Q1 2021 Fate Therapeutics Inc Earnings Call

[music].

Good day, ladies and gentlemen.

Operator: and welcome to the fate therapeutics first quarter 2021 financial results conference call. This call is being webcast live on the investors section of fate.com

Welcome to the fate Therapeutics first quarter 2021 financial results Conference call. This call is being webcast live on the investors section of feet.

Operator: A Fate Therapeutics website at fatetherapeutics.com at this

<unk> Therapeutics website at fate Therapeutics Dot com at this time all participants are in a listen only mode. Later, we will conduct a question and answer session and instructions will follow at the time if anyone should require operator assistance. Please press Star then one sorry.

Operator: At this time, all participants are in a listen-only mode. Later, we will conduct a question-and-answer session.

Operator: And instructions will follow at the time. If anyone should require operator assistance, please press star 1.

Operator: Please press star, then 1. Sorry, press star zero on your touch tone phone. As a reminder, this call will be recorded. I will now turn the call over to Scott Walshco, President and CEO of Fate Therapeutics. Scott, you may.

Sorry Press Star Zero on your Touchtone phone as a reminder, this call will be recorded I will now turn the call over to Scott Washco, President and CEO of fate Therapeutics, Scott you may begin.

Scott Walshco: Thank you. Good afternoon, and thanks, everyone, for joining us for the Fate Therapeutics first quarter 2021 financial results call. Shortly after 4 p.m. Eastern Time today, we issued a press release with these results, which can be found on the Investors section of our website under Press Release. In addition, our Form 10-Q for the quarter-ended March 31, 2021, was filed shortly thereafter and can be found on the Investors section of our website under Financial Information.

Thank you good afternoon, and thanks, everyone for joining us for the fate Therapeutics first quarter 2021 financial results call.

Shortly after four P M. Eastern time today, we issued a press release with these results, which can be found on the investors section of our website under press releases. In addition, our form 10-Q for the quarter ended March 31, 2021 was filed shortly thereafter and can be found on the investors section of our <unk>.

Website under financial information.

Scott Walshco: Before we begin, I would like to remind everyone that, except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements.

Before we begin I would like to remind everyone that except for statements of historical facts. The statements made by management and responses to questions. On this conference call are forward looking statements under the Safe Harbor provisions of the private Securities Litigation Reform Act of 1095.

These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward looking statements.

Scott Walshco: Please see the forward-looking statement disclaimer in the company's earnings press release issued after the close of market today, as well as the risk factors included in our Form 10-Q for the quarter ended March 31, 2021 that was filed with the SEC. Undue reliance should not be placed on forward-looking statements, which speak only as of the date they are made, as facts and circumstances underlying these forward-looking statements may change. Except as required by law, Fate Therapeutics disclaims any obligation to update these forward-looking statements to reflect future information, events, or circumstances.

Please see the forward looking statement disclaimer on the company's earnings press release issued after the close of market today as well as the risk factors included in our form 10-Q for the quarter ended March 31, 2021 that was filed with the SEC today.

Undue reliance should not be placed on forward looking statements, which speak only as of the day. They are made as facts and circumstances underlying these forward looking statements may change.

Sept as required by law fate therapeutics disclaims any obligation to update these forward looking statements.

<unk> future information events or circumstances.

Scott Walshco: Joining me on today's call are Dr. Wayne Hsu, our Senior Vice President of Clinical Development, Ed Dulac, our Chief Financial Officer, and Bob Valamehr, our Chief Research and Development Officer. Today, we will highlight our clinical progress and plans for each of our disease franchises, including our plans to share interim clinical data for off-the-shelf, IPS-derived NK cell programs in acute myeloid leukemia and in B We will also discuss the expansion of our FT538 program into solid tumors, where our IND application was recently approved by the FDA for the conduct of a multi-dose, multi-cycle, phase one clinical trial in combination with certain monoclonal antibodies targeting tumor-associated antigens, EGFR, HER2, and PD-L1.

Joining me on today's call our Doctor Wayne Chu, our senior Vice President of clinical development, Ed do Lark, our Chief Financial Officer, and Bob <unk>, Our Chief Research and development Officer.

Today, we will highlight our clinical progress and plans for each of our disease franchises, including our plans to share interim clinical data for off the shelf Ips derived NK cell programs in acute myeloid leukemia and in B cell malignancies.

We will also discuss the expansion of our ft, $5 38 program into solid tumors, where our R&D application was recently allowed by the FDA for conduct of a multi dose multi cycle phase one clinical trial in combination with certain monoclonal antibodies.

Getting the tumor targeting tumor associated antigens egfr her two and PDL one.

Scott Walshco: This marks the 12th IND allowed by the FDA for our IPSC product platform, alongside the 24th annual American Society of Gene and Cell Therapy meeting being held virtually next week. We plan to share interim phase one clinical data for FT516 and FT538 programs in relapsed refractory AML. We believe this clinical update will be insightful on multiple fronts.

This marks the 12th IMD allowed by the FDA for our <unk> product platform.

Alongside the 24th annual American Society of Gene and cell therapy meeting being held virtually next week, we plan to share interim phase one clinical data for ft, 516 ft, $5 38 programs in relapsed refractory AML.

We believe this clinical update will be insightful on multiple fronts.

Scott Walshco: For example, there is clinical precedent across numerous single-center, investigator-initiated academic studies that donor NK cells can drive anti-leukemic activity. However, these approaches rely on the use of NK cells that are matched to the patient, that are manufactured solely for that patient, and that are delivered to that patient in a hospital setting following intensive conditioning therapy. FT-516 and FT-538 are iPSC-derived and K-cell product candidates that are administered off-the-shelf, in the outpatient setting, and without patient care.

For example, there is clinical precedent across numerous single center investigator initiated academic studies that donor NK cells can drive anti leukemic activity.

However, these approaches rely on the use of NK cells that are matched to the patient that are manufactured solely for that patient and that are delivered to that patient in a hospital setting following intensive conditioning therapy.

$5 16, an FTE $5 38, our Ips derived NK cell product candidates that are administered off the shelf in the outpatient setting and without patient matching.

Scott Walshco: Additionally, these Phase I clinical studies of FT-516 and FT-538 are designed to assess the inherent capacity of the product candidate to target and kill leukemic blasts as a monotherapy. As we have shown, encouraging phase 1 clinical data of FT-516 in combination with rituximab in relapsed refractory B-cell lymphoma. We believe there is an opportunity to build off of this foundation and combine it with ADCC-competent monoclonal antibodies in relapsed refractory AML.

Additionally, these phase one clinical studies of Ft 516 in Ft, 538 are designed to assess the inherent capacity of the product candidate to target and kill leukemic blasts as a mono therapy as.

As we have shown encouraging phase one clinical data of ft 516 in combination with Rituximab in relapsed refractory B cell lymphoma. We believe there is an opportunity to build off of this foundation and combine with ADC competent monoclonal antibodies in relapsed refractory.

Scott Walshco: To this end, an investigator-initiated study of FT538 in combination with daratumab designed to target CD38 positive leukemic blasts and further enhance anti-leukemic activity is expected to begin later this year. Finally, although patients have been treated in the first dose cohort only with FT538, we are assessing early translational observations that might indicate whether FT538, with its additional engineered modalities, has superior Patients with relapsed refractory AML often have high leukemic blast burns, prolonged impairment of hematopoietic function, and exceptionally poor output.

AML.

To this end an investigator initiated study of <unk> $5 38 in combination with Dara two mab designed to target CD 38 positive leukemic blasts and further enhance anti leukemic activity is expected to begin later this year.

Finally, although patients have been treated in the first dose cohort only with ft. $5 38, we are assessing early translational observations that might indicate whether ft 538 with its additional engineered modalities has superior functionality.

<unk> two ft 516.

Patients with relapsed refractory AML, often have high leukemic blast burden.

Prolonged impairment of hematopoietic function and exceptionally poor outcomes.

Scott Walshco: Median overall survival rates are less than 6 months, and 5-year overall survival rates are 10-15%. The only proven curative therapy is allogeneic stem cell transplants. However, many patients are often ineligible due to their leukemic burden or not deemed fit to tolerate the procedure due to the intensity of chemotherapy. There is a significant need for therapies that can clear the bone marrow of leukemic blasts, which can enable patients to qualify for allogeneic transplant or can enable a durable response without further therapy.

Median overall survival rates are less than six months and five year overall survival rates are 10% to 15%.

The only proven curative therapy is allogeneic stem cell transplant. However, many patients are often in eligible due to their leukemic burden or not deemed fit to tolerate the procedure due to the intensity of chemotherapy conditioning.

There is a significant need for therapies that can clear the bone marrow of leukemic blasts, which can enable patients to qualify for allogeneic transplant or can enable a durable response without further therapy.

Scott Walshco: For example, a recent study in relapsed refractory AML showed that patients achieving an initial response per the 2017 ELN response criteria, defined as either achieving a complete response, CR, a complete response with incomplete hematologic recovery, CRI, or a morphologic leukemia-free state, MLFS, had statistically significant improvement in overall survival. Given the significant unmet need for patients with AML, several therapies have been approved in recent years based on single-arm studies demonstrating response rates of 20% to 30% with 8 to 12 months median duration of response.

For example, a recent study in relapsed refractory AML showed that patients achieving an initial response per the 2017 <unk> criteria defined as either achieving a complete response CR.

<unk> response, with incomplete hematologic recovery, Cri or morphologic leukemia free state MLR FES.

Had statistically significant improvement in overall survival.

Given the significant unmet need for patients with AML. Several therapies have been approved in recent years based on single arm studies, demonstrating response rates of 20% to 30% with eight to 12 months median duration of response. These include therapies designed to target specific mute.

Scott Walshco: These include therapies designed to target specific mutations that cause bone marrow dysfunction, such as IDH1, IDH2, and FLT3 inhibitors. Emerging therapies, including T-cell engagers in CAR T-cells, have also shown similar response rates in early phase tests. However, significant toxicities have been reported, including rates of cytokine release syndrome in excess of 50 percent. In many respects, our interest in off-the-shelf IPS-derived NK cell therapy dates back to conversations in early 2015 with Dr. Jeff Miller, professor of medicine at the University of Minnesota and deputy director of the Masonic Cancer Center, and Dr. Sarah Cooley, who was at the time a leading clinical investigator in the emerging field of NK cell therapy at the University of Minnesota and now is senior vice president of translational medicine at Fate Therapeutic

Patients that cause bone marrow dysfunction, such as <unk>, <unk> and flit three inhibitors.

Emerging therapies, including T cell engages in car T cells have also shown similar response rates in early phase testing, however, significant toxicities have been reported including rates of cytokine release syndrome in excess of 50%.

In many respects our interest in off the shelf Ips derived NK cell therapy dates back that conversation in early 2015 with Dr. Jeff Miller Professor of Medicine University of Minnesota, and Deputy director of the Masonic Cancer Center and Dr. Sarah Cooley, who was at the time of leading clinics.

Investigator in the emerging field of NK cell therapy at the University of Minnesota, and now as senior Vice President Translational medicine at fate Therapeutics doctors Miller and coolly, we're conducting studies using ex vivo cytokines activated peripheral blood NK cells to treat patients with <unk>.

Refractory AML with the goal of bridging patients to transplant.

In single Center investigator initiated academic studies ex vivo cytokines activated donor NK cell therapy has shown responses of 20% to 35%, including an studies run by doctors Miller on coolly.

And while we believe these response rates are comparable to recently approved therapies significant challenges have limited clinical advancement of donor NK cell therapy. For example, the current paradigm of donor NK cell therapy resembles a transplant like process.

Scott Walshco: Doctors Miller and Cooley were conducting studies using ex vivo cytokine-activated peripheral blood NK cells to treat patients with relapsed refractory AML with the goal of bridging patients to transplant. In single-center investigator-initiated academic studies, ex vivo cytokine-activated donor and K-cell therapy has shown responses of 20 to 35 percent, including in studies run by Drs. Miller and Miller.

Patients are hospitalized.

<unk> intense lymphoma depleting chemotherapy.

And are administered NK cells from donors that are specifically manufactured for and matched to the patient.

Additionally, very large numbers of NK cells, often times in excess of several billion cells per dose on.

Scott Walshco: And while we believe these response rates are comparable to recently-approved therapies... Significant challenges have limited clinical advancement of donor NK cell therapy. For example, the current paradigm of donor and case cell therapy resembles a transplant-like process. Patients are hospitalized, receive intense lympho-depleting chemotherapy, and are administered NK cells from donors that are specifically manufactured for and matched to the patient. Additionally, very large numbers of NK cells, oftentimes in excess of several billion cells per dose, are required to be administered to patients to achieve a response.

Are required to be administered to patients to achieve responses and production of such large numbers of NK cells, often necessitates weeks of complex manufacturer, while the patient remains untreated and is at high risk for disease progression.

In contrast, our ft 516 in Ft, $5 38 programs are off the shelf Ips derived cell products, which are available on demand for administration in the outpatient setting without patient matching and therefore have the potential to efficiently and effectively.

Many patients with AML.

The phase one study of <unk> as a monotherapy has enrolled the first and second dose cohorts of $90 million and 300 million cells per dose.

Scott Walshco: And production of such large numbers of NK cells often necessitates weeks of complex manufacture while the patient remains untreated and is at high risk for disease progression. In contrast, our FT-516 and FT-538 programs are off-the-shelf, IPS-derived sell-products that are available on demand for administration in the outpatient setting with outpatient matching, and therefore have the potential to efficiently and effectively treat many patients with AMI.

And dose escalation is ongoing with enrollment in the third dose cohort of 90 million cells per dose.

The phase one study of Ft 538, as a mono therapy is ongoing with enrollment in the first dose cohort of 100 million cells per dose.

As a reminder, AML is a very heterogeneous disease and patient outcomes do vary depending on cytogenetics mutation status and leukemic burden.

Key objectives in dose escalation, our safety of our engineered Ips derived NK cell products tolerability of the off the shelf multi dose treatment schedule.

<unk> anti leukemic activity, including in consideration of patient and disease baseline characteristics.

Scott Walshco: The Phase I study of FT516 as a monotherapy has enrolled the first and second dose cohorts of 90 million and 300 million cells per dose, and dose escalation is ongoing with enrollment in the third dose cohort of 90 million cells per dose. The Phase I study of FT538 as a monotherapy is ongoing, with enrollment in the first dose cohort of 100 million cells per dose. As a reminder, AML is a very heterogeneous disease, and patient outcomes do vary depending on cytogenetics, mutation status, and leukemic burden.

Certainly we will consider objective responses in dose escalation based on the established 2017, <unk> response criteria, which is broadly accepted as the gold standard for assessing AML patient outcomes as encouraging evidence that our off the shelf IP.

<unk> derived NK cell franchise may hold therapeutic promise for patients with AML.

We are also interested in early translational comparisons between ft 516 in FTE $5 38.

Scott Walshco: Key objectives in dose escalation are the safety of our engineered, IPS-derived NK cell products, tolerability of the Off-the-Shelf Multi-Dose Treatment Schedule, and Anti-Leukemic Activity, including in consideration of patient and disease baseline characteristics. Certainly, we will consider objective responses in dose escalation based on the established 2017 ELN response criteria, which is broadly accepted as the gold standard for assessing AML patient outcomes, as encouraging evidence that our off-the-shelf, IPS-derived, and K-Cell franchise may hold therapeutic promise for patients with AMS.

At our feature symposium at AST GCT. Dr. Miller is scheduled to highlight the unique properties of <unk> $5 38, resulting from the deletion of the CD 38 gene and.

In preclinical models, the engineered functionality of ft, $5 38 in parts metabolic transcriptional and functional properties that are substantially similar to those of adaptive NK cells, a discreet subset of memory like NK cells that exhibit increased cytokine production.

<unk> enhanced persistence resistance to oxidative stress and potent cereal cytotoxicity.

We look forward to reviewing early clinical data of our Ft 538 program that might indicate whether it's engineered functionality confers superior therapeutic advantages.

Scott Walshco: We are also interested in early translational comparisons between FT-516 and FT-538. At a feature symposium at ASGCT, Dr. Miller is scheduled to highlight the unique properties of FT538 resulting from the deletion of the CD38. In preclinical models, the engineered functionality of FT538 imparts metabolic, transcriptional, and functional properties that are substantially similar to those of adaptive NK cells, a discrete subset of memory-like NK cells that exhibit increased cytokine production, enhanced persistence, resistance to oxidative stress, and potent serial cytotoxicity.

At the 2021 American Society of clinical oncology annual meeting being held virtually from June <unk> through the eighth.

We plan to present, new clinical data from our phase one study of <unk> hundred 16 in combination with Rituximab for the treatment of relapsed refractory B cell lymphoma, we believe the interim phase one clinical data of Ft 516 in combination with Rituximab previous.

We presented at our Investor event in December were compelling and suggest that ft 516 can be administered in the outpatient setting.

The high affinity non cleavable CD 16 receptor of Ft, 516 can effectively synergize with <unk> with Rituximab in patients that have relapsed following or are refractory to rituximab containing regimens ft 516 may have a differentiate it.

Scott Walshco: We look forward to reviewing early clinical data of our FT538 program that might indicate whether its engineered functionality confers superior therapeutic advantages at the 2021 American Society of Clinical Oncology Annual Meeting being held virtually from June 4th through the 8th.

Safety profile.

Compared to T cell based therapies, including T cell engaging <unk> and car T cell therapies and Ft 516 may confer rates of response in relapsed refractory B cell lymphoma that are similar to those of T cell based therapies.

The <unk> presentation will cover a total of 13 patients that have completed dose escalation at the first three dose levels of 300 million cells 900 million cells and 300 million cells per dose.

Scott Walshco: We plan to present new clinical data from our phase one study of FT516 in combination with rituximab for the treatment of relapsed refractory B-cell lymphoma. We believe the interim Phase I clinical data of FT516 in combination with rituximab previously presented at our investor event in December were compelling and suggest that FT516 can be administered in the outpatient setting. The high-affinity, non-cleavable CD16 receptor of FT5-16 can effectively synergize with rituximab in patients that have relapsed following or are refractory to rituximab-containing regimens.

Note that the Ft 516 clinical protocol does allow for patient backfill in the event of dose level has cleared toxicity and shown activity.

That more than three patients may be enrolled at a given dose level.

Dose escalation in our phase one study is currently ongoing with enrollment at 900 million cells per dose. We are preparing to initiate multiple dose expansion cohorts. We are also preparing to explore combinations of ft 516 with standard of care.

<unk> containing CD 20 targeted therapy and without Cy flew chemotherapy conditioning to assess its therapeutic potential in earlier lines of therapy.

Scott Walshco: FT 516 may have a differentiated safety profile compared to T-cell based therapies, including T-cell engagers and CAR T-cell therapy, and FT-516 may confer rates of response in relapsed refractory B-cell lymphoma that are similar to those of T-cell based therapy. The ASCO presentation will cover a total of 13 patients that have completed dose escalation at the first three dose levels of 300 million cells, 900 million cells, and 300 million cells per dose.

We continue to be pleased with the progress in our phase one clinical trial of Ft 596 are off the shelf Ips derived car NK cell product candidate designed to target multiple antigens through its high affinity non cleavable CD 16 receptor and its CD 19 targeted.

Car.

And approach that we believe may hold best in class potential for the treatment of B cell malignancies.

<unk> escalation in our phase one study of <unk> hundred 96 is ongoing with enrollment in the third single dose cohorts of 300 million cells as mono therapy and debt 300 million cells in combination with Rituximab for B cell lymphoma.

Scott Walshco: Note that the FT-516 clinical protocol does allow for patient backfill in the event a dose level has cleared toxicity and shown activity, so that more than three patients may be enrolled at a given dose level. Dose escalation in our Phase 1 study is currently ongoing with enrollment at 900 million cells per dose, and we are preparing to initiate a multiple-dose expansion cohort.

As well as in the first single dose cohort of 30 million cells as mono therapy for chronic lymphocytic leukemia.

We plan to begin enrollment in combination with <unk> upon clearance of this first mono therapy dose cohort in CLO.

Scott Walshco: We're also preparing to explore combinations of FT516 with standard of care regimens containing CD20 targeted therapy and without CyFlu chemotherapy conditions to assess its therapeutic potential in earlier-line therapy. We continue to be pleased with the progress in our Phase 1 clinical trial of FT596, an off-the-shelf iPSC-derived CAR and K-cell product candidate designed to target multiple antigens through its high-affinity non An approach that we believe may hold best-in-class potential for the treatment of B-cell malignancies.

In addition, since we believe that relapsed refractory patients with aggressive cancers will be best served by administration of multiple doses during the first weeks of treatment we.

We have now submitted a protocol amendment to enable multi dose treatment schedules for ft 596. In addition to the current single dose treatment schedule.

We plan to introduce the multi dose treatment schedule in each of the four regimens at the highest dose level cleared for the single dose treatment schedule in that particular regimen.

In late July early August we plan to hold an investor event to feature our Ft, 596 program, where we expect to share interim phase one clinical data covering approximately 20 patients.

Scott Walshco: Dose escalation in our Phase 1 study of FT596 is ongoing with enrollment in the third single-dose cohort of 300 million cells as monotherapy and at 300 million cells in combination with rituximab for B-cell lymphoma, as well as in the first single-dose cohort of 30 million cells as monotherapy for chronic lymphocytic leukemia. We plan to begin enrollment in combination with ibinitu In addition, since we believe that relapsed refractory patients with aggressive cancer will be best served by the administration of multiple doses during the first weeks of treatment.

In the second quarter, we expect to initiate clinical investigation of our Ips C product platform in multiple myeloma.

Similar to our approach in lymphoma, we are beginning clinical investigation in multiple myeloma by leveraging our high affinity non cleavable CD 16 receptor and we're combining ft $5 38, with Dara two mab to maximize ADC.

While Dara to map effectively targets CD 38 expressed on myeloma cells and induces cell death.

It also induces NK cell fracture side, which significantly impairs the effectiveness of ADC.

In addition, NK cell function is often impaired in patients with multiple myeloma.

Further reducing the potential therapeutic activity of <unk>.

Scott Walshco: We have now submitted a protocol amendment to enable multi-dose treatment schedules for FT596 in addition to the current single-dose treatment schedule. We plan to introduce the multi-dose treatment schedule in each of the four regimens, at the highest dose level cleared for the single dose treatment schedule in that particular regimen.

Collectively preclinical and clinical observations suggest a potential therapeutic benefit of maintaining NK cell numbers and function.

Enrollment of <unk> $5 38 in combination with Dara <unk> will commence at 100 million cells per dose.

We are also preparing to initiate a phase one clinical trial of <unk> hundred 76 are off the shelf Ips derived car NK cell product candidate designed to target multiple antigens through its high affinity non cleavable, CD 16 receptor and its <unk> targeted car and.

Scott Walshco: In late July or early August, we plan to hold an investor event to feature our FT-596 program, where we expect to share interim Phase I clinical data covering approximately 20 patients. In the second quarter, we expect to initiate clinical investigation of our IPSC product platform in multiple myelomas. Similar to our approach in lymphoma, we are beginning clinical investigation in multiple myeloma by leveraging our high affinity non-cleavable CD16 receptor, and we are combining FT538 with Dora2Mab to maximize ADCC.

<unk> that we believe may hold best in class potential for the treatment of multiple myeloma.

At the American Association for Cancer Research annual meeting in April we presented preclinical data demonstrating that the multi antigen targeting functionality of ft 507, six exhibits greater in vivo efficacy compared to the combination of <unk>.

CMA targeted car T cells, and a gamma secretase inhibitor.

The clinical protocol for a phase one clinical trial of <unk> hundred 76 includes dose escalation, both as monotherapy and in combination with Dara to map to enable dual antigen targeting of <unk> and <unk> 38 on myeloma cells.

Scott Walshco: While DARA2MAP effectively targets CD38 expressed on myeloma cells and induces cell death, it also induces NK cell fracture, which significantly impairs the effectiveness of ADC. In addition, NK cell function is often impaired in patients with multiple myeloma, further reducing the potential therapeutic activity of ADC. Collectively, preclinical and clinical observations suggest a potential therapeutic benefit of maintaining NK cell numbers and function.

Additionally, the protocol includes assessment of both single dose and multi dose treatment regimens to maximize the therapeutic index. During the first 30 days following infusion.

As I mentioned during our last quarterly update we are enthusiastic about the potential of NK cells to treat a wide range of solid tumors.

And we are pleased with the progress we are making in building our pipeline of off the shelf multiplexed engineered product candidates.

Scott Walshco: Enrollment of FT538 in combination with daratumab will commence at 100 million cells per dose. We are also preparing to initiate a Phase I clinical trial of FT576. Our off-the-shelf IPS-derived CAR and K-cell product candidate designed to target multiple antigens through its high-affinity non-cleavable CD16 receptor and its BCMA-targeted CAR, an approach that we believe may hold best-in-class potential for the treatment of multiple myeloma.

An initial therapeutic strategy of particular interest to us is exploiting ADC, which is a potent anti tumor mechanism by which NK cells recognize bind and kill antibody coated cancer cells, and which has been shown to improve progression free survival.

In patients with solid tumors.

However, significant limitations in the functional capacity of a patients NK cells, which are often depleted a number or impaired including through CD 16, shedding can compromise the potency of <unk> ADC in patients with solid tumors.

Scott Walshco: At the American Association for Cancer Research annual meeting in April, we presented preclinical data demonstrating that the multi-antigen targeting functionality of FT576 exhibits greater in vivo efficacy compared to the combination of BCMA-targeted CAR T-cells and agamase secretase inhibitors. The clinical protocol for a Phase I clinical trial of FT576 includes dose escalation, both as monotherapy and Additionally, the protocol includes assessment of both single-dose and multi-dose treatment regimens to maximize the therapeutic index during the first 30 days following infection.

We believe a off the shelf administration of an ADC optimized NK cell can augment the activity of monoclonal antibodies that are currently approved for the treatment of many solid tumors to this end. We are currently enrolling patients in the third dose cohort of our phase one.

Study of Ft, 516 in combination with a value mab and <unk> ADC competent anti PD lone checkpoint inhibitor therapy.

I am pleased to announce today that we are significantly expanding on this therapeutic strategy.

Last month, the FDA allowed our IND application for clinical investigation of Ft 538 in combination within our array of monoclonal antibodies, including those that target the tumor associated antigens Egfr her two and PDL one.

Scott Walshco: As I mentioned during our last quarterly update, we are enthusiastic about the potential of NK cells to treat a wide range of solid tumors, and we are pleased with the progress we are making in building our pipeline of off-the-shelf, multiplexed engineered products.

This marks the 12th IND allowed by the FDA for our Ips C product platform.

Under the clinical protocol each patient is eligible to receive up to two ft 538 treatment cycles.

Scott Walshco: An initial therapeutic strategy of particular interest to us is exploiting ADC, which is a potent anti-tumor mechanism by which NK cells recognize, bind, and kill antibody-coded cancer cells, and which has been shown to improve progression-free survival in patients with solid tumors. However, significant limitations in the functional capacity of a patient's NK cells, which are often depleted in number or impaired, including through CD16 shedding, can compromise the potency of ADCC in patients with solid tumors. We believe off-the-shelf administration of an ADCC-optimized NK cell can augment the activity of monoclonal antibodies that are currently approved for the treatment of many solid tumors.

With each cycle, consisting of three days of outpatient linfield conditioning, three once weekly infusions of ft, $5, 38, and monoclonal antibody therapy.

We intend to initiate clinical investigation of three independent regimens, combining ft 538, with Egfr targeted cetuximab her two targeted trastuzumab and PDL, one targeted <unk> and we expect to initiate enrollment in the second half of 'twenty.

'twenty one.

Finally, I would like to take a moment and sincerely. Thank the patients caregivers and investigators who participated in the protect study of programming.

While our full attention and resources are focused on our deep pipeline of off the shelf Ips derived cancer Immunotherapies. We are disappointed to announce that the protect study did not meet its primary endpoint of prevention of acute graft versus host disease following allogeneic stem.

Scott Walshco: To this end, we are currently enrolling patients in the third dose cohort of our phase one study of FT5-16 in combination with Aveliumab, an ADCC-competent anti-PD-L1 checkpoint inhibitor therapy. I am pleased to announce today that we are significantly expanding on this therapeutic strategy. Last month, the FDA approved our IND application for clinical investigation of FT538 in combination with an array of monoclonal antibodies, including those that target the tumor-associated antigens EGFR, HER2, and PD-L1.

Cell transplant, and we will stop all further development of premium.

We intend to share the clinical results of the protect study with our investigators and the broader transplant community to assist in their continuing efforts to improve the curative potential of allogeneic transplant for patients.

I would now like to turn the call over to Ed to highlight our first quarter financial results.

Scott Walshco: This marks the 12th IND allowed by the FDA for our IPSC product platform. Under the clinical protocol, each patient is eligible to receive up to two FT-538 treatment cycles, with each cycle consisting of 3 days of outpatient lymphoconditioning, 3 once-weekly infusions of FT538, and monoclonal antibody therapy. We intend to initiate clinical investigation of three independent regimens, combining FT-538 with EGFR-targeted cetuximab, HER2-targeted tristuzumab, and PD-L1-targeted evalumab, and we expect to initiate enrollment in the second half of 2020.

Thank you Scott turning to our financial results revenue was $11 1 million for the first quarter of 2021 compared to $2 5 million for the same period last year.

Revenue in the current quarter was derived from our collaboration with Janssen and Ono Pharmaceuticals.

Research and development expenses for the first quarter of 2021 for $44 $9 million compared to $29 3 million for the same period last year the.

The increase in our R&D expenses was attributable primarily to an increase in employee head count and compensation, including share based compensation and <unk> expenses associated with clinical trial costs.

General and administrative expenses for the first quarter of 2021 were $12 5 million compared to $7 7 million from the same period last year.

Scott Walshco: Finally, I would like to take a moment and sincerely thank the patients, caregivers, and investigators who participated in the PROTECT study of protein. While our full attention and resources are focused on our deep pipeline of off-the-shelf IPS-derived cancer immunotherapies, we are disappointed to announce that the PROTECT study did not meet its primary endpoint of prevention of acute graft-first host disease following allogeneic stem cell transplant, and we will stop all further development approaches.

The increase in our G&A expenses was attributable primarily to an increase in head count and employee compensation, including share based compensation.

Total operating expenses for the first quarter of 2021 were $44 $4 million net of $13 million and noncash share based compensation expense.

In the first quarter, we recorded a noncash zero point $7 million non operating benefit associated with the fair value of contingent milestone payments under our Ips derived car T cell collaboration with Memorial Sloan Kettering.

In the event a certain clinical milestone is achieved with an Ips derived car T cell product candidate up to three milestone payments may be owed to MSA based on subsequent trading values of the company's common stock ranging from 50 to $150 per share.

Scott Walshco: We intend to share the clinical results of the PROTECT study with our investigators and the broader transplant community to assist in their continuing efforts to improve the curative potential of allogeneic transplantation for patients. I would now like to turn the call over to Ed to highlight our first quarter financial results.

These milestone payments in the aggregate total up to $75 million and no amounts have been paid or are currently owed to Ms. Kay.

Edward J. Dulac: Thank you, Scott. Turning to our financial results, revenue was $11.1 million for the first quarter of 2021, compared to

We will re measure of this liability currently valued in the aggregate at $47 million on a quarterly basis.

And changes in the fair value will be recorded in our earnings as a non operating income or expense.

Edward J. Dulac: 2021, compared to $2.5 million for the same period last year. Revenue in the current quarter was derived from our collaborations with Janssen and Ono Pharmaceutical.

In January we completed a public offering of common stock whereby we issued five 1 million common shares.

In addition in lieu of common stock, we issued 257 pre funded warrants.

Edward J. Dulac: Research and development expenses for the first quarter of 2021 were $44.9 million, compared to $29.3 million for the same period last year. The increase in our R&D expenses is attributable primarily to an increase in employee headcount and compensation, including share-based compensation, and in expenses associated with clinical trial costs. General and administrative expenses for the first quarter of 2021 were $12.5 million, compared to $7.7 million for the same period last year. The increase in our G&A expenses was attributable primarily to an increase in headcount and employee compensation, including share-based compensation.

The net proceeds from the financing were approximately $432 million.

The company ended the first quarter of 2021 with $888 million of cash cash equivalents and investments.

Common stock outstanding was 94 million shares and preferred convertible stock outstanding was $2 8 million shares each of which is convertible into five shares of common stock under certain conditions.

I would now like to open the call up to any questions.

Thank you, ladies and gentlemen, Hey, do you have a question at this time. Please press Star then the one on you touched on phone. If your question has been answered or you wish to remove yourself from the queue. Please press the pound key.

And we do have our first question from Robyn.

So im curious securities.

Yeah.

Robyn if debt.

Edward J. Dulac: Total operating expenses for the first quarter of 2021 were $44.4 million, net of $13 million in non-cash, share-based compensation expense. In the first quarter, we recorded a non-cash $0.7 million non-operating benefit associated with the fair value of contingent milestone payments under our IPSC-derived CAR T-cell collaboration with Memorial Sloan Kettering. In the event that a certain clinical milestone is achieved with an IPSC-derived CAR T-cell product candidate, up to three milestone payments may be owed to MSK based on the subsequent trading values of the company's common stock, ranging from 50 to $150 per share.

Good day count slightly Robyn thanks for taking my question and so much on the call.

Let's just start off net.

Next week, and then you have a lot of data coming.

You talked that you update us on the call you talked about yet.

Kate on FTC.

Non cyclical lucky.

Slide 38.

Maybe you can give us some color about the patient baseline how many patients what we see how many doses.

Hmm.

We'll.

See them treated with and how should we think about your strategy in ammo.

On the Big picture, how do we digest this data and how do we set the expectation Platt Inc.

Sure.

So Robyn I mean, we will have a fairly comprehensive event from now I think it's next Thursday, so seven to eight days from now we'll have a fairly comprehensive event.

We'll walk through.

What has historically been done with respect to NK cell treatment in AML.

Edward J. Dulac: These milestone payments in the aggregate total up to $75 million, and no amounts have been paid or are currently owed to MSK. We will remeasure this liability, currently valued in the aggregate at $47 million, on a quarterly basis, and changes in the fair value will be recorded in our earnings as a non-operating income or expense. In January, we completed a public offering of common stock, whereby we issued 5.1 million common shares.

We will provide some detail on the preclinical results that we have seen for instance, with ft 538, including comparing ft $5 38 to <unk> 16.

And then Wayne will spend a significant amount of time walking through.

The history of patients that we've treated you will see patients.

On a patient you'll see detail on a patient by patient basis. So we plan on providing the detail for each and every patient and you will see baseline characteristics you will see whether that patient is relapsed to refractory you will see most recent therapy you will see.

Edward J. Dulac: In addition, in lieu of common stock, we issued 257,000 pre-funded warrants. The net proceeds from the financing were approximately $432 million. The company ended the first quarter of 2021 with $888 million of cash, cash equivalents, and investment. Common stock outstanding was 94 million shares. And preferred convertible stock outstanding was 2.8 million shares, each of which is convertible into five shares of common stock under certain conditions. I would now like to open the call to any questions.

This.

For instance, risk profile associated with each and every patient and then importantly, you will obviously see anti leukemic activity and responses associated with each and every patient. So there will be a tremendous amount of detail there will be it will be very transparent on a patient by patient basis and we expect to include in that about in total 12 patients.

And strategy in solid tumors.

I mean going forward, that's a big one for yes, sorry, more clarity there and excited about that.

On a strategy in solid tumors, absolutely I mean, clearly we think there are multiple monoclonal antibodies that are improved in solid tumors for instance, whether it be herceptin herbs.

<unk> others.

And part of their mechanism of action is dependent on antibody dependent cellular cytotoxicity ADC and we think NK cells play a really important role there. We actually think there is plenty of evidence to suggest that ADC today is not being optimized that the NK cell <unk>.

Operator: Thank you. Ladies and gentlemen, if you have a question at this time, please press star, then the number on your touchtone phone. If your question has been answered, or you wish to remove yourself from the queue, please press the pound key.

<unk> essentially that exist within patients.

Operator: And we do have our first question from Robin from Truist Securities. Thanks for taking my question, and so much on the call. So, let's just start off with, you know, next week, and then you have a lot of data coming. You've talked about, you updated on the call, you talked about how you updated on FT6516 and FT538. Maybe you could give us some color about the patient baseline, how many people...

His check to or compromised.

That by coming in with a wave of NK cells better designed to synergize with the monoclonal antibody. We think we can substantially augment responses. That's step one and we are started to initiate that obviously with ft 516.

Obviously, increasing our investment based on our conviction in ADC by moving Ft, 538, now into solid tumors across a fairly broad set of monoclonal antibodies in solid tumors.

Operator: How many patients will we see? How many doses?

Ultimately, though as you know we think of that as a stepping stone.

Operator: What will we see them treated with and how do we think about your strategy and ML? Sort of the big picture; how do we digest this data, and how do we set the expectations for it? Thanks.

What we're doing for instance in lymphoma, what we're doing in myeloma, where were utilizing for instance, CD 16. In addition to engineered car functionality. We are doing the same exact thing in solid tumors, where we have product candidates are emerging in the <unk>.

Scott Walshco: So, Robin, I mean, we will have a fairly comprehensive event from now on. I think it's next Thursday, so seven, eight days from now, we'll have a fairly comprehensive event.

Second half of this year.

Building off of the Ft, $5 38, backbone engineering and cars for instar first IMD will be engineering, a car against the MC gain mcbee stress ligands. We recently presented data where we the engineered in a car into the ft 538 backbone against <unk> three.

Scott Walshco: We will walk through what has historically been done with respect to NK cell treatment in AML. We will provide some detail on the preclinical results that we have seen, for instance, with FT-538, including comparing FT-538 to FT-516. And then Wayne will spend a significant amount of time walking through the history of patients that we've treated. You will see patients, on a patient-by-patient basis. So we plan on providing details for each and every patient, and you will see baseline characteristics.

Re as a solid tumor targeting strategy and in addition, we expect that the first IND actually under the Janssen collaboration will be a car NK cell product for solid tumors.

Alright, Thanks, again, you've mined blown me about how many different product lines.

I don't know all day, but thank you so much I appreciate it.

Sure.

And we do have our next question.

Net 10 half Piper Sandler.

And what's the total Hudson.

I'm on a call up a little bit.

<unk> net we're going to help your event later this year and more datasets.

Scott Walshco: You will see whether that patient is relapsed or refractory. You will see the most recent therapy. You will see, for instance, the risk profile associated with each and every patient. And then, importantly, you will obviously see anti-leukemic activity and responses associated with each and every patient. So there will be a tremendous amount of detail. There will be, and it'll be very transparent on a patient by patient basis. And we expect to include them in that.

With all of these different approaches of the solid tumor side, how do you ultimately envisioned this playing at all do you expect growth there will be certain cell types.

That may be better and different kinds of cancers with different kinds of <unk>.

Through the combinations.

Ultimately see a penalty on that product like submit J mcbee.

Give us a little bit more color on sort of where your thinking is there. Thank you.

Sure.

I think it's early for us to have a definitive strategy and solid tumors with multiplexed engineered cell therapy since.

We are breaking new ground I do think generally there are certain solid tumors that may actually be more amenable to NK cell therapy, we've talked in the past for instance that there are various mechanisms of resistance.

Scott Walshco: and Strategy and Policy. I mean, going forward, that's a big one for you. Yeah, no, sorry. More clarity there.

Scott Walshco: Adopting solid tumors? Absolutely.

Scott Walshco: I mean, clearly, we think there are multiple monoclonal antibodies that are improved in solid tumors, for instance, whether it be Herceptin, Erbitux, Avelumab, others. And, you know, part of their mechanism of action is dependent on antibody-dependent cellular cytosine toxicity, ADCC. And we think NK cells play a really important role there. We actually think, you know, there's plenty of evidence to suggest that ADCC today is checked or compromised and that by coming in with a wave of NK cells that are designed to synergize with the monoclonal antibody, we think we can substantially augment the response.

Solid tumors utilize to escape recognition of the immune system, whether it's T cells or NK cells. One of the more significant mechanisms of resistance is actually where the tumor works to down regulate MHC class one.

And there is loss of antigen presentation through that downregulation of MHC class, one because of that T cells can.

Can no longer recognize those tumors.

The exact cell type that an NK cell tenant in fact recognize and often times the cells the tumor cells debt down regulate MHC class one our high expresses of stress ligands again. These are that these are for instance.

Scott Walshco: That's step one, and we are starting to initiate that obviously with FT516, but we're obviously increasing our investment based on our conviction in ADCC by moving FT538 now into solid tumors across a fairly broad set of monoclonal antibodies in solid tumors. Ultimately, though, as you know, we think of that as a stepping stone.

Hughes for NK cells to recognize and attack. So I think that is one area of solid tumor biology that we are really interested in with respect to NK cells and in particular, the <unk> product candidate since it's designed to key in on stress law.

Scott Walshco: What we're doing, for instance, in lymphoma, what we're doing in myeloma, where we're utilizing, for instance, CD16 in addition to engineered CAR functionality. We are doing the same exact thing in solid tumors, where we have product candidates emerging in the second half of this year, building off of the FT-538 backbone. Engineering cars, for instance, our first IND will be engineering a car against the MIC-A and MIC-B stress ligands. We recently presented data where we engineered a car into the FT538 backbone against B7H3 as a solid tumor targeting strategy. And in addition, we expect that the first IND, actually under the Janssen collaboration, will be a car and case cell product for solid tumors.

Gans and even overcome resistance.

That exists with downregulation of stress ligands are shedding of stress ligands, but in addition, I also think there is going to be a fundamental role for combination with monoclonal antibody.

Monoclonal antibodies are used our own fleet and often successfully reached solid tumors.

And.

Part of their marketing mechanisms action is ADC in NK cell dependent.

And so we're really excited for instance, with respect to <unk>, $5, 38, and being able to combine that with monoclonal antibody therapy against a broad array of solid tumors.

Excellent.

The events coming up on more data this year.

Thank you.

And we do have a next question from Lisa Yang from Cantor.

Hey, guys. Thanks for taking my question and congrats on all the progress and looking forward to next week for sure.

I guess I just wanted that maybe it's a philosophical.

Robin: Again, you've mind-blown me about how many different products you have to focus on, so I'm writing them all down. But thank you so much; I appreciate it.

And practical question just.

How important is durability after after kind of a single dose or understanding that are having a kind of a perception of that end like this data set and the other of other upcoming datasets as well and then also can you just talk a little bit about the PDL, one thats kind of the better target versus PD, one just curious about that as well. Thanks.

Operator: And we do have our next question from Ted Tenhof on Piper Sandler.

Ted Tenhof: Hey guys, thanks so much for taking the question. I want to kind of follow up a little bit, and I'm appreciating that we're going to have the event later this year and more data.

Sure.

The last question I mean, we're obviously early in exploration with respect to combination of monoclonal antibodies in solid tumors, we started with <unk>.

Ted Tenhof: With all these different approaches on the solid tumor side, how do you ultimately protect the environment?

It doesn't it doesn't mean it was the right place to start, but we start with the volume out because obviously PDL one is op regulated.

Ted Tenhof: Do you expect that there will be certain cell types that may be better in different kinds of cancers with different kinds of therapeutic combinations? Do you ultimately see a penultimate product like MIC-A or MIC-B?

On the tumor itself. So we thought at least it provided a means by which the NK cell could target in combination with a volume at a.

Target expressed on a tumor as opposed to PD one PD one.

Scott Walshco: Give us a little bit more color on sort of where you're thinking is there. Thank you. Sure. I mean, I think it's early for us to have an opinion.

With respect to durability of the doses I mean again. This is something that we are we are exploring and we're experimenting with different treatment regimens and schedules to begin to tease out the differences that might exist between treatment schedules, whether thats one dose whether thats for instance up to six doses I think it is.

Scott Walshco: I mean, I think it's early for us to have a definitive strategy in solid tumors with multiplexed engineered cell therapy since we are breaking new ground. I do think, however, that there are certain solid tumors that may actually be more amenable to NK cell therapy. We've talked in the past, for instance, that there are various mechanisms of resistance that solid tumors utilize to escape recognition by the immune system, whether it's T-cells or NK-cells.

Too early to know the answer to that question I think fundamentally we believe two things that there is a period of time.

Especially for aggressive cancers, where you need to hit the tumor hard.

And that may be the first two weeks, maybe thats. The first four weeks, maybe thats the first six weeks.

But there is a period of time, where we believe a therapy really needs to aggressively attack the tumor to lead to.

Scott Walshco: One of the more significant mechanisms of resistance is where the tumor works to down-regulate MHC class 1, and there is loss of antigen presentation through that downregulation of MHC class one. Because of that, T cells can no longer recognize those tumors. That's the exact cell type that an NK cell can, in fact, recognize. And oftentimes, the cells, the tumor cells that down-regulate MHC class 1 are high expressors of stress ligands.

Deep durable responses.

And I would also say our belief system today is that the best way to drive that deep durable kill during that window again, whether it be 246 weeks.

Is through multi dosing and.

And the reason for that is because when you administer sell into a patient I think theres lots of data on emerging that that cell profoundly changes with respect to its function properties anti tumor killing ability.

Scott Walshco: Again, these are, for instance, cues for NK cells to recognize an attack. So I think that is one area of solid tumor biology that we are really interested in with respect to NK cells and, in particular, the CARMIC-A-MICB product candidate, since it's designed to key in on stress ligands and even overcome resistance that exists with downregulation of stress ligands or shedding of stress ligands. But in addition, I also think there is gonna be a fundamental role for combination therapy with monoclonal antibodies.

During that window of kill and so our belief is that to really maximize activity and because the cells administered to patients do change within the patient that are multi dose strategy is likely going to be the best strategy and I would say finally, we.

Similar to that.

Believe on multi targeting strategy is going to be the most effective strategy.

Okay. That's helpful.

<unk>.

And we do have our next question from Eagle <unk> from Citi.

Scott Walshco: I mean, monoclonal antibodies are used early and often, successfully, to treat solid tumors, and part of their mechanisms of action is ADCC and NK cell-dependent. And so we're really excited, for instance, with respect to FT538 and being able to combine that with monoclonal antibody therapy against a broad array of solid tumors.

Hi, Thank you very much for taking the question Pat in your prepared remarks on AML you mentioned.

<unk> team are being correlated with improved overall survival. Obviously some of the more recent approved therapies for AML targeted therapies, such as <unk> and <unk> inhibitors were approved based on a narrower and narrower measure of CRC or range that I was just wondering is there any specific reason with respect cell therapies.

Operator: And we do have our next question from Alisa Young from Cantor. Hey guys, thanks for taking my question and congratulations on all the progress. We're looking forward to next week, for sure.

Focus should be on <unk> as opposed to vs.

CRH.

Case for their targeted therapies in the add on.

Any discussions with the FDA on this nuance.

Alisa Young: I guess I just wanted to, maybe it's a philosophical and a little bit practical question, just, you know, how important is durability after, after kind of a single dose or understanding that or having a, you know, kind of perception of that in this data set and other, other upcoming data sets as well. And then also, can you just talk a little bit about whether it's PD-L1 that's kind of the better target versus PD-1? I'm just curious about that as well.

No I have not had any discussions with the FDA at this point, we're using what we believe to be an updated criteria.

Using 2017 El N. We think it is the gold standard we can have an interesting discussion on maybe Wayne can jump in with respect to CRH vs. Cri, we actually believe under the 2017, Elo El and criteria.

<unk> is a higher bar than CRH.

Cry.

Wires, either full recovery of neutrophils or platelets.

CRH does not require full recovery of either.

Scott Walshco: I'll start with the last question. I mean, you know, we're obviously early in exploration with respect to the combination of monoclonal antibodies in solid tumors. We started with Velumab. It doesn't mean it was the right place to start, but we started with Velumab because, you know, obviously PD-L1 is upregulated on the tumor itself. So we thought at least it provided a means by which the NK cell could target, in combination with Velumab, a target expressed on a tumor, as opposed to PD-L1.

Okay.

So under the 2007 <unk> criteria, we actually believe Cri is a higher bar than CRH and Wayne I don't know you may want to comment on that.

So just one comment I mean I think.

Yes.

Our certainly assessing our response to subjectively objectively based on the 2017 at Yale and criteria. We are very aware of some of the recent approvals for example, with some of the <unk> inhibitors, where the approval was based on.

Positive CR in CRH and I think it is important to emphasize debt as we're in because we're only in early phase one study.

Scott Walshco: With respect to durability of the doses, I mean, again, this is something that we are exploring, and we're experimenting with different treatment regimens and schedules to begin to tease out the differences that might exist between treatment schedules, whether that's one dose or whether that's, for instance, up to six doses. I think it's too early to know the answer to that question.

Early part of a phase one dose escalation.

We're not holding fast to specific endpoints like CR CRH has a path to registration. We when you look at the responses that early indicators of activity that might confer a clinical benefit.

So I would caution just a little bit about.

Scott Walshco: I think fundamentally we believe two things. First, that there is a period of time, especially for aggressive cancers, where you need to hit the tumor hard. And that may be the first two weeks; maybe that's the first four weeks; maybe that's the first six weeks. But there's a period of time where we believe a therapy really needs to aggressively attack the tumor to lead to a deep, durable response. I would also say our belief system today is that the best way to drive that deep, durable response during that window, again, whether it be two, four, six weeks, is through multi-dose.

Committing to a particular response criteria at this early stage of the game.

But certainly as our dataset matures and we get more data.

Understanding some of the relationships.

Tween response, and durability and even survival as we get enough patients.

It will allow us the opportunity to further refine some of these relationships when we apply other criteria like CRE.

Okay. Thank you very much I just had one other question maybe you commented on this in the past, but if you could remind us could you just explain why the starting dose for $5 38 in myeloma is 100 million cells, whereas for $5 16 of $5 96, a threefold lower at 30 million cells and also what is going to.

Scott Walshco: And the reason for that is because when you administer a cell to a patient, I think there's lots of data emerging that that cell profoundly changes with respect to its function, properties, and anti-tumor killing ability during that window of time. And so our belief is that to really maximize activity, and because the cells administered to patients do change within the patient, a multi-dose strategy is likely going to be the best strategy. And I would say, similar to that, we believe a multi-targeting strategy is going to be the most effective strategy. Great, thanks. That's helpful.

The expected starting dose for $5 76.

Yeah.

Wouldn't read too much into it other than just time and experience. If you go back on.

Obviously, the initial experiences with Ft 516, we're talking about an Ips derived.

<unk> therapy Ft 516 at the time that was engineered with <unk> 16.

Very little clinical experience experience and so we started and proposed to start at 30 million cells per dose as we've gotten more advanced and built up clinical experience over time, we've gotten comfortable with the safety profile quite honestly.

Operator: Great. Thanks. That's helpful. And we do have our next question from Yigal Nochomovitz from Citi.

What we're seeing with our Ips derived NK cell therapies, including at much higher doses and so when we submitted our protocol for FTE 538, as well as FTE 576, now given all of the safety history, we do have with our platform going back two years.

Yigal Dov Nochomovitz: Hi, thank you very much for taking the questions. Scott, any prepared remarks on...

Scott Walshco: AML, you mentioned, alluded to ORR being correlated with improved overall survival.

Scott Walshco: Overall Survival, and obviously some of the more recent approved therapies for AML, targeted therapies such as split-3 and IDH inhibitors were approved based on the narrower measure of CRCRH. So I was just wondering, is there any specific reason why, with respect to cell therapies, the focus should be on OOR as opposed to CRCRH, as is the case for targeted therapies, and do you have any discussions with the FDA on this new one?

<unk>.

We opted to start at a higher dose 100 million cells per dose and the FDA was comfortable with that.

Alright, thank you.

Sure.

And we do have our next question from Michael <unk> from Jefferies.

Hey, Scott.

Congrats on all the progress we have two questions one was going back to expectations around AML.

You've previously said, 20% to 30% CR rate has been seen in literature, you've talked about the various I guess limitations for some of those programs.

Is that the right bar to think about 456.

And how to put that into context with the fact that you will have some $5 38 data next week as well. So maybe just compare and contrast, those programs versus the expectations you've laid out and also how important is durability. So that's question. One is on AML and question two is similar and that is with lymphoma in the summer.

Scott Walshco: No, we've not had any discussions with the FDA at this point. We're using what we believe to be an updated criteria using the 2017 ELN. We think it is the gold standard.

Scott Walshco: We can have an interesting discussion, and maybe Wayne can jump in with respect to CRH versus CRI. We actually believe that under the 2017 ELN criteria, CRI is a higher bar than CRH. CRI requires either full recovery of neutrophils or platelets, while CRH does not require full recovery of either. So under the 2007 ELN criteria, we actually believe CRI is a higher bar than CRH. And Wayne, I don't know; you may want to comment. So, just one comment, I mean, I think... Yes, I mean, we are certainly assessing our...

We know the data at Ash and I think you had two prior <unk>.

Our ability seems to be a question that would be important can you just help us understand expectations around.

Our ability given the only two showers, but car T is 30% to 50% durable CR, maybe make some comments on durability. Thank you.

Sure. So yeah, obviously I think starting on AML, I think theres going to be a lot of interest in trying to compare for instance, ft 516, with four or <unk> $5 38, with the expense the historical experience with donor derived NK cell therapy.

And I do think donor derived NK cell therapy as I've mentioned in the sort of single center academic studies have shown 20% to 30%, 35% response rates I understand the natural the desire to do that comparison I think there are significant differences that have existed with donor derived NK cell therapy.

Operator: Dr. Michael Yee, Andrea Tan, William Maughan, Tyler Buren, Jack Allen, Michael Ulz, and Tazeen

Versus the paradigm that we're pursuing and I touched on some of them. We could talk about just right off the top of the lymphoma conditioning regimen is significantly different we have a lighter we have a lighter conditioning, we give we deliver the product to outpatient historically the paradigm for donor derived NK cell therapy has been transplant like.

Operator: We're not holding fast to specific endpoints like CRCR.

Operator: Dr. Michael Yee, Andrea Tan, William Maughan, Tyler Buren, Jack Allen, Michael Ulz, and Tazeen

Significant lymphoma, depletions such that patients are hospitalized.

Operator: Relationships When We Apply Other Criteria Like CRE

So I do think I do understand the natural comparison I think there's differences.

Operator: Okay, thank you very much. I just had one other question.

That said.

The reason I'm focused on 20% to 30% is not the comparison with donor derived NK cell therapy is because I think thats, the right bar to determine whether or not we actually potentially have a product.

Operator: Maybe you've commented on this in the past, but if you could remind us, could you just explain why the starting dose for 538 in myeloma is 100 million cells, whereas for 516 and 596 it's three-fold lower at 30 million cells? And also, what is going to be the expected starting dose for 576?

Going back to my comments that I made on some recent approvals in AML given the unmet need there have been multiple approvals in the past two years or three years, where the response rate has been about let's call it somewhere between the high teens in the mid twenties.

And so when I focus on response rate of the 20% to 30% I'm not actually looking at that in the context of gosh donor derived NK cell therapy on looking at it in the context of two I actually think we on a product that can be advanced into a registration study and that's how I'm thinking about that bar in AML.

Scott Walshco: 576. Yeah, I

Scott Walshco: Yeah, I wouldn't read too much into it other than just time and experience. If you go back, you know, obviously the initial experiences with FT516, we're talking about an IPS-derived therapy, FT516, at the time that it was engineered with CD16, with very little clinical experience. And so we started and proposed to start at 30 million cells per dose. As we've gotten more advanced and built up clinical experience over time, we've gotten comfortable with the safety profile, quite honestly, of what we're seeing with our IPS-derived NK cell therapies, including at much higher doses.

Yes, we will see we will see obviously, we'll share the data with respect to ft 516 in ft, 538, I have been pretty upfront about it when people have asked look at preclinical ft 530, it's a better product it just as preclinical euro.

Hey, some head to head turn on turn times.

In 10 different races, 530, it's always going to win whether that plays out in the clinic or not.

It'll be interesting to see that.

With respect to <unk> and 516 in lymphoma.

We provided a little bit of data initially there will be a much more robust update at <unk> with respect to ft 516.

And we're encouraged to share that data I think.

Durability I think it's a fair question. The durability of the response I think is a fair question I think that is still a bit early to assess we're not even at the we're not we haven't even advanced through the top dose level, yet and our patients are still relatively speaking only on study for sure.

Scott Walshco: And so when we submitted our protocol for FT-538, as well as FT-576, Now, given all the safety history we do have with our platform going back two years, we opted to start at a higher dose, 100 million cells per dose, and the FDA was fine with that.

<unk> period of time.

I think by Ash, we will have a very clear view of durability of ft 516, plus rituximab.

Thank you Greg.

Operator: And we do have our next question from Michael Yee on behalf of Jeff.

And we do have a next question from Peter Lawson from Barclays.

Michael Jonathan Yee: Hey Scott, congrats on all the progress. We had two questions. One was going back to expectations around AML. You've previously said a 20-30% CR rate has been seen in literature. You talked about the various, I guess, limitations of some of those programs. Is that the right bar to think about for 5.1.6 and how to put that into context with the fact that you will have some 5.38 data next week as well?

Scott Thanks, so much for.

All the detail.

I guess going back to low.

Next question around.

The response rate or the bar for AML lists.

Are you focused on Cri CRH.

Is that response rate that 20% to 35% response rate in AML or is that more of a J.

Our number.

<unk>.

Its the number that I've.

Described.

Is a composite of CR.

Hi.

Yes.

There's just a very interesting paper that was released and published on <unk> actually in relapsed refractory AML.

Michael Jonathan Yee: So maybe just compare and contrast those programs versus the expectations you've laid out and also how important durability is. So question one is on AML. And question two is similar, and that is with lymphoma in the summer.

Where the data that I referred to on a reference I made was a comparison.

<unk> patients.

Using the 2017 El N criteria.

That achieved CR cri.

MLR FES versus patients that did not.

There is a clear survival benefit between those two groups CR Cri MLR FES versus non responders clear survival benefit statistically significant debt extend out over 30 months.

Scott Walshco: We know the data at ASH, and I think you had two prior CRs. Durability seems to be a question that would be important. Can you just help us understand expectations around durability given that there are only two CRs but CAR-T is 33-50% durable.

Good day.

Would you be I guess more content with a high.

Roy.

Versus high CRH.

On a gauge so CR Cri CRH is not part of the 2007 <unk> criteria.

Scott Walshco: Durable CR. So maybe make some comments on durability. Thank you.

It's part of our criteria that and regionally existed in 'twenty.

Scott Walshco: Sure. So, yeah, obviously, starting with AML, I think there's going to be a lot of interest in trying to compare, for instance, FT516 or FT538 with the historical experience with donor-derived NK cell therapy. And I do think donor-derived NK cell therapy, as I've mentioned in these sort of single-center academic studies, has shown 20 to 30 percent, 35 percent response rates. I understand the natural desire to do that comparison. I think there are significant differences that have existed with donor-derived NK cell therapy versus the paradigm that we're pursuing, and I've touched on some of them. We can talk about just right off the top, the lymphoconditioning regimen is significantly different. We have lighter conditioning.

2003.

I agree there are paths forward, where approvals have been achieved based on CR CRH Theres also paths forward where products have been approved on CR Cri.

There are two different response criteria is both of them are very viable.

Great. Thank you and then just your comment around no.

Using our site flow.

Really appealing.

Are you thinking of other ways to deplete the bone marrow through other methods or.

Yes, yes, I think I think there I think I think this comes down to a question that philosophical question and scientific question on what is the purpose of Psi flow.

I think Thats an open question. There is I think a lot of speculation around what the purpose of site flu is.

But I don't think Theres any magic to Si flu and cell therapy, where XI flu has to be delivered with cell therapy site flow has a biological effect.

It is probably multifactorial one of those biological effects is for instance, cigna.

Significantly increasing cytokines within patients as a result of the <unk> flow.

Scott Walshco: We deliver the product to outpatients. Historically, the paradigm for donor-derived NK cell therapy has been transplant-like, with significant lymphodepletion, such that patients are hospitalized.

And so I do think as we look forward and think about what is the ultimate cell therapy paradigm for patients I think looking at ways for instance, where we can.

Significantly reduced tsai flu.

Scott Walshco: So, I do think, I do understand the natural comparison, but I think there's differences. That said... The reason I'm focused on 20-30% is not the comparison with donor-derived NK cell therapy. It's because I think that's the right bar to determine whether or not we actually potentially have a product. Going back to my comments that I made on some recent approvals in AML given the unmet need, there have been multiple approvals in the past two or three years where the response rate has been about, let's call it somewhere between the high teens and the mid-20s.

It is important and we are very interested in exploring that and it's actually one of the reasons why we're engineering in cytokines support into ourselves.

Great.

Thank you so much which I appreciate sure sure.

And we do have our next question from testing on that from Bank of America.

<unk> are you on mute.

Sorry can you hear me now.

I can yes, excellent sorry about that.

Thanks for taking my questions.

From 516 on $5 nine thanks, I just wanted to drill in a little bit into the pursuit of <unk> indication.

On the last year, there's obviously been a number of companies that have had on drugs approved in this space from Seattle genetics similar focus stimulus recently.

Scott Walshco: And so when I focus on the response rate of 20 to 30%, I'm not actually looking at that in the context of, gosh, donor-derived NK cell therapy. I'm looking at it in the context of, do I actually think we have a product? that can be advanced into a registration. And that's how I'm thinking about that bar in AMI.

<unk> therapeutics and they're all different mechanisms, obviously from what youre pursuing but wanted to get your thoughts about how you view the opportunity overall in <unk>, and where you see NK cells potentially fitting into the treatment paradigm.

Scott Walshco: We'll see. Obviously, we'll share the data with respect to FT516 and FT538. I've been pretty upfront about it when people have asked. Look, preclinically, FT538's a better product. It just is, preclinically.

And then on second question is more of.

In general Whats your strategy for re dosing NK cells and how many doses can a patient potentially receive and can you just remind us what's the highest number of doses any patient has received across your program. So far thanks.

Scott Walshco: If you race them head-to-head 10 out of 10 times in 10 different races, 538's always going to win. Whether that plays out in the clinic or not, it'll be interesting to see. With respect to ASCO and 516 and lymphoma, yeah, we provided a little bit of data initially. There will be a much more robust update at ASCO with respect to FT 516, and we're encouraged to share that data. I think, you know, durability is a fair question.

Sure. So I'll tackle the last question first so the most doses that we have the maximum number of doses that we have administered to a patient is six.

And this goes back to first started with actually Ft 500.

And it was actually the reason we sort of ran this experiment with Ft 500, we gave two days of outpatient lymphoma conditioning.

Followed by.

Doses of Ft 500 on day, one day seven day 14.

Scott Walshco: The durability of the response, I think, is a fair question. I think that is still a bit early to assess. We're not even at the, we haven't even advanced through the top dose level yet, and our patients are still, relatively speaking, only on study for a short period of time. I think by ASH, we will have a very clear view of the durability of FT516 plus Rituxan.

Then the patient was off therapy for two weeks.

And we did a safety assessment and then we actually re dosed. The next month day $1 7 million in 14.

Without lymphoseek conditioning.

And so that was essentially you could think about it is six doses over 45 days following light outpatient <unk> conditioning in the entire experiment at some level initially was set up to assess whether or not a patient could tolerate multi dosing in that form.

Operator: Thank you. Great. And we do have our next question from Peter Lawson from Barclays.

Peter Richard Lawson: I guess, going back to... Mike's question around...

For instance would there be mechanisms of profound immune rejection that would arise.

Peter Richard Lawson: The response rate, or the BAFA AML, is... Are you focused on CRI or CRH?

That was one of the very early things we were looking at right would there be for instance, a form of Crs that would emerge because you would administer essentially a cell unmatched to a patient and that the patient would be building up allo reactivity to that so we did not see that with.

Peter Richard Lawson: Or is that more of just an ORR number?

Scott Walshco: It's the number that I've... is a composite of CR, CRI, and MLFF. There's just been a very interesting paper that was released and published about venetoclax, actually, in relapsed refractory AML, where the data that I referred to in the reference I made was a comparison of Patience, using the 2017 ELN criteria, that achieved CR, CRI, and MLFS versus patients that did not. There is a clear survival benefit between those two groups, CR, CRI, and MLFS versus non-responders. A clear survival benefit, statistically significant, that extends out over 30 months. And would you be, I guess, more content with a high?

<unk> 500, and we've not seen that with Ft 516 ft 516 has been dosed up to six doses.

And we've not seen that with any of our other product candidates to date now ft 596, we've given a single dose and then they can repeat that single dose cycle, but generally speaking we've.

We feel really confident about our ability to re dose and I'm certainly demonstrated our ability to re dose safely with tolerability up to six doses over a 45 day period.

With respect to where we think NK cells fit within sort of the b cell lymphoma <unk> landscape.

There's lots of opportunity here I mean, clearly we've started out in a position where we are.

Operator: https://www.kenhub.com

Scott Walshco: CRH is not part of the 2007 ELN criteria. It's part of a criteria that originally existed in 20... in 2003. I agree, there are paths forward where approvals have been achieved based on CR, and CRH. There's also Paths Forward, where products have been approved on CR, and CRI. There are two different response criteria. Both of them are very loud.

You can think about it as sort of third line.

Where patients have failed multiple lines of Rituximab and we're really excited about what we've seen in that setting where we've combined ft 516 for instance, with rituximab in patients that have either relapsed or failed rituximab.

We think there's a great opportunity there given the response rates that we're seeing with ft 516.

And Additionally, like we discussed we actually think if the product candidate really does synergize effectively with Rituxan and if it really does continue to show a differentiated safety profile compared to T cell therapies, whether they be engaged <unk> or.

Scott Walshco: Thank you. And then just your comment around not using CyFlu is really appealing. Um, so are you thinking of other ways to deplete the bone marrow through other methods or not? Yes. Yes. I think, uh, I think there, I think, I think this comes down to a question, the philosophical question and scientific question about what is the purpose of CyFlu? I think that's an open question.

Car T cells, we think we have a terrific opportunity to go very early line with ft, 516, or ft 590 <unk>.

Okay. Thank you.

Sure.

And we do have a next question from Michael Schmidt from Guggenheim.

Okay.

Yeah.

Scott Walshco: There's, I think, a lot of speculation around what the purpose of PSY-Flu is, but I don't think there's any magic to PSY-Flu and cell therapy where PSY-Flu has to be delivered with cell therapy. If PSY-Flu has a biological effect, it is probably multifactorial. One of those biological effects is, for instance, significantly increasing cytokines within patients as a result of the PSY flu. And so I do think, you know, as we look forward and think about what the ultimate cell therapy paradigm for patients is, I think looking at ways, for instance, where we can significantly reduce the PSY flu is important, and we are very interested in exploring that. And it's actually one of the reasons why we're engineering cytokine support into our.

Hey, guys. This is kelsey on for Michael Thanks for taking our question.

First I guess.

Quick from me Ken The protocol amendments are $5 960, <unk> implemented. It my guess is there any chance you could provide some insight into maybe the number of proportion of patients to date that has Scott in a second dose.

In other words, I guess could we read into the fact that you are now at the point that you had filed this amendment maybe more than just that single case study patients.

And then secondly could you, possibly provide an update on where you stand.

On a and lunch.

Phase one trial threat from 819, and what maybe some guidance there before you start treating patients.

That's it thanks sure.

Sure.

First question first so.

With respect to the protocol Amendment.

Protocol Amendment, we believe.

Can be IRB approved and active.

Scott Walshco: Great. Thank you so much. I very much appreciate it. Sure. Sure. And we do have our next question from Tazeen Ahmad from Bank of America.

Let's call it by.

At the end of June.

It's submitted.

Given the FDA an opportunity to comment on that protocol, we're taking that protocol to multiple <unk> and we think by the end of June we may be in a position to begin to implement a multi dose treatment schedule with respect to FTE 596.

Operator: Yes. Oh, excellent.

Operator: https://www.kenhub.com

Operator: Seattle Genetics, Timorphosis, and most recently, ADC Therapeutics. They're all different mechanisms, obviously, from what you're pursuing, but I wanted to get your thoughts about how you view the opportunity overall in DLBCL and where you see NK cells potentially fitting into the treatment paradigm.

I think one of the reasons that I have alluded to this in the past.

We've taken some time to file that amendment is we clearly wanted to get experience with.

Administering more than one dose of ft, 596, and clearly the patient debt we.

We disclosed at Ash of last year did go on to a second cycle.

Operator: https://www.globalonenessproject.org

We've had lots of experience now with patients in lymphoma, receiving multiple cycles of ft, 516, and yes. There have been other patients that have been retreated with ft 596.

Operator: https://www.yigalnochomovitz.com

Scott Walshco: Sure, so I'll tackle the last question first. So the most doses that we have, the maximum number of doses that we have administered to a patient is six. And this goes back to, actually, FT500, where we, and this was actually the reason we sort of ran this experiment with FT500. We gave two days of outpatient lymphoconditioning, followed by doses of FT500 on day 1, day 7, day 14, and the patient was off therapy for two weeks, and we did a safety assessment. And then we actually re-dosed.

That I think was your first question. Your second question with respect to 2019.

We actually have just recently completed.

Two additional manufacturing runs with 819.

And we believe that those manufacturing runs will be released shortly.

We will be in a position to treat patients with FCA 19 quickly upon release and so yes in the next call it weeks to months.

Next weeks, we'll I think we'll be in a position to treat patients with <unk> 19.

Okay perfect. Thanks, so much.

Scott Walshco: The next month, day one, seven, and 14, without lymphoconditioning. And so that was essentially, you could think about it as six doses over 45 days following light outpatient lymphoconditioning. And the entire experiment, at some level, was initially set up to assess whether or not a patient could tolerate multi-dosing in that form. For instance, would there be mechanisms of, you know, profound immune rejection that would arise? That was one of the very early things we were looking at.

Sure.

Thank you and we do have our next question from Dana <unk> from Seb.

Hi, Thanks for the question or two from day, one to follow up on the moving away from site flu I guess I Wonder why you are starting with I think you said 516 cohort given that it does not have the membrane bound IL 15 that could reduce dependence on site flu.

Impact on decline.

And then the second question is on durability of response and you have many many trials in cohort.

I Wonder, which one do you think is most likely to first give the best opportunity to test durability of response.

Scott Walshco: Would there be, for instance, a form of CRS that would emerge because you would administer essentially a cell unmatched to a patient and that the patient would be building up alloreactivity to that cell? We did not see that with FT500, and we've not seen that with FT516. FT516 has been dosed up to six doses. And we haven't seen that with any of our other product candidates to

Meaning it won't have the complexity of many patient going on to transplant App you can get from most CR or PR.

Yes. So last your last question first I think ft 516 in lymphoma is a perfect example to test durability of response I just don't know if we're far along with I don't think we're far along enough with respect to time on study.

Scott Walshco: Now, FT596, we've given a single dose, and then they can repeat that single dose cycle. I feel really confident about our ability to re-dose and have certainly demonstrated our ability to re-dose safely with tolerability up to six doses over a 45-day period. With respect to where we think NK cells fit within sort of the B-cell lymphoma, DLB, and BCL landscape, I think there's lots of opportunity here.

Sure.

We're certainly not cleared the entire dose escalation.

To answer the question.

On an informative way with respect to durability of response, but I think the ft. 516 study is a really great study to judge durability of response.

I continue to believe Ft 596, given it is dual antigen targeting.

Will show improvement over and above 516, but that remains to be seen I think 50 596 of the best in class product candidate <unk>.

Super excited with what we're seeing with 516, but I do believe ft, 596 of the best and price product candidate, but.

Scott Walshco: I mean, clearly, we've started out in a position where we are, you know, you can think of it as sort of a third line where patients have failed multiple lines of rituximab. And we're really excited about what we've seen in that setting where we've combined FT-516, for instance, with rituximab in patients that have either relapsed or failed rituxim We think there's a great opportunity there given the response rates that we're seeing with FT-516.

But I do think the first sort of benchmark with respect to durability response can be assessed using ft 516, plus rituximab absolutely.

With respect to Si flu and where we're starting with that and Wi Fi was 16, 5% 16 is given being administered with IL two.

That in mind $5 38 is not but $5 16 is and so even though we may for instance, significantly reduced tsai flu or move to a different form of conditioning, we will likely still administer with some degree of cytokine support from <unk>.

Scott Walshco: And additionally, like we discussed, we actually think if the product candidate really does synergize effectively, and if it really does continue to show a differentiated safety profile compared to T-cell therapies, whether they be in gaugers or CAR T-cells, we think we have a terrific opportunity to go very early with FT-516 or FT-596.

Got it so I guess, what's your opinion on that to completion removes the IL <unk> sink I think that's the other idea knock on that just increase the cytokines that that all of those cells that you don't deplete them Osaka by all the IL assets there yes.

Why the experiment needs to be done I think it's a fair I think it's a fair question because I think that is one of the things that Si flu may do as well is while it provides in a better field for competition for the Adaptively transferred cells.

Operator: And we do have our next question from Michael Schmidt from...

Operator: Question from Michael Schmidt from Guggenheim.

And so I think that guidance.

Operator: Hey, guys. This is Kelsey on for Michael.

I think that I think that'll be an interesting observation with ft 516, because there may be competition. There obviously with ft 538, it doesn't it doesn't need to fight that fight because it has its own cytokine support building.

Operator: Thanks for taking our question. First, I guess, how quickly can the protocol amendment for 596 be approved and implemented? And I guess, is there any chance you could provide some insight into maybe the number of proportional patients to date that have gotten the second dose? In other words, could we read into the fact that you're now at the point where you can file this amendment that there's maybe more than just that single case study patient?

And we do have our next question from Mara Goldstein from Mizuho.

Hi, great. Thanks for taking the question.

On slide 38 in multiple myeloma.

I think we have seen peripheral neuropathy emerge as a potential issue Pfizer you snap a pause on it by specific and I believe Andrew.

On to AMG for Tony how does he reported incidences of crushed car T studies targeting before may have.

Operator: And then secondly, could you possibly provide an update on where you stand kind of in phase one trial prep for 819 and what maybe still needs to be done there before you start treating patients? That's it. Thank you.

Reported debt, so I understand on multiple myeloma patients will likely.

Had been treated as a neuro toxic prior therapies, but I'm curious as to your thoughts on.

Scott Walshco: Sure. First question first, so with respect to the protocol amendment, the protocol amendment, we believe, can be IRB approved and active by the end of June. Let's call it that. It's been submitted.

In this setting for $5 38.

What you would anticipate with respect to peripheral neuropathy.

For for that work and then also if I can just ask on the J&J payment was that tied to any.

Scott Walshco: We're giving the FDA an opportunity to comment on that protocol, and we're taking that protocol to multiple IRBs. And we think, by the end of June, we may be in a position to begin to implement a multi-dose treatment schedule with respect to epidemiology. I think one of the reasons, and I have alluded to this in the past..., that we've taken some time to file that amendment is that we clearly wanted to get experience with administering more than one dose of FT-596.

Any team of any specific milestone on our way.

Clinical.

R&D work.

So on the last question that J&J is is just revenue we did not trigger any milestone with J&J this quarter.

That contributed to revenue so the revenue contributors from J&J, we're sort of typical recognized recognizing upfront the allocation of the upfront as well as J&J does fully fund all of the work under the collaboration so we obviously get paid for.

For the work that we do and that gets recognized as revenue.

Scott Walshco: And clearly, the patient that we disclosed at ASH last year did go on to a second cycle. We've had lots of experience now with patients in lymphoma receiving multiple cycles of FT-516. And yes, there have been other patients that have been retreated with FT-596. That, I think, was your first question. Your second question with respect to 819; we actually have just recently completed two additional manufacturing runs with 819. And we believe that those manufacturing runs will be released shortly, and we'll be in a position to treat patients with AFT819 quickly upon release. And so, yeah, in the next weeks to months, or next week. I think we'll be in a position to treat patients with AIDS. Okay, perfect. Thanks.

With respect to <unk> 35, 38 in myeloma, I mean, I'll, let <unk> comment on that I mean, the one thing I will say right off the bat. The initial experience with ft. $5 38 is obviously in combination with Dara <unk> has a well established history with respect to see on its profile, but I'll, let <unk> comment on that.

No I mean, I think that's a really good question and we've been following the peripheral neuropathy is.

Observed with some of the more T cell based therapy I guess.

One hypothesis that we hope to address with the $5 38 study in myeloma is whether or not a different effect yourself.

E on NK cell.

One.

Combined with our tumor that may have a different safety profile than what's been observed with some of the.

More T cell directed therapies like bi specifics in the car Ts.

Mhm.

But I mean on solar.

The clinical experiment that we obviously will.

Conduct.

Right, but there is no exclusion criteria based on fire personal neuropathy, so stay low.

Operator: Okay, perfect. Thanks so much.

Okay alright, thank you.

Operator: Thank you. And we do have our next question from Daina Graybosch here.

Yep.

Okay.

And we do have our next question from do Kim from BMO.

Operator: Andrea Graybosch from SVB Hi, thanks for the question.

Hi, This is James from Alberto Thanks for taking my questions and congrats on the progress I guess, it's a two part question.

Operator: For me, one is a follow-up on the move away from PsyFlu. I just wonder why you are starting it.

Operator: with, I think you said, an ST516 cohort, given that it doesn't have the membrane-bound IL-15 that could reduce.

Given the MD Anderson data using NK cells, combined with <unk> NK cell engagement and.

Operator: Reduced dependence on PSI flu and impact on cytokine. And then the second question is about durability.

In Hodgkin's lymphoma, how do you view that combo regimen versus your car financing.

Phil.

And do you think there is any merit and doing a preloaded NK cell within engineered using something like 7500.

Operator: https://www.youtube.com

Operator: Most likely to first give the best opportunity to test

Operator: https://www.youtube.com

I think today, our strategy has been to leverage our CD 16 receptor Inc.

Operator: The complexity of many patients going on to transplant after you get them in a CR or PR.

In combination with a variety of well established.

<unk> approved modalities and I think that will continue to be our strategy I think the idea of being able to promote ADC with ft, 516, or <unk> $5 38.

Scott Walshco: Yeah, so your last question first. I think FT516 in lymphoma is a perfect example to test durability of response. I just don't know if we're far along. I don't think we're far along enough with respect to time on study, or we're certainly not cleared of the entire dose escalation phase to answer the question in an informative way with respect to durability of response. But I think the FT-516 study is a really great study to judge durability of response. I continue to believe FT-596, given it is dual antigen targeting, will show improvement over and above FT-516. But that remains to be seen.

And synergize with agents that are used early and often in both hematologic malignancies and solid tumors I think it's an exciting opportunity to leverage <unk> 16 in ADC and that's the strategy that we are pursuing.

People can have different beliefs systems.

<unk> around what they think is more.

Product ties or is he.

Better patient reach.

Reach.

I personally believe and off the shelf cell therapy combined with a monoclonal antibody that is also delivered if you will off the shelf or in fact engineering.

Scott Walshco: I think FT-596 is a best-in-class product candidate. I'm super excited about what we're seeing with 516, but I do believe FT-596 is a best-in-class product candidate. But I do think the first sort of benchmark with respect to durability response can be assessed using FT-516 plus rituximab, absolutely. With respect to CyFlu and where we're starting with that and why 516 is given, 516 is given administered with IL-2. Keep that in mind. 538 is not, but 516 is.

And NK cell to target for instance, an antigen is a much.

Better strategy than manufacturing.

Product patient by patient.

That requires.

Essentially combinations.

On cryo preservation and construction of products through.

Through a manufacturing paradigm.

That's a personal belief.

Great. Thanks that was incredibly helpful.

Thanks, again, and looking forward to the update next week.

And we do have our next question from Nick Abbott from Wells Fargo.

Thanks for taking my question I missed the.

EBITDA Nicole.

Scott Walshco: And so even though we may, for instance, significantly reduce CyFlu or move to a different form of conditioning, we will likely still administer with some degree of cytokine support for 516. About it. So I guess what's your opinion on that the depletion removes the

We'll see down I don't know if you're on the call, but you will be missed going forward.

And then a couple of questions you've mentioned sort of light.

And then from conditioning regimen on a few times. So can you competitors day rates.

<unk> regimen, the incident zone conditioning regimen related grade three four talks and talks versus what has been reported on spend.

Scott Walshco: I think that's the other idea, not that it just increases side effects but that all those cells that you don't deplete them will suck up all the IL-2 you would need. Yeah, no, I've...

On conditioning regimens and then I have a phone.

Thanks.

Yeah honestly I don't have those figures off the top of my.

Had her fingertip, so I would not want to provide those but I would say just generally.

Lymphoma conditioning.

Scott Walshco: Yeah, so that's why the experiment needs to be done. I think it's a fair question because I think that is one of the things that PsyFlu may do as well, because while, you know, it provides a better field for competition for the adoptively transferred cell. And so I think that'll be an interesting observation with FT516 because there may be competition there. Obviously, with FT538, it doesn't need to fight that fight because it has its own cytokine support building.

Does have toxicity associated with it and I do think where the field will go and we have to recognize this is that the better therapies will be therapies and a better experience for patients.

We'll be.

Therapies that have lighter conditioning regimens.

And therefore less toxicity as opposed to cranking up.

On the conditioning.

And I think the field needs to recognize that and I think it's one of the things that we're very focused on.

Okay. Thanks, and then.

If you want to if for instance, if you want to go early line therapy, whether its hematologic malignancies or solid tumors, there's no way you're conditioning patients putting them in the hospital or significantly increasing the risk of for instance, infection and it's just not going on.

Operator: And we do have our next question from Mara Goldstein from Missoula.

Operator: Great. Thanks for taking the question.

Operator: Hey, on ST-538 and multiple myeloma, I think we've seen peripheral neuropathy emerge as a potential issue. Pfizer just announced a pause on its bispecific, and I believe Amgen's AMG-420 had a few reported grade 3 incidences, and of course, CAR-T studies targeting DCMA have reported this. So I understand that multiple myeloma patients are likely to have been treated with neurotoxic prior therapies, but I'm curious as to your thoughts in this setting for 538, what you would anticipate with respect to peripheral neuropathy for that work. And then also, if I could just ask, on the J&J payment, was that tied to any achievement of any specific milestone, or was it just clinical?

I don't think Thats, the way to maximize patient reach your benefit.

True.

No.

We recently Elissa trial.

Now moving to demand.

With me on.

On 16, and so can you talk a little bit about the Genesis of the trial.

$2016 38.

De risking for 573 yield based on the ninth Street coffee.

Oh.

You're talking about are you talking are you referring to the ovarian study.

The Minnesota trial, yes, Okay, yes, okay.

<unk>.

So.

Yes.

[laughter].

Our little eye.

Wasn't aware it was I wasn't aware it was public to be honest with you.

But okay.

Yes to be fair, we're starting with Ft 516, as a monotherapy.

Suspect the trial will transition from <unk> 16 to <unk> 38, as a mono therapy.

Scott Walshco: R&D work. So in the last question, J&J is just revenue. We did not trigger any milestone with J&J this quarter that contributed to revenue. So the revenue contributors from J&J were sort of typical, recognizing up front, the allocation of the up front, as well as J&J does fully fund all of the work under the collaboration. So obviously, we get paid for the work that we do, and that gets recognized as revenue.

Okay.

We will likely with.

With progress begin to combine locally.

With the <unk> III engage her.

However, as you know we are developing a product candidate that is in fact engineered with a seven percentage III.

Okay.

Okay. Thanks, a lot.

Sure.

And when do you have on last question from Robert range from HC Wainwright.

Scott Walshco: With respect to FT-538 and myeloma, I mean, I'll let Wayne comment on that, but I will say right off the bat, the initial experience with FT-538 was obviously in combination with daratumumab, and daratumumab has a well-established history with respect to safety and its profile, but I'll let Wayne comment on that. No, I mean, I think that's a really good question, you know, and we've been following.

Hey, everyone could shape for Rob I just.

I have a couple of very quick questions. One is on Ft 548, and please excuse me if you've provided guidance in the past, but on clinical trials. Gov. You also have to the mob is one of the potential combination arms are you still evaluating their arm or are you just focused on debt at the moment on the.

The last one on the Ft 500 can we still expect further data datasets in.

Patients who are refractory to anti PD ones.

Sure.

Operator: .. .. .. .. .. .. .. You know, one hypothesis that we hope to

Tumor types like non small cell lung cancer.

Operator: https://www.kenhub.com

Yes. So your last question, we will be providing a solid tumor update likely in the second half of this year, probably sometime in the third quarter, we'll discuss what we're seeing in solid tumors with ft 500 ft 516 in combination with <unk>.

Operator: is, you know, whether or not a different effector cell is involved.

Operator: https://www.kenhub.com

Operator: Combined with thera-tumor, this may have a different safety profile than what's been observed with some of the more T-cell-directed therapies like bispecifics and CAR-Ts.

And also we will be providing an update at that time with respect to our broader solid tumor strategy as it relates to for instance, Carmike mcbee.

Operator: Bahram Valamehr. It's a... It's a...

Operator: It's a clinical experiment that we, you know, we obviously will need to...

Discuss <unk> III as well as the J&J product for <unk> under the J&J collaboration.

Operator: will meet Conduct. Right, but there's no exclusion.

As solid tumor targeted so in the second half of this year will provide a fairly fulsome update on our solid tumor efforts.

Operator: Right, but there's no exclusion criteria based on prior personal neuropathy, you know, in case those patients have been treated. Nope. Okay. All right. Thank you. Yes.

Sorry, what was your first question.

So on clinical trial, Doug you also have the slammer assets.

Yeah, sorry.

Yeah, No we're very focused on combining with our tune that theyre different regimens in the regimen that we're focused on today is the combination with our timna.

Operator: And we do have our next question from Du Kim from VMI.

Operator: Hi, this is James Pernod-Bordeaux. Thanks for taking our questions and congratulations on the progress. I guess this is a two-part question. Given the MD Anderson data using NK cells combined with Apimed's NK cell engager in Hodgkin's lymphoma, how do you view that combo regimen versus your CAR-I NK cells?

Okay, great. Thank you.

Sure.

And I am showing that there are no more questions at this time.

Perfect.

You everyone for your time today, we look forward to providing a full update on our initial clinical.

<unk> with Ft, 516, and up to $5 38 next week.

Operator: And do you think there's any merit in doing a preloaded IMK cell with an engager using something like your FD500?

Thank you ladies and gentlemen.

And this concludes today's conference.

Scott Walshco: I think to date our strategy has been to leverage our CD16 receptor in combination with a variety of well-established FDA-approved modes, and I think that will continue to be our strategy. I think the idea of being able to promote ADCC with FT516 or FT538 and synergize with agents that are used early and often in both hematologic malignancies and solid tumors is an exciting opportunity to leverage CD16 and ADCC. And that's the strategy that we are pursuing.

You may now disconnect.

Okay.

[music].

Scott Walshco: People can have different belief systems around what they think is more..., productized, or has better patient reach. I personally believe in off-the-shelf cell therapy combined with a monoclonal antibody that is also delivered, if you will, off-the-shelf. In fact, engineering an NK cell to target, for instance, an antigen is a much better strategy than manufacturing a product patient by patient that requires, essentially, combinations of cryopreservations and construction of products through a manufacturing paradigm. That's a personal belief I hold. Great

Operator: Great. Thanks. That was incredibly helpful. Thanks again, and I'm looking forward to the update next week.

Operator: And we do have our next question from Nick Abbott from Wells Fargo.

Operator: Well, good afternoon, and thanks for taking my questions. I missed the beginning of the call, but the first thing I'd like to say is that, obviously, Dan, I don't know if you're on the call, but you will be missed going forward. And then I have a couple of questions.

Operator: Scott, you've mentioned this sort of light outpatient lymphoconditioning regimen a few times. So can you compare, first, the rates of the regimen, the insulin flow conditioning regimen-related grade 3-4 tox and heme tox? This is what has been reported for standard.

Operator: And then I have a follow-up question. Thanks.

Scott Walshco: Yeah, honestly, I don't have those figures off the top of my head or fingertips, so I would not want to provide those, but I would say, just generally, you know, lymphoconditioning does have toxicity associated with it. And I do think where the field will go, and we have to recognize this, is that the better therapy will be therapies, and a better experience for patients, will be therapies that have lighter conditioning regimens and therefore less toxicity as opposed to cranking up the conditioning.

Scott Walshco: And I think the field needs to recognize that, and I think it's one of the things that we're very focused on. For instance, if you want to go early-line therapy, whether it's hematologic malignancies or solid tumors, there's no way you're conditioning patients, putting them in the hospital, or significantly increasing their risk of, for instance, infection. It's just not going to happen. I don't think that's the way to maximize patient reach or benefit. And I noticed that you've recently listed a trial of...

Operator: for all of Enoblacuzumab, with

Operator: with 516, and so can you talk a little bit about the genesis of the trial and why 516, not 538? Is this de-risking for 573 or B7H3, Kelsey?

Operator: Are you talking about the, are you referring to the ovarian study?

Operator: Yeah, the Minnesota trial. OK, yeah, OK. So.

Operator: So, yes, thank you for that.

Scott Walshco: I wasn't aware it was public, to be honest with you. But okay, yes, to be fair, we're starting with FT-516 as a monotherapy. I suspect the trial will transition from FT-516 to FT-538 as monotherapy. We will likely, with progress, begin to combine locally with a B7H3 engagement. However, as you know, we are developing a product candidate that is, in fact, engineered with a B7H3.

Operator: And we do have our last question from Robert Burns from HC Wainwright.

Operator: Hey, everyone, this is Chait for Rob. I just have a couple of very quick questions. One is on FT-538, and please excuse me if you've provided guidance in the past, but on clinicaltrials.gov, you also have Illituzumab as one of the potential combination arms. Are you still evaluating their arm, or are you just focused on datatumumab? And the last one on FT-500; can we still expect further data sets in patients who are refractory to anti-PD1s in chemotypes like non-small cell lung cancer? Yes, so your last question.

[music].

Operator: Yes, so your last question. We will be providing a solid tumor update later this year, probably sometime in the third quarter. We'll discuss what we're seeing in solid tumors with FT500 and FT516 in combination with Velumab, and also we'll be providing an update at that time with respect to our broader solid tumor strategy as it relates to, for instance, CAR-MIC-A, MIC-B, we just discussed B7H3, as well as the J&J product, the first IND under the J&J collaboration, which So, in the second half of this year, we'll provide a fairly comprehensive update on our solid tumor strategy.

Operator: Sorry, what was your first question? So on clinicaltrials.gov, you also have the slam it. Oh, yeah. Sorry, Yeah, no, we're very focused on combining with R2MEM.

Scott Walshco: Yeah, no, we're very focused on combining it with dartumimab. They're different regimens, and the regimen that we're focused on today is the combination of dartumimab.

Operator: And I'm showing that there are no more questions at this time.

Operator: Perfect. Thank you everyone for your time today. We look forward to providing a full update on our initial clinical observations with FT516 and FT538 next week. Thank you, ladies and gentlemen. This concludes today's conference. You may now disconnect. Outro Music

Operator: Thank you, ladies and gentlemen. This concludes today's conference.

Operator: Good day, ladies and gentlemen, and welcome to the Fate Therapeutics First Quarter 2021 Financial Results Conference call. This call is being webcast live on the Investors section of Fate Therapeutics' website at www.fatetherapeutics.com

Operator: at fatetherapeutics.com. At this time, all participants are in a listen-only mode. Later, we will conduct a question and answer session.

Operator: And instructions will follow at the time. If anyone

Operator: And once you require operator assistance, please press star, then 1. Sorry, press star zero on your touch-tone phone. As a reminder, this call will be recorded. I will now turn the call over to Scott Walshco, President and CEO of...

Operator: and CEO of Fate Therapeutics. Scott, you may begin.

Scott Walshco: Thank you. Good afternoon, and thank you everyone for joining us for the Fate Therapeutics first quarter 2021 financial results call. Shortly after 4 p.m. Eastern Time today, we issued a press release with these results, which can be found on the Investors section of our website under Press Release. In addition, our Form 10-Q for the quarter-ended March 31, 2021, was filed shortly thereafter and can be found on the Investors section of our website under Financial Information.

Scott Walshco: Before we begin, I would like to remind everyone that, except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements.

Scott Walshco: Please see the forward-looking statement disclaimer in the company's earnings press release issued after the close of market today, as well as the risk factors included in our Form 10-Q for the quarter ended March 31, 2021, that was filed with the SEC. Undue reliance should not be placed on forward-looking statements, which speak only as of the date they are made, as facts and circumstances underlying these forward-looking statements may change. Except as required by law, Fate Therapeutics disclaims any obligation to update these forward-looking statements to reflect future information, events, or circumstances.

Scott Walshco: Joining me on today's call are Dr. Wayne Hsu, our Senior Vice President of Clinical Development, Ed Dulac, our Chief Financial Officer, and Bob Valamehr, our Chief Research and Development Officer. Today, we will highlight our clinical progress and plans for each of our disease franchises, including our plans to share interim clinical data for off-the-shelf, IPS-derived NK cell programs in acute myeloid leukemia and in B We will also discuss the expansion of our FT538 program into solid tumors, where our IND application was recently approved by the FDA for the conduct of a multi-dose, multi-cycle, phase one clinical trial in combination with certain monoclonal antibodies targeting tumor-associated antigens, EGFR, HER2, and PD-L1.

[music].

Scott Walshco: This marks the 12th IND allowed by the FDA for our IPSC product platform, alongside the 24th annual American Society of Gene and Cell Therapy meeting being held virtually next week. We plan to share interim Phase I clinical data for FT-516 and FT-538 programs in relapsed refractory AML. We believe this clinical update will be insightful on multiple fronts.

Scott Walshco: For example, there is clinical precedent across numerous single-center, investigator-initiated academic studies that donor NK cells can drive anti-leukemic activity. However, these approaches rely on the use of NK cells that are matched to the patient, that are manufactured solely for that patient, and that are delivered to that patient in a hospital setting following intensive conditioning therapy. FT-516 and FT-538 are iPSC-derived and K-cell product candidates that are administered off-the-shelf, in the outpatient setting, and without patient care.

Scott Walshco: Additionally, these Phase I clinical studies of FT-516 and FT-538 are designed to assess the inherent capacity of the product candidate to target and kill leukemic blasts as a monotherapy. As we have shown, encouraging phase 1 clinical data of FT-516 in combination with rituximab in relapsed refractory B-cell lymphoma. We believe there is an opportunity to build off of this foundation and combine it with ADCC-competent monoclonal antibodies in relapsed refractory AML.

Good day, ladies and gentlemen, and welcome to the fate Therapeutics first quarter 2021 financial results Conference call. This call is being webcast live on the investors section of fate.

Fate Therapeutics website at fate Therapeutics Dot com at this time all participants are in a listen only mode. Later, we will conduct a question and answer session and instructions will follow at the time if anyone should require operator assistance. Please press star then one.

Scott Walshco: To this end, an investigator-initiated study of FT538 in combination with daratumab designed to target CD38-positive leukemic blasts and further enhance anti-leukemic activity is expected to begin later this year. Finally, although patients have been treated in the first dose cohort only with FT-538, we are assessing early translational observations that might indicate whether FT-538, with its additional engineered modalities Patients with relapsed refractory AML often have high leukemic blast burns, prolonged impairment of hematopoietic function, and an exceptionally poor outcome. The median overall survival rates are less than 6 months, and 5-year overall survival rates are 10-15%.

Sorry Press Star zero on your touch on phone.

As a reminder, this call will be recorded I will now turn the call over to Scott Washco, President and CEO of fate Therapeutics, Scott you may begin.

Thank you good afternoon, and thanks, everyone for joining us for the fate Therapeutics first quarter 2021 financial results call.

Shortly after four P M. Eastern time today, we issued a press release with these results, which can be found on the investors section of our website under press releases. In addition, our form 10-Q for the quarter ended March 31, 2021 was filed shortly thereafter and can be found on the investors section of our web.

Site under financial information.

Before we begin I would like to remind everyone that except for statements of historical facts. The statements made by management and responses to questions. On this conference call are forward looking statements under the Safe Harbor provisions of the private Securities Litigation Reform Act of 1095 <unk>.

Scott Walshco: The only proven curative therapy is allogeneic stem cell transplants. However, many patients are often ineligible due to their leukemic burden or not deemed fit to tolerate the procedure due to the intensity of their chemotherapy conditions. There is a significant need for therapies that can clear the bone marrow of leukemic blasts, which can enable patients to qualify for allogeneic transplantation or can enable a durable response without further therapy. For example, a recent study in relapsed refractory AML showed that patients achieving an initial response per the 2017 ELN response criteria, defined as either achieving a complete response, CR, a complete response with incomplete hematologic recovery, CRI, or a morphologic leukemia-free state, MLFS, had statistically significant improvement in overall survival.

These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward looking statements. Please see the forward looking statement disclaimer on the company's earnings press release issued after the close of market today as well as the risk factors included in.

Our form 10-Q for the quarter ended March 31, 2021 that was filed with the SEC today.

Undue reliance should not be placed on forward looking statements, which speak only as of the day. They are made as facts and circumstances underlying these forward looking statements may change, except as required by law fate therapeutics disclaims any obligation to update these forward looking statements to reflect future information.

Events or circumstances.

Joining me on today's call our Doctor Wayne Chu, our senior Vice President of clinical development, and do Lark, Our Chief Financial Officer, and Bob <unk>, Our Chief Research and development Officer.

Scott Walshco: Given the significant unmet need for patients with AML, several therapies have been approved in recent years based on single-arm studies demonstrating response rates of 20 to 30% with 8 to 12 months median duration of response. These include therapies designed to target specific mutations that cause bone marrow dysfunction, such as IDH1, IDH2, and FLT3 inhibitors. Emerging therapies, including T-cell engagers in CAR T-cells, have also shown similar response rates in early phase tests. However, significant toxicities have been reported, including rates of cytokine release syndrome in excess of 50%.

Today, we will highlight our clinical progress and plans for each of our disease franchises, including our plans to share interim clinical data for off the shelf Ips derived NK cell programs in acute myeloid leukemia and in B cell malignancies, we.

We will also discuss the expansion of our ft, $5 38 program into solid tumors, where our R&D application was recently allowed by the FDA for conduct of a multi dose multi cycle phase one clinical trial in combination with certain monoclonal antibodies.

Getting the tumor targeting tumor associated antigens egfr her two and PDL one.

This marks the 12th IMD allowed by the FDA for our Ips C product platform.

Scott Walshco: In many respects, our interest in off-the-shelf IPS-derived NK cell therapy dates back to conversations in early 2015 with Dr. Jeff Miller, professor of medicine at the University of Minnesota and deputy director of the Masonic Cancer Center, and Dr. Sarah Cooley, who was at the time a leading clinical investigator in the emerging field of NK cell therapy at the University of Minnesota and now is senior vice president of translational medicine at Fate Therapeutic Doctors Miller and Cooley were conducting studies using ex vivo cytokine-activated peripheral blood NK cells to treat patients with relapsed refractory AML with the goal of bridging patients to transplant. In single-center investigator-initiated academic studies, ex vivo cytokine-activated donor and case cell therapy has shown responses of 20 to 35 percent, including in studies run by Drs. Miller and Miller.

Alongside the 24th annual American Society of Gene and cell therapy meeting being held virtually next week, we plan to share interim phase one clinical data for ft, 516, and ft $5 38 programs in relapsed refractory AML.

We believe this clinical update will be insightful on multiple fronts.

For example, there is clinical precedent across numerous single center investigator initiated academic studies that donor NK cells can drive anti leukemic activity.

However, these approaches rely on the use of NK cells that are matched to the patient that are manufactured solely for that patient and that are delivered to that patient in a hospital setting following intensive conditioning therapy.

Ft 516 in Ft, 538, our Ips derived NK cell product candidates that are administered off the shelf in the outpatient setting and without patient matching.

Scott Walshco: And while we believe these response rates are comparable to recently-approved therapies... Significant challenges have limited clinical advancement of donor NK cell therapy. For example, the current paradigm of donor and case-file therapy resembles a transplant-like process.

Additionally, these phase one clinical studies of <unk> 16 on Ft, $5 38 are designed to assess the inherent capacity of the product candidate to target and kill leukemic blasts as a mono therapy as.

As we have shown encouraging phase one clinical data of ft 516 in combination with Rituximab in relapsed refractory B cell lymphoma. We believe there is an opportunity to build off of this foundation and combine with ADC competent monoclonal antibodies in relapsed refractory.

Scott Walshco: Patients are hospitalized, receive intense lympho-depleting chemotherapy, and are administered NK cells from donors that are specifically manufactured for and matched to the patient. Additionally, very large numbers of NK cells, oftentimes in excess of several billion cells per dose, are required to be administered to patients to achieve a response. And production of such large numbers of NK cells often necessitates weeks of complex manufacture while the patient remains untreated and is at high risk for disease progression.

A M L.

To this end an investigator initiated study of <unk> $5 38 in combination with Dara two mab designed to target CD 38 positive leukemic blasts and further enhance anti leukemic activity is expected to begin later this year.

Finally, although patients have been treated in the first dose cohort only with ft. 538, we are assessing early translational observations that might indicate whether ft $5 38 with its additional engineers modalities has superior functionality.

Scott Walshco: In contrast, our FT-516 and FT-538 programs are off-the-shelf, IPS-derived sell-products that are available on demand for administration in the outpatient setting with outpatient matching, and therefore have the potential to efficiently and effectively treat many patients with AMS.

<unk> two ft 516.

Patients with relapsed refractory AML, often have high leukemic blast burden.

Pro longed impairment of hematopoietic function and exceptionally poor outcomes.

Scott Walshco: The Phase I study of FT516 as a monotherapy has enrolled the first and second dose cohorts of 90 million and 300 million cells per dose, and dose escalation is ongoing with enrollment in the third dose cohort of 90 million cells per dose. The Phase I study of FT538 as a monotherapy is ongoing with enrollment in the first dose cohort of 100 million cells per dose. As a reminder, AML is a very heterogeneous disease, and patient outcomes do vary depending on cytogenetics, mutation status, and leukemic burden.

Median overall survival rates are less than six months and five year overall survival rates are 10% to 15%.

The only proven curative therapy is allogeneic stem cell transplant. However, many patients are often ineligible due to their leukemic burden or not deemed fit to tolerate the procedure due to the intensity of chemotherapy conditioning.

There is a significant need for therapies that can clear the bone marrow of leukemic blasts, which can enable patients to qualify for allogeneic transplant or can enable a durable response without further therapy.

For example, a recent study in relapsed refractory AML showed that patients achieving an initial response per the 2017 <unk> criteria defined as either achieving a complete response CR a complete response with incomplete hematologic recovery.

Scott Walshco: Key objectives in dose escalation are the safety of our engineered IPS-derived NK cell products, tolerability of the Off-the-Shelf Multi-Dose Treatment Schedule, and Anti-Leukemic Activity, including in consideration of patient and disease baseline characteristics. Certainly, we will consider objective responses in dose escalation based on the established 2017 ELN response criteria, which is broadly accepted as the gold standard for assessing AML patient outcomes, as encouraging evidence that our off-the-shelf, IPS-derived, and K-Cell franchise may hold therapeutic promise for patients with AMS.

Hi, or morphologic leukemia free state MLS S.

Had statistically significant improvement in overall survival.

Given the significant unmet need for patients with AML. Several therapies have been approved in recent years based on single arm studies, demonstrating response rates of 20% to 30% with eight to 12 months median duration of response. These include therapies designed to target specific mute.

Patients that cause bone marrow dysfunction, such as <unk>, <unk> and <unk> inhibitors.

Emerging therapies, including T cell engages in car T cells have also shown similar response rates in early phase testing.

Scott Walshco: We are also interested in early translational comparisons between FT-516 and FT-538. At a feature symposium at ASGCT, Dr. Miller is scheduled to highlight the unique properties of FT538, resulting from the deletion of the CD38. In preclinical models, the engineered functionality of FT538 imparts metabolic, transcriptional, and functional properties that are substantially similar to those of adaptive NK cells, a discrete subset of memory-like NK cells that exhibit increased cytokine production, enhanced persistence, and resistance to oxidative stress. We look forward to reviewing early clinical data from our FT538 program that might indicate whether its engineered functionality confers superior therapeutic advantages. At the 2021 American Society of Clinical Oncology Annual Meeting being held virtually from June 4th through the 8th.

However, significant toxicities have been reported including rates of cytokine release syndrome in excess of 50%.

In many respects our interest in off the shelf Ips derived NK cell therapy dates back that conversation in early 2015 with Dr. Jeff Miller Professor of Medicine University of Minnesota, and Deputy director of the Masonic Cancer Center and Dr. Sarah Cooley, who was at the time of leading clinic.

Investigator in the emerging field of NK cell therapy at the University of Minnesota, and now as senior Vice President Translational medicine at fate Therapeutics doctors Miller and clearly we're conducting studies using ex vivo cytokines activated peripheral blood NK cells to treat patients with <unk>.

<unk> refractory AML with the goal of bridging patients to transplant.

In single Center investigator initiated academic studies ex vivo cytokines activated donor NK cell therapy has shown responses of 20% to 35%, including an studies run by doctors Miller on coolly.

And while we believe these response rates are comparable to recently approved therapies significant challenges have limited clinical advancement of donor NK cell therapy. For example, the current paradigm of donor NK cell therapy resembles a transplant like process.

Scott Walshco: We plan to present new clinical data from our phase one study of FT516 in combination with rituximab for the treatment of relapsed refractory B-cell lymphoma. We believe the interim phase one clinical data of FT516 in combination with rituximab previously presented at our investor event in December were compelling and suggest that FT516 can be administered in the outpatient setting. The high-affinity, non-cleavable CD16 receptor of FT516 can effectively synergize with rituximab in patients that have relapsed following or are refractory to rituximab-containing regimens.

Patients are hospitalized.

<unk> intense lymphoma depleting chemotherapy.

Our administered NK cells from donors that are specifically manufactured for and matched to the patient.

Additionally, very large numbers of NK cells, often times in excess of several billion cells per dose are required to be administered to patients to achieve responses.

And production of such large numbers of NK cells, often necessitates weeks of complex manufacturer, while the patient remains untreated and is at high risk for disease progression.

In contrast, our ft 516 in Ft, $5 38 programs are off the shelf Ips derived cell products, which are available on demand for administration in the outpatient setting without patient matching and therefore have the potential to efficiently and effectively.

Scott Walshco: FT 516 may have a differentiated safety profile compared to T-cell based therapies including T-cell engagers and CAR T-cell therapies, and FT-516 may confer rates of response in relapsed refractory B-cell lymphoma that are similar to those of T-cell based therapy. The ASCO presentation will cover a total of 13 patients that have completed dose escalation at the first three dose levels of 300 million cells, 900 million cells, and 300 million cells per dose.

Many patients with AML.

The phase one study of <unk> 16, as a mono therapy has enrolled the first and second dose cohorts of $90 million and 300 million cells per dose.

And dose escalation is ongoing with enrollment in the third dose cohort of 90 million cells per dose.

Scott Walshco: Note that the FT-516 clinical protocol does allow for patient backfill in the event a dose level has cleared toxicity and shown activity, so that more than three patients may be enrolled at a given dose level. Dose escalation in our Phase 1 study is currently ongoing with enrollment at 900 million cells per dose, and we are preparing to initiate multiple dose expansion cohorts.

The phase one study of Ft 538, as a mono therapy is ongoing with enrollment in the first dose cohort of 100 million cells per dose.

As a reminder, AML is a very heterogeneous disease and patient outcomes do vary depending on cytogenetics mutation status and leukemic burden.

Key objectives in dose escalation, our safety of our engineered Ips derived NK cell products tolerability of the off the shelf multi dose treatment schedule.

Scott Walshco: We're also preparing to explore combinations of FT516 with standard of care regimens containing CD20 targeted therapy and without CyFlu chemotherapy conditions to assess its therapeutic potential in earlier-line therapy. We continue to be pleased with the progress in our Phase 1 clinical trial of FT596, an off-the-shelf iPSC-derived CAR and K-cell product candidate designed to target multiple antigens through its high-affinity non-cleavable CD16 receptor and its CD19-targeted CAR, an approach that we believe may hold best-in-class potential for the treatment of B-cell malignancies.

<unk> anti leukemic activity, including in consideration of patient and disease baseline characteristics. Certainly we will consider objective responses in dose escalation based on the established 2017, <unk> response criteria, which is broadly accept.

It is the gold standard for assessing AML patient outcomes as encouraging evidence that our off the shelf Ips derived NK cell franchise may hold therapeutic promise for patients with AML.

We are also interested in early translational comparisons between ft 516 in FTE $5 38.

At a feature symposium at AST GCT. Dr. Miller is scheduled to highlight the unique properties of <unk> $5 38, resulting from the deletion of the CD 38 gene and.

Scott Walshco: Dose escalation in our Phase 1 study of FT596 is ongoing with enrollment in the third single-dose cohort of 300 million cells as monotherapy and at 300 million cells in combination with rituximab for B-cell lymphoma, as well as in the first single-dose cohort of 30 million cells as monotherapy for chronic lymphocytic leukemia. We plan to begin enrollment in combination with ibinitu In addition, since we believe that relapsed refractory patients with aggressive cancer will be best served by the administration of multiple doses during the first weeks of treatment.

In preclinical models, the engineered functionality of ft, $5 38 in parts metabolic transcriptional and functional properties that are substantially similar to those of adaptive NK cells, a discreet subset of memory like NK cells that exhibit increased cytokine production.

<unk> enhanced persistence resistance to oxidative stress and potent cereal cytotoxicity.

We look forward to reviewing early clinical data of our Ft 538 program that might indicate whether it's engineered functionality confers superior therapeutic advantages.

At the 2021 American Society of clinical oncology annual meeting being held virtually from June <unk> through the Ace.

Scott Walshco: We have now submitted a protocol amendment to enable multi-dose treatment schedules for FT596 in addition to the current single-dose treatment schedule. We plan to introduce the multi-dose treatment schedule in each of the four regimens, at the highest dose level cleared for the single-dose treatment schedule in that particular regimen.

We plan to present, new clinical data from our phase one study of <unk> hundred 16 in combination with Rituximab for the treatment of relapsed refractory B cell lymphoma, we believe the interim phase one clinical data on <unk> 16 in combination with Rituximab previous.

We presented at our Investor event in December were compelling and suggest that ft 516 can be administered in the outpatient setting.

Scott Walshco: In late July or early August, we plan to hold an investor event to feature our FT-596 program, where we expect to share interim Phase I clinical data covering approximately 20 patients. In the second quarter, we expect to initiate clinical investigation of our IPSC product platform in multiple myelomas. Similar to our approach in lymphoma, we are beginning clinical investigation in multiple myeloma by leveraging our high affinity non-cleavable CD16 receptor, and we are combining FT538 with Daratumab to maximize ADCC.

A high affinity non cleavable CD 16 receptor of Ft, 516 can effectively synergize with <unk>.

With Rituximab in patients that have relapsed following or are refractory to rituximab containing regimens ft 516 may have a differentiated safety profile.

Compared to T cell based therapies, including T cell engaging <unk> and car T cell therapies and Ft 516 may confer rates of response in relapsed refractory B cell lymphoma that are similar to those of T cell based therapies.

Scott Walshco: While DARA2MAP effectively targets CD38 expressed on myeloma cells and induces cell death, it also induces NK cell fracture, which significantly impairs the effectiveness of ADC. In addition, NK cell function is often impaired in patients with multiple myeloma, further reducing the potential therapeutic activity of dark.

<unk> presentation will cover a total of 13 patients that have completed dose escalation at the first three dose levels of 300 million cells 900 million cells and 300 million cells per dose.

Note that the Ft 516 clinical protocol does allow for patient backfill in the event of dose level has cleared toxicity and shown activity.

Scott Walshco: Collectively, preclinical and clinical observations suggest a potential therapeutic benefit of maintaining NK cell numbers and function. Therefore, enrollment of FT538 in combination with daratumab will commence at 100 million cells per dose. We are also preparing to initiate a Phase I clinical trial of FT576, our off-the-shelf IPS-derived core and K-cell product candidate designed to target multiple antigens through its high-affinity non-cleavable CD16 receptor and its BCMA-targeted CAR, an approach that we believe may hold best-in-class potential for the treatment of multiple myeloma.

So that more than three patients may be enrolled at a given dose level.

Dose escalation in our phase one study is currently ongoing with enrollment at 900 million cells per dose. We are preparing to initiate multiple dose expansion cohorts. We are also preparing to explore combinations of ft 516 with standard of care.

Emmons containing CD 20 targeted therapy and without Cy flew chemotherapy conditioning to assess its therapeutic potential in earlier lines of therapy.

We continue to be pleased with the progress in our phase one clinical trial of Ft 596 are off the shelf Ips derived car NK cell product candidate designed to target multiple antigens through its high affinity non cleavable CD 16 receptor and its CD 19 targeted.

Scott Walshco: At the American Association for Cancer Research annual meeting in April, we presented preclinical data demonstrating that the multi-antigen targeting functionality of FT576 exhibits greater in vivo efficacy compared to the combination of BCMA-targeted CAR T-cells and agamase secretase inhibitors. The clinical protocol for a Phase I clinical trial of FT576 includes dose escalation, both as monotherapy and Additionally, the protocol includes assessment of both single-dose and multi-dose treatment regimens to maximize the therapeutic index during the first 30 days following infection.

Car and.

And the approach that we believe may hold best in class potential for the treatment of B cell malignancies.

Dose escalation in our phase one study of <unk> hundred 96 is ongoing with enrollment in the third single dose cohorts of 300 million cells as monotherapy.

And at 300 million cells in combination with Rituximab for B cell lymphoma.

As well as in the first single dose cohort of 30 million cells as mono therapy for chronic lymphocytic leukemia, we.

We plan to begin enrollment in combination with <unk> upon clearance of this first monotherapy dose cohort in CLO.

Scott Walshco: As I mentioned during our last quarterly update, we are enthusiastic about the potential of NK cells to treat a wide range of solid tumors, and we are pleased with the progress we're making in building our pipeline of off-the-shelf, multiplexed engineered products.

In addition, since we believe that relapsed refractory patients with aggressive cancers will be best served by administration of multiple doses during the first weeks of treatment with.

We have now submitted a protocol amendment to enable multi dose treatment schedules for ft $5 96. In addition to the current single dose treatment schedule.

Scott Walshco: An initial therapeutic strategy of particular interest to us is exploiting ADC, which is a potent anti-tumor mechanism by which NK cells recognize, bind, and kill antibody-coded cancer cells, and which has been shown to improve progression-free survival in patients with solid tumors. However, significant limitations in the functional capacity of a patient's NK cells, which are often depleted in number or impaired, including through CD16 shedding, can compromise the potency of ADCC in patients with solid tumors. We believe off-the-shelf administration of an ADCC-optimized NK cell can augment the activity of monoclonal antibodies that are currently approved for the treatment of many solid tumors.

We plan to introduce the multi dose treatment schedule in each of before regimens at the highest dose level cleared for the single dose treatment schedule in that particular regimen.

In late July early August we plan to hold an investor event to feature our Ft, 596 program, where we expect to share interim phase one clinical data covering approximately 20 patients.

In the second quarter, we expect to initiate clinical investigation of our Ips C product platform in multiple myeloma.

Similar to our approach in lymphoma, we are beginning clinical investigation in multiple myeloma by leveraging our high affinity non cleavable CD 16 receptor and we're combining FTE $5 38, with Dara two mab to maximize ADC.

Scott Walshco: To this end, we are currently enrolling patients in the third dose cohort of our phase one study of FT5-16 in combination with Aveliumab, an ADCC-competent anti-PD-L1 checkpoint inhibitor therapy. I am pleased to announce today that we are significantly expanding on this therapeutic strategy. Last month, the FDA approved our IND application for clinical investigation of FT538 in combination with an array of monoclonal antibodies, including those that target the tumor-associated antigens EGFR, HER2, and PD-L1.

While Dara to map effectively targets CD 38 expressed on myeloma cells and induces cell death.

It also induces NK cell fracture side, which significantly impairs the effectiveness of ADC.

In addition, NK cell function is often impaired in patients with multiple myeloma.

Further reducing the potential therapeutic activity of <unk>.

Collectively preclinical and clinical observations suggest a potential therapeutic benefit of maintaining NK cell numbers and function.

Enrollment of <unk> $5 38 in combination with Dara <unk> will commence at 100 million cells per dose.

We are also preparing to initiate a phase one clinical trial of <unk> hundred 76 are off the shelf Ips derived car NK cell product candidate designed to target multiple antigens through its high affinity non cleavable CD 16 receptor and its be CMA targeted car and.

Scott Walshco: This marks the 12th IND allowed by the FDA for our IPSC product platform. Under the clinical protocol, each patient is eligible to receive up to two FT-538 treatment cycles, with each cycle consisting of 3 days of outpatient lymphoconditioning, 3 once-weekly infusions of FT538, and monoclonal antibody therapy. We intend to initiate clinical investigation of three independent regimens, combining FT-538 with EGFR-targeted cetuximab, HER2-targeted tristuzumab, and PD-L1-targeted evalumab, and we expect to initiate enrollment in the second half of 2021.

<unk> that we believe may hold best in class potential for the treatment of multiple myeloma.

At the American Association for Cancer Research annual meeting in April we presented preclinical data demonstrating that the multi antigen targeting functionality of <unk> hundred 76 exhibits greater in vivo efficacy compared to the combination of beef.

CMA targeted car T cells, and a gamma secretase inhibitor.

The clinical protocol for a phase one clinical trial of <unk> hundred 76 includes dose escalation, both as monotherapy and in combination with Dara to map to enable dual antigen targeting of <unk> and <unk> 38 on myeloma cells.

Scott Walshco: Finally, I would like to take a moment and sincerely thank the patients, caregivers, and investigators who participated in the PROTECT study of proteins. While our full attention and resources are focused on our deep pipeline of off-the-shelf IPS-derived cancer immunotherapies, we are disappointed to announce that the PROTECT study did not meet its primary endpoint of prevention of acute graft-first host disease following allogeneic stem cell transplant, and we will stop all further development approaches.

Additionally, the protocol includes assessment of both single dose and multi dose treatment regimens to maximize the therapeutic index. During the first 30 days following infusion.

As I mentioned during our last quarterly update we are enthusiastic about the potential of NK cells to treat a wide range of solid tumors.

And we are pleased with the progress we are making in building our pipeline of off the shelf multiplexed engineered product candidates.

An initial therapeutic strategy of particular interest to us is exploiting ADC, which is a potent anti tumor mechanism by which NK cells recognize find and kill antibody coated cancer cells, and which has been shown to improve progression free survival.

Scott Walshco: We intend to share the clinical results of the PROTECT study with our investigators and the broader transplant community to assist in their continuing efforts to improve the curative potential of allogeneic transplantation for patients. I would now like to turn the call over to Ed to highlight our first quarter financial results.

In patients with solid tumors.

However, significant limitations in the functional capacity of a patients NK cells, which are often but depleted a number or impaired including through CD 16, shedding can compromise the potency of <unk> ADC in patients with solid tumors.

Edward J. Dulac: Thank you, Scott. Turning to our financial results, revenue was $11.1 million for the

Edward J. Dulac: first quarter of 2021, compared to $2.5 million for the same period last year. Revenue in the current quarter was derived from our collaborations with Janssen and Ono Pharmaceuticals.

We believe a off the shelf administration of an ADC optimized NK cell can augment the activity of monoclonal antibodies that are currently approved for the treatment of many solid tumors to this end. We are currently enrolling patients in the third dose cohort of our phase one.

Edward J. Dulac: Research and development expenses for the first quarter of 2021 were $44.9 million, compared to $29.3 million for the same period last year. The increase in our R&D expenses is attributable primarily to an increase in employee headcount and compensation, including share-based compensation, and in expenses associated with clinical trial costs. General and administrative expenses for the first quarter of 2021 were $12.5 million, compared to $7.7 million for the same period last year. The increase in our G&A expenses was attributable primarily to an increase in headcount and employee compensation, including share-based compensation.

Study of Ft, 516 in combination with the volume up and Asia, ADC competent anti PD lone checkpoint inhibitor therapy.

I am pleased to announce today that we are significantly expanding on this therapeutic strategy.

Last month, the FDA allowed our IND application for clinical investigation of Ft 538 in combination within our array of monoclonal antibodies, including those that target the tumor associated antigens Egfr her two and PDL one.

This marks the 12th IND allowed by the FDA for our Ips C product platform.

Under the clinical protocol each patient is eligible to receive up to two ft 538 treatment cycles.

Edward J. Dulac: Total operating expenses for the first quarter of 2021 were $44.4 million, net of $13 million in non-cash, share-based compensation expense. In the first quarter, we recorded a non-cash, $0.7 million non-operating benefit associated with the fair value of contingent milestone payments under our IPSC-derived CAR T-cell collaboration with Memorial Sloan Kettering. In the event that a certain clinical milestone is achieved with an IPSC-derived CAR T-cell product candidate, up to three milestone payments may be owed to MSK based on the subsequent trading values of the company's common stock, ranging from 50 to $150 per share.

With each cycle, consisting of three days of outpatient linfield conditioning, three once weekly infusions of ft, $5, 38, and monoclonal antibody therapy.

We intend to initiate clinical investigation of three independent regimens, combining ft 538, with Egfr targeted to <unk> her two targeted trastuzumab and PDL, one targeted <unk> and we expect to initiate enrollment in the second half of 'twenty.

'twenty one.

Finally, I would like to take a moment and sincerely. Thank the patients caregivers and investigators who participated in the protect study of programming.

While our full attention and resources are focused on our deep pipeline of off the shelf Ips derived cancer Immunotherapies. We are disappointed to announce that the protect study did not meet its primary endpoint of prevention of acute graft versus host disease following allogeneic stem.

Edward J. Dulac: These milestone payments in the aggregate total up to $75 million, and no amounts have been paid or are currently owed to MSK. We will remeasure this liability, currently valued in the aggregate at $47 million, on a quarterly basis, and changes in the fair value will be recorded in our earnings as a non-operating income or expense. In January, we completed a public offering of common stock, whereby we issued 5.1 million common shares. In addition, in lieu of common stock, we issued 257,000 pre-funded warrants. The net proceeds from the financing were approximately $432 million, and the company ended the first quarter of 2021 with $888 million in cash equivalents.

Cell transplant, and we will stop all further development of premium we intend to share the clinical results of the protect study with our investigators and the broader transplant community to assist in their continuing efforts to improve the curative potential of allogeneic transplant for patients.

<unk>.

I would now like to turn the call over to Ed to highlight our first quarter financial results.

Thank you Scott turning to our financial results revenue was $11 1 million for the first quarter of 2021 compared to $2 5 million for the same period last year.

Revenue in the current quarter was derived from our collaboration with Janssen and Ono Pharmaceuticals.

Operator: [inaudible] CommonStock: outstanding

Research and development expenses for the first quarter of 2021 were $44 9 million compared to $29 3 million for the same period last year the.

Operator: Common stock outstanding was 94 million shares, and preferred convertible stock outstanding was 2.8 million shares, each of which is convertible into five shares of common stock under certain conditions. I would now like to open the call to any questions.

The increase in our R&D expenses was attributable primarily to an increase in employee head count and compensation, including share based compensation and in expenses associated with clinical trial costs.

General and.

Operator: Thank you. Ladies and gentlemen, if you have a question at this time, please press star, then the number on your touchtone phone.

Administrative expenses for the first quarter of 2021 or $12 5 million.

Compared to $7 $7 million from the same period last year the.

Operator: If your question has been answered or you wish to remove yourself from the queue, please press the pound key. And we do have our first question from Robin from Truist Securities. Thanks for taking my question and so much on the call. So, let's just start off with next week, and you have a lot of data coming. You've talked about, you've updated, on the call you talked about, how do you update on FT6516 and FT538? Maybe give us some color about that.

The increase in our G&A expenses was attributable primarily to an increase in head count and employee compensation, including share based compensation.

Total operating expenses for the first quarter of 2021 were $44 $4 million net.

Net of $13 million and noncash share based compensation expense.

In the first quarter, we recorded a non cash zero point $7 million non operating benefit associated with the fair value of contingent milestone payments under our Ips derived car T cell collaboration with Memorial Sloan Kettering.

In the event a certain clinical milestone is achieved with an Ips derived car T cell product candidates up to three milestone payments may be owed to MSA based on subsequent trading values of the company's common stock ranging from 50 to $150 per share.

Operator: Patient baseline. How many patients will we see? How many doses? What will we see them treated with? And how do we think about your strategy in AML? In a nutshell, how do we digest this data, and how do we set the expectations for it?

These milestone payments in the aggregate total up to $75 million and no amounts have been paid or are currently owed to Ms. Kay.

Operator: Thanks.

Operator: So, Robin, I mean, we will have a fairly comprehensive event from now on. I think it's next Thursday, so seven, eight days from now, we'll have a fairly comprehensive event.

We will re measure of this liability currently valued in the aggregate at $47 million on a quarterly basis and changes in the fair value will be recorded in our earnings as a non operating income or expense.

Operator: We will walk through what has historically been done with respect to NK cell treatment in AML. We will provide some detail on the preclinical results that we have seen, for instance, with FT-538, including comparing FT-538 to FT-516. And then Wayne will spend a significant amount of time walking through the history of patients that we've treated. You will see patients, on a patient basis, you'll see detail on a patient by patient basis, so we plan on providing detail for each and every patient.

In January we completed a public offering of common stock whereby we issued five 1 million common shares in.

In addition in lieu of common stock, we issued 257 pre funded warrants.

The net proceeds from the financing were approximately $432 million.

The company ended the first quarter of 2021 with $888 million of cash cash equivalents and investments.

Common stock outstanding was 94 million shares and preferred convertible stock outstanding was $2 8 million shares each of which is convertible into five shares of common stock under certain conditions.

Operator: And you will see baseline characteristics. You will see whether that patient is relapsed or refractory. You will see the most recent therapy. You will see the, for instance, risk profile associated with each and every patient. And then importantly, you will obviously see anti-leukemic activity and responses associated with each and every patient. So there will be a tremendous amount of detail. There will be, it'll be very transparent on a patient-by-patient basis, and we expect to include in that about 12 in total.

I would now like to open the call up to any questions.

Thank you, ladies and gentlemen, Hey, do you have a question at this time. Please press Star then the one on you touched on phone. If your question has been answered or you wish to remove yourself from the queue. Please press the pound key.

And we do have our first question from Robyn.

From a security.

Yeah.

Robin can play out.

Hi, everyone. Good day.

Thanks for taking my question then so much on the call.

We'll just start off with you know next week and then you have a lot of data coming.

Operator: I mean, going forward, that's a big one for you. Yeah, no, sorry. Need more clarity there.

You've talked that you can update us on the call you talked about yet.

Kate on Etsy.

Non cyclical lucky.

Operator: Strategy in solid tumors? Absolutely.

Slide 38.

Maybe you can give us some color about the patient baseline how many patients what we see how many doses.

Operator: I mean, clearly, we think there are multiple monoclonal antibodies that are improved in solid tumors, for instance, whether it be Herceptin, Erbitux, Avelumab, and others. And part of their mechanism of action is dependent on antibody-dependent cellular cytosol toxicity, ADCC. And we think NK cells play a really important role there. We actually think, you know, there's plenty of evidence to suggest that ADCC today is not being optimized, that the NK cell compartment essentially that exists within patients is checked or compromised, and that by coming in with a wave of NK cells that are designed to synergize with the monoclonal antibody, we think we can substantially augment the response.

Hmm.

We'll.

See them treated with and how should we think about your strategy on ammo.

On the Big picture, how do we digest this data and how do we put the expectation Platt Inc.

Sure.

So Robyn I mean, we will have a fairly comprehensive event from now I think it's next Thursday, so seven to eight days from now we'll have a fairly comprehensive event.

We'll walk through.

What has historically been done with respect to NK cell treatment in AML.

We will provide some detail on the pre clinical results that we have seen for instance, with ft, $5 38, including comparing ft $5 38 to ft 516.

And then Wayne will spend a significant amount of time walking through.

The history of patients that we've treated you will see patients.

Operator: That's step one, and we are starting to initiate that obviously with FT516, but we're obviously increasing our investment based on our conviction in ADCC by moving FT538 now into solid tumors across a fairly broad set of monoclonal antibodies in solid tumors. Ultimately, though, as you know, we think of that as a stepping stone.

On a patient you'll see detail on a patient by patient basis. So we plan on providing the detail for each and every patient and you will see baseline characteristics you will see whether that patient is relapsed or refractory you will see most recent therapy you will see.

That's the.

For instance, risk profile associated with each and every patient and then importantly, you will obviously see anti leukemic activity and responses associated with each and every patient. So there will be a tremendous amount of detail there will be it will be very transparent on a patient by patient basis and we expect to include in that about in total 12 patients.

Operator: What we're doing, for instance, in lymphoma, what we're doing in myeloma, where we're utilizing, for instance, CD16, in addition to engineered CAR functionality, we are doing the same exact thing in solid tumors where we have product candidates emerging in the second half of this year, building off of the FT-538 backbone. Engineering in cars, for instance, our first IND will be engineering We recently presented data where we engineered a car into the FT538 backbone against B7H3 as a solid tumor targeting strategy. And in addition, we expect that the first IND, actually under the Janssen collaboration, will be a car and case cell product for solid tumors.

And strategy in solid tumors.

I mean going forward, that's a big one for you.

Sorry, one more clarity there and excited about that.

On a strategy in solid tumors, absolutely I mean, clearly we think there are multiple monoclonal antibodies that are improved in solid tumors for instance, whether it be herceptin.

<unk>, others and part of their mechanism of action is dependent on antibody dependent cellular cytotoxicity ADC and we think NK cells play a really important role there. We actually think there is plenty of evidence to suggest that ADC today is not <unk>.

Operator: Thanks, Scott. Again, you've mind-blown me about how many different products you have to focus on. I'm writing them all down.

<unk> optimized that the NK cell compartment essentially that exist within patients.

Operator: I'm writing them all down. But thank you so much. I appreciate it. Sure. And we do have our next question from Ted Tenhof on Piper Sandler.

Is check to or compromised and that by coming in with a wave of NK cells better designed to synergize with the monoclonal antibody. We think we can substantially augment responses. That's step one and we are started to initiate that.

Operator: Hey guys, thanks so much for taking the question.

Operator: event later this year.

Operator: With all these different approaches on the solid tumor side, how do you ultimately envision this playing out? Do you expect that there will be certain cell types?

With Ft 516, but we're obviously increasing our investment based on our conviction in ADC by moving Ft 538, now into solid tumors across a fairly broad set of monoclonal antibodies in solid tumors ultimately though.

Operator: that may be better in different kinds of cancers with different kinds of therapy.

Operator: of Therapeutic Combinations. Do you ultimately see a penultimate product like the MIC-A or MIC-B? Give us a little bit more color on sort of where you're thinking is going on there, thank you. Sure.

As you know, we think of that as a stepping stone.

What we're doing for instance in lymphoma, what we're doing in myeloma, where were utilizing for instance, CD 16. In addition to engineered car functionality.

Operator: I mean, I think it's early for us to have a definitive strategy in solid tumors with multiplexed engineered cell therapy since we are breaking new ground. I do think, however, that there are certain solid tumors that may actually be more amenable to NK cell therapy. We've talked in the past, for instance, that there are various mechanisms of resistance that solid tumors utilize to escape recognition by the immune system, whether it's T-cells or NK-cells.

We are doing the same exact thing in solid tumors, where we have product candidates are emerging in the second half of this year.

Building off of the Ft, $5 38, backbone engineering and cars for installed <unk> will be engineering, a car against to make gain mcbee stress ligands. We recently presented data where we the engineered in a car into the ft 538 backbone against <unk> three.

Operator: One of the more significant mechanisms of resistance is actually where the tumor works to downregulate MHC class 1, so there is loss of antigen presentation through that downregulation of MHC class one. Because of that, T cells can no longer recognize those tumors. But that's the exact cell type that an NK cell can, in fact. And oftentimes, the cells, the tumor cells that downregulate MHC class 1 are high expressors of stress ligands.

Re as a solid tumor targeting strategy and in addition, we expect that the first <unk> D actually under the Janssen collaboration will be a car NK cell product for solid tumors.

Alright, Thanks, again, you've mined blown me about how many different product lines.

I don't know all day, but thank you so much I appreciate it.

Sure.

And we do have our next question from <unk>.

Net 10 half Piper Sandler.

Operator: Again, these are, for instance, cues for NK cells to recognize an attack. So I think that is one area of solid tumor biology that we are really interested in with respect to NK cells and, in particular, the CAR-MicA-MicB product candidate since it's designed to key in on stress ligands and even overcome resistance that exists with downregulation of stress ligands or shedding of stress ligands. But in addition, I also think, you know, there is gonna be a fundamental role for combination with monoclonal antibodies.

So from a cyclical question.

I wanted to follow up a little bit.

Given that we're going to have your event later this year and more datasets.

With all of these different approaches of the solid tumor side, how do you ultimately envisioned this playing at all do you expect growth there will be certain cell types.

That may be better and different kinds of cancers with different kinds of <unk>.

Through the combination.

Ultimately see a penalty on that product line from Mr. Mcbee.

Chemical and put more color on sort of where your thinking is there. Thank you.

Sure.

I think it's early for us to have a definitive strategy and solid tumors with multiplexed engineered cell therapy since.

Operator: I mean, you know, monoclonal antibodies are used early and often, successfully, to treat solid tumors. And part of their mechanisms of action is ADCC and NK cell dependent. And so we're really excited, for instance, with respect to FT538 and being able to combine that with monoclonal antibody therapy against a broad array of solid tumors. Thanks, everybody. Thank you.

We are breaking new ground I do think generally there are certain solid tumors that may actually be more amenable to an NK cell therapy, we've talked in the past for instance that there are various mechanisms of resistance.

Net solid tumors utilize to escape recognition of the immune system, whether it's T cells or NK cells. One of the more significant mechanisms of resistance is actually where the tumor works to down regulate MHC class one.

Operator: Excellent. Well, I'm excited about the events coming up and more data.

And there is loss of antigen presentation through that downregulation of MHC class, one because of that T cells can.

Operator: And we do have our next question from Alisa Young from Cantor. Hey guys, thanks for taking my question and congratulations on all the progress. I'm looking forward to next week for sure.

Can no longer recognize those tumors.

The exact cell type that an NK cell tenant in fact recognize and often times the cells the tumor cells debt down regulate MHC class one our high expresses of stress ligands again. These are that these are for instance.

Operator: I guess I just wanted to maybe ask a philosophical and a little bit practical question. Just, you know, how important is durability after kind of a single dose or understanding that or having a, you know, kind of perception of that in this data set and other upcoming data sets as well? And then also, can you just talk a little bit about whether it's PD-L1 that's kind of the better target versus PD-1? I'm just curious about that as well.

Hughes for NK cells to recognize and attack. So I think that is one area of solid tumor biology that we are really interested in with respect to NK cells and in particular, the <unk> product candidate since it's designed to key in on stress law.

Operator: I'll start with the last question. I mean, you know, we're obviously early in exploration with respect to the combination of monoclonal antibodies in solid tumors. We started with Velumab. It doesn't mean it was the right place to start, but we started with Velumab because, you know, obviously PD-L1 is upregulated on the tumor itself. So we thought at least it provided a means by which the NK cell could target, in combination with Velumab, a target expressed on a tumor as opposed to PD-L1.

Gans and even overcome resistance.

That exists with downregulation of stress ligands are shedding of stress ligands, but in addition, I also think there is going to be a fundamental role for combination with monoclonal antibody.

Monoclonal antibodies are used them early and often successfully reached solid tumors.

And.

Part of their marketing mechanisms as action is ADC in NK cell dependent and so we're really excited for instance, with respect to <unk> $5, 38, and being able to combine that with monoclonal antibody therapy.

Against a broad array of solid tumors.

Excellent coverage of the events coming up on more data this year.

Thank you.

And we do have a next question from Lisa Yang from Cantor.

Operator: With respect to durability of the doses, I mean, again, this is something that we are exploring, and we're experimenting with different treatment regimens and schedules to begin to tease out the differences that might exist between treatment schedules, whether that's one dose or whether that's, for instance, up to six doses. I think it's too early to know the answer to that question.

Hey, guys. Thanks for taking my question and congrats on all the progress we're looking forward to next week for sure.

I guess I just wanted to maybe it's a philosophical.

Practical question, just how important is durability. After after kind of a single dose or understanding that are having a kind of a perception of that end like this data set and the other upcoming datasets as well and then also can you just talk a little bit about the PDL. One that's kind of the better target versus PD, one just curious about that as well. Thanks.

Operator: I think fundamentally we believe two things. First, that there is a period of time, especially for aggressive cancers, where you need to hit the tumor hard. And that may be the first two weeks; maybe that's the first four weeks; maybe that's the first six weeks. But there's a period of time where we believe a therapy really needs to aggressively attack the tumor to lead to a deep, durable response. I would also say our belief system today is that the best way to drive that deep, durable response during that window, again, whether it be two, four, six weeks, is through multi-dose.

Sure.

What was the last question I mean, we're obviously early in exploration with respect to combination of monoclonal antibodies in solid tumors, we started with a volume app.

It doesn't it doesn't mean it was the right place to start, but we start with the volume out because obviously PDL one is up regulated.

On the tumor itself. So we thought at least it provided a means by which the NK cell could target in combination with a volume at.

A target expressed on a tumor as opposed to PD one PD one.

With respect to durability of the doses I mean again. This is something that we are we are exploring an.

Experimenting with different treatment regiments and schedules to begin to tease out the differences that might exist between treatment schedules, whether thats one dose whether thats for instance up to six doses I think it's too early to know the answer to that question I think fundamentally we believe two things.

Operator: And the reason for that is because when you administer a cell to a patient, I think there's lots of data emerging that that cell profoundly changes with respect to its function, properties, and anti-tumor killing ability during that window of time. And so our belief is that to really maximize activity, and because the cells administered to patients do change within the patient, a multi-dose strategy is likely going to be the best strategy. And I would say, similar to that, we believe a multi-targeting strategy is going to be the most effective strategy. Thanks. That's very helpful.

Net.

There is a period of time.

Especially for aggressive cancers, where you need to hit the tumor hard.

And that may be the first two weeks, maybe thats. The first four weeks, maybe thats. The first six weeks, but there is a period of time, where we believe a therapy really needs to aggressively attack the tumor to lead to.

Deep durable responses.

And I would I would also say our belief system today is that the best way to drive that deep durable kill during that window again, whether it be 246 weeks is through multi dosing.

Operator: And we do have our next question from Yigal Nochomovitz from Citi.

Operator: Hi, thank you very much for taking the question. Scott, any prepared remarks on AMS?

And the reason for that is because when you administer sell into a patient I think theres lots of data on emerging that that cell profoundly changes with respect to its function properties anti tumor killing ability.

Operator: https://youtu.beo.com

Operator: Targeted therapies such as CLIT3 and IDH inhibitors have been approved based on their effectiveness.

Operator: Narrow Measure of CRCRH. No, we've not had any discussions with the FDA at this point. We're using what we believe to be an updated criteria using the 2017 ELN. We think it is the gold standard.

During that window of kill and so our belief is that to really maximize activity and because the cells administered to patients do change within the patient that are multi dose strategy is likely going to be the best strategy and I would say finally, we.

Operator: We can have an interesting discussion, and maybe Wayne can jump in with respect to CRH versus CRI. We actually believe that under the 2017 ELN criteria, CRI is a higher bar than CRH. CRI requires either full recovery of neutrophils or platelets, while CRH does not require full recovery of either. So under the 2007 ELN criteria, we actually believe CRI is a higher bar than CRH. And Wayne, I don't know, you may want to comment on that. So just one comment. I mean, I think. Yes, I mean, we certainly are...

Similar to that.

Believe on multi targeting strategy is going to be the most effective strategy.

Yeah.

Okay. That's helpful.

And we do have our next question from Eagle <unk> from Citi.

Hi, Thank you very much for taking the question Scott on your prepared remarks on AML you mentioned.

Alluded to <unk> being correlated with improved overall survival, obviously some of the more recent approved therapies for AML targeted therapies, such as the 390 <unk> inhibitors were approved based on a narrower and narrower measure of CRC. Our range. I was just wondering is there any specific reason with respect to cell therapies.

Focus should be on <unk> as opposed to CRH.

CRH that's been the case for their targeted therapies and have you had any discussions with the FDA on this nuance.

No I have not had any discussions with the FDA at this point, we're using what we believe to be an updated criteria.

Operator: Assessing Our Responses objectively, based on the 2017 ELN criteria

Using 2017 El N. We think it is the gold standard we can have an interesting discussion on maybe Wayne can jump in with respect to CRH vs. Cri, we actually believe under the 2017 Elo El N criteria.

Operator: It's important to emphasize that as we're in, you know, because we're only in the early phase.

Operator: Phase I study, you know, the early part of Phase I dose escalation, you know.

<unk> is a higher bar than CRH cri.

Operator: We're not holding fast to specific endpoints like CRCRIH as a path to registration.

Wires, either full recovery of neutrophils or platelets.

CRH does not require full recovery of either.

Operator: We look at the responses as early indicators of activity that might confer clinical benefit. So I would caution just a little bit about committing to a particular response criteria at this early stage of the game. But certainly, as our data set matures and we get more data, then understanding some of the relationships between...

So under the 2007 <unk> criteria, we actually believe Cri is a higher bar than CRH and Wayne I don't want you may want to comment on that.

So just one comment I mean I think.

Yes, we are.

We're certainly assessing our response to subjectively objectively based on the 2017 Gail on criteria. We are very aware of some of the recent approvals for example, with some of the <unk> inhibitors, where the approval was based on a composite CR in CRH and I think it is important to emphasize debt.

Operator: Response and durability and even survival as we get enough patients will allow us the opportunity to further refine some of these.

As we're in because we're only in early phase one study.

Early part of a phase one dose escalation.

Operator: https://www.cdc.gov.au

We're not holding fast to specific <unk>.

Operator: Okay, thank you very much. I just had one other question. Maybe you've commented on this in the past.

<unk> is a path to registration we when you look at the response is that early indicators of activity that might confer a clinical benefit.

Operator: If you could remind us, could you just explain why the...

I would caution just a little bit about <unk>.

Operator: The starting dose for 538 in myeloma is 100 million cells, whereas for 516 and 596, it's three-fold lower at 30 million cells. And also, what is going to be the expected starting dose for...

Committing to a particular response criteria at this early stage of the game.

But certainly as our dataset matures and we get more data than understanding some of the relationships between.

Operator: Thank you for joining us for 576. Yeah.

Sponsor and durability and even survival as we get enough patients.

Operator: Yeah, I wouldn't read too much into it other than just time and experience. If you go back, you know, obviously the initial experiences with FT516, we're talking about an IPS-derived therapy, FT516, at the time that it was engineered with CD16, with very little clinical experience. And so we started and proposed to start at 30 million cells per dose. As we've gotten more advanced and built up clinical experience over time, we've gotten comfortable with the safety profile, quite honestly, of what we're seeing with our IPS-derived NK cell therapies, including at much higher doses.

It will allow us the opportunity to further refine some of these relationships when we apply other criteria like CRE.

Okay. Thank you very much I just had one other question maybe you commented on this in the past, but if you could remind us could you just explain why the starting dose for $5 38 in myeloma is 100 million cells, whereas for $5 16 on $5 96, a threefold lower at 30 million cells and also what is going to be the <unk>.

<unk> starting dose for 576.

Yeah.

I wouldn't read too much into it other than just time and experience if you go back.

Obviously, the initial experiences with Ft 516, we're talking about an Ips derived.

<unk> therapy Ft 516 at the time that was engineered with <unk> 16, very little clinical experience experience and so we started and proposed to start at 30 million cells per dose as we've gotten more advanced and built up clinical experience over time.

Operator: And so when we submitted our protocol for FT-538, as well as FT-576, Now, given all the safety history we do have with our platform going back two years, we opted to start at a higher dose, 100 million cells per dose, and the FDA was comfortable with that.

We've gotten comfortable with the safety profile quite honestly of what we're seeing with our Ips derived NK cell therapies, including at much higher doses and so when we submitted our protocol for Ft 538, as well as FTE 576, now given all.

Operator: And we do have our next question from Michael Yee of Jeffrey.

Operator: Hey Scott, congrats on all the progress. We had two questions. One was going back to expectations around AML. You've previously said that a 20 to 30 percent CR rate has been seen in literature. You talked about the various, I guess, limitations with some of those programs. Is that the right bar to think about for 5.1.6 and how to put that into context with the fact that you will have some 5.38 data next week as well?

The safety history, we do have with our platform going back two years, we opted to start at a higher dose 100 million cells per dose and the FDA was comfortable with that.

Great. Thank you.

Sure.

And we do have our next question from Michael <unk> from Jefferies.

Hey, Scott.

Congrats on all the progress we have two questions one was going back to expectations around AML.

You've previously said, 20% to 30% CR rate has been seen in literature, you've talked about the various I guess limitations for some of those programs is that the right bar to think about 456.

Operator: So maybe just compare and contrast those programs versus the expectations you've laid out and also how important durability is. So that's question one on AML. And question two is similar, and that is with lymphoma in the summer. We know the data from ASH, and I think you had two prior CRs. Durability seems to be a question that would be important. Can you just help us understand expectations around durability given that there are only two CRs, but CAR T is 33 to 50 percent durable CR.

And how to put that into context with the fact that you will have some $5 38 data next week as well. So maybe just compare and contrast, those programs versus the expectations you've laid out and also how important is durability. So that's question. One is on AML and question two is similar and that is with lymphoma in the summer.

We know the data at Ash and I think you had two prior CR.

Ability seems to be a question that would be important can you just help us understand expectations around <unk>.

Our ability given the only two showers, but car T is.

<unk>, 33% to 50% durable CR.

Operator: So maybe you could make some comments on durability. Thank you. Sure. So, yeah, obviously, I think, starting in AML, I think there's going to be a lot of interest in trying to compare, for instance, FT516 with, or FT538, with the historical experience with donor-derived NK cell therapy. And I do think donor-derived NK cell therapy, as I've mentioned in these sort of single-center academic studies, has shown 20 to 30 percent, 35 percent response rates.

Maybe make some comments on durability. Thank you.

Sure. So yeah, obviously I think starting on AML, I think theres going to be a lot of interest in trying to compare for instance, ft 516, with four or <unk> $5 38 with the expense the historical.

<unk> experience with donor derived NK cell therapy.

I do think donor derived NK cell therapy as I've mentioned in the sort of single center academic studies have shown 20% to 30%, 35% response rates I understand the natural the desire to do that comparison I think there are significant differences that have existed with donor derived NK cell therapy.

Operator: I understand the natural desire to do that comparison. I think there are significant differences that have existed with donor-derived NK cell therapy versus the paradigm that we're pursuing, and I've touched on some of them. We can talk about, just right off the top, the lymphoconditioning regimen is significantly different. We have lighter conditioning.

Versus the paradigm that we're pursuing and I'll touch on some of them. We can talk about just right off the top the lymphoma conditioning regimen is significantly different we have a lighter we have a lighter conditioning, we give we deliver the product to outpatient historically the paradigm for donor derived NK cell therapy has been transplant low.

Operator: We deliver the product outpatiently. Historically, the paradigm for donor-derived NK cell therapy has been transplant-like, with significant lymphodepletion, such that patients are hospitalized.

On significant lymphoma, depletions such that patients are hospitalized.

Operator: So, I do think, I do understand the natural comparison, but I think there's differences. That said... The reason I'm focused on 20-30% is not the comparison with donor-derived NK cell therapy. It's because I think that's the right bar to determine whether or not we actually potentially have a product. Going back to my comments that I made on some recent approvals in AML given the unmet need, there have been multiple approvals in the past two or three years where the response rate has been about, let's call it somewhere between the high teens and the mid-twenties.

So I do think I do understand the natural comparison I think there's differences.

That said.

The reason I'm focused on 20% to 30% is not the comparison with donor derived NK cell therapy is because I think thats, the right bar to determine whether or not we actually potentially have a product.

Going back to my comments that I made on some recent approvals in AML given the unmet need there have been multiple approvals in the past two years or three years, where the response rate has been about let's call it somewhere between the high teens in the mid twenties.

Operator: And so when I focus on the response rate of 20 to 30%, I'm not actually looking at that in the context of, gosh, donor-derived NK cell therapy. I'm looking at it in the context of, do I actually think we have a product? that can be advanced into a registrar.

And so when I focus on response rate of the 20% to 30% I'm not actually looking at that net in the context of gosh donor derived NK cell therapy on looking at it in the context of two I actually think we have a product that can be advanced into a registration study and that's how I'm thinking about that bar.

Operator: And that's how I'm thinking about that bar in a. We'll see. Obviously, we'll share the data with respect to FT-516 and FT-538. I've been pretty upfront about it when people have asked. Look, preclinically, FT-538 is a better product. It just is, preclinically.

No.

Yes, we will see we will see obviously, we'll share the data with respect to ft 516 in ft, 538, I have been pretty upfront about it when people have asked look at preclinical ft 530, it's a better product. It just as pre clinically you raise some head to head turn on turn times.

Operator: If you race them head-to-head 10 out of 10 times in 10 different races, 538 is always going to win. Whether that plays out in the clinic or not, it'll be interesting to see. With respect to ASCO and 516 and lymphoma, yeah, we provided a little bit of data initially. There will be a much more robust update at ASCO with respect to FT 516, and we're encouraged to share that data.

In 10 different races, 530, it's always going to win whether that plays out in the clinic or not.

It'll be interesting to see that.

With respect to <unk> and 516 in lymphoma.

We provided a little bit of data initially there will be a much more robust update at <unk> with respect to ft 516.

And we're encouraged to share that data I think.

Operator: I think, you know, durability is a fair question. The durability of the response, I think, is a fair question. I think that is still a bit early to assess. We're not even at the, we haven't even advanced through the top dose level yet, and our patients are still, relatively speaking, only on study for a short period of time. I think by ASH, we will have a very clear view of the durability of FT516 plus Rituximab.

Durability I think it's a fair question. The durability of the response I think is a fair question I think that is still a bit early to assess we're not even at the we're not we haven't even.

Through the top dose level yet.

Our patients are still relatively speaking only on study for a short period of time.

I think by Ash, we will have a very clear view of durability of ft 516, plus rituximab.

Operator: Thank you. Great. And we do have our next question from Peter Lawson from Barclays.

Thank you Greg.

And we do have a next question from Peter Lawson from Barclays.

Scott Thanks, so much.

All the details.

Operator: I guess going back to... Mike's question around.

I guess going back to <unk>.

Mikes question around.

Operator: The response rate, or the BAFA AML, is... Are you focused on CRI or CRH? Has that response rate, that 20-35% response rate in AML, or is that more of just an O or R number? It's the number that I've, is a composite of CR.

The response rate or the bar for AML lists.

Are you focused on Cri CRH as debt.

Response rate that 20% to 35% response rate in AML.

That more of a J.

On the.

That's the number that I had.

Described.

Is a composite of CR.

Operator: CRI, MLFS. There's just a very interesting paper that was released and published about venetoclax, actually, in relapsed refractory AML, where the data that I referred to in the reference I made was a comparison of Patience, using the 2017 ELN criteria, that achieved CR, CRI. MLFS versus patients that did not. There is a clear survival benefit between those two groups, CR-CRI-MLFS versus non-responders. A clear survival benefit, statistically significant, that extends out over 30 months. And would you be, I guess, more content with a high... CRI versus the PI-CRH? I'm just trying to gauge how much.

Hi.

LFS.

There's just a very interesting paper that was released and published on <unk> actually in relapsed refractory AML.

Where the data that I referred to in the reference I made was a comparison.

<unk> patients using the 2017 El N criteria.

That achieved CR cri.

MLR FES versus patients that did not.

There is a clear survival benefit between those two groups CR Cri MLS us versus non responders clear survival benefit statistically significant that extended out over 30 months.

Good day.

Would you be I guess more content with a high.

Roy.

Versus high CRH.

To gauge so CR Cri CRH is not part of the 2007 El N criteria.

Operator: So CRH is not part of the 2007 ELN criteria. It's part of a criteria that originally existed in 20... in 2003. I agree, there are paths forward where approvals have been achieved based on CR, and CRA. There's also Paths Forward, where products have been approved on CR, and CRI. There are two different response criteria. Both of them are very vile.

It's part of our criteria that and regionally existed in 'twenty two.

2003.

I agree there are paths forward, where approvals have been achieved based on CR CRH Theres also paths forward where products have been approved on CR Cri.

There are two different response criteria is both of them are very viable.

Operator: Thank you. And then just your comment around not using CyFlu is really appealing. So are you thinking of other ways to deplete the bone marrow through other methods or not? Yes. Yes. I think I think there I think I think this comes down to a question of a philosophical question and scientific question about what the purpose of CyFlu is. I think that's an open question.

Great. Thank you and then just your comment around no.

Using our soy flow.

Really appealing.

Are you thinking of other ways to deplete the bone marrow through other methods all.

Yes, yes, I think I think there I think I think this comes down to a question that philosophical question and scientific question on what is the purpose of Psi flow.

I think Thats an open question. There is I think a lot of speculation around what the purpose of site flu is.

Operator: There's, I think, a lot of speculation around what the purpose of PSY-Flu is. But I don't think there's any magic to PSY-Flu and cell therapy, where PSY-Flu has to be delivered with cell therapy. PSY-Flu has a biological effect, and it is probably multifactorial. One of those biological effects is, for instance, significantly increasing cytokines within patients as a result of the PSY flu. And so I do think, you know, as we look forward and think about what the ultimate cell therapy paradigm for patients, I think looking at ways, for instance, where we can significantly reduce PSY flu is important, and we are very interested in exploring that. And it's actually one of the reasons why we're engineering in cytokine support into our.

But I don't think Theres any magic to Si flu and cell therapy, where XI flu has to be delivered with cell therapy site flu has a biological effect.

It is probably multifactorial one of those biological effects is for instance significantly.

Significantly increasing cytokines within patients as a result of the <unk> flow.

And so I do think as we look forward and think about what is the ultimate cell therapy paradigm for patients I think looking at ways for instance, where we can sit.

Significantly reduced site flu.

It is important and we are very interested in exploring that and it's actually one of the reasons why we're engineering in cytokines support into ourselves.

Operator: Thank you so much. Sure. Sure. And we do have our next question from Tazeen Ahmad from Bank of America.

Great.

Thank you so much much free.

Sure sure.

And we do have our next question from testing on that from Bank of America.

Operator: Tazeen, are you on mute? Sorry, can you hear me now? I can, yes.

<unk> are you on mute.

Sorry can you hear me now.

I can yes, excellent sorry about that.

Operator: Oh, excellent. Sorry about that. No problem. Thanks for taking my question.

Yeah, Brian Thanks for taking my questions.

From 516 on $5 nine thanks, I just wanted to drill in a little bit into the pursuit of the <unk> indication.

Operator: https://www.youtube.com

On the last year, there's obviously been a number of companies that have had on drugs approved in this space from Seattle genetics similar focus stimulus recently.

Operator: I wanted to get your thoughts about how you view the opportunity overall and how you view

Operator: and where you see NK cells potentially fitting into

<unk> therapeutics and they're all different mechanisms, obviously from what youre pursuing but wanted to get your thoughts about how you view the opportunity overall in <unk>, and where you see NK cells potentially fitting into the treatment paradigm.

Operator: K-Cells Potentially Fitting into the Treatment Paradigm. And then the second question is more of, you know, in general, what's your strategy for re-dosing NK cells and how many doses could a patient potentially receive? Can you just remind us what the highest number of doses any patient has received?

And then the second question is more of.

In general Whats your strategy for re dosing NK cells and how many doses can a piece on potentially receive and can you just remind us what's the highest number of doses any piece and has received across your program. So far.

Operator: has received across your program so far. Thanks.

Operator: Sure, so I'll tackle the last question first. So the most doses that we have, the maximum number of doses that we have administered to a patient is six. And this goes back to, actually, FT500, where we, and this was actually the reason we sort of ran this experiment with FT500. We gave two days of outpatient lymphoconditioning, followed by doses of FT500 on day 1, day 7, day 14, and the patient was off therapy for two weeks, and we did a safety assessment. And then we actually re-dosed.

Sure. So I'll tackle the last question first so the most doses that we have the maximum number of doses that we have administered to a patient is six.

And this goes back to first started with actually Ft 500.

And it was actually the reason we sort of ran this experiment with Ft 500, we gave two days of the outpatient lymphoma conditioning.

Followed by.

Doses of Ft 500 on day, one day seven day 14.

Then the patient was off therapy for two weeks.

And we did a safety assessment and then we actually re dosed. The next month day, one 7% and 14.

Operator: The next month, day one, seven, and 14, without lymphoconditioning. And so that was essentially, you could think about it as six doses over 45 days following light outpatient lymphoconditioning. And the entire experiment, at some level initially, was set up to assess whether or not a patient could tolerate multi-dosing in that form. For instance, would there be mechanisms of profound immune rejection that would arise? That was one of the very early things we were looking at.

Without lymphoseek conditioning.

And so that was essentially you could think about it is six doses over 45 days following light outpatient <unk> conditioning in the entire experiment at some level initially was set up to assess whether or not a patient could tolerate multi dosing in that form.

For instance would there be mechanisms of profound immune rejection that would arise.

That was one of the very early things we were looking at right would there be for instance, a form of Crs that would emerge because you would administer essentially a cell unmatched to a patient and that the patient would be building up allo reactivity to that so we did not see that with.

Operator: Would there be, for instance, a form of CRS that would emerge because you would administer essentially a cell unmatched to a patient and that the patient would be building up alloreactivity to that cell? We did not see that with FT500, and we have not seen that with FT516. FT516 has been dosed up to six times, and we've not seen that with any of our other product candidates to date. Now, FT596, we give a single dose, and then patients can repeat that single dose cycle.

<unk> 500, and we've not seen that with Ft 516 ft 516 has been dosed up to six doses.

And we've not seen that with any of our other product candidates to date now ft 596, we've given a single dose and then they can repeat that single dose cycle, but generally speaking we've.

Operator: But generally speaking, we've, I feel really confident about our ability to re-dose and have certainly demonstrated our ability to re-dose safely with tolerability up to six doses over a 45-day period. With respect to where we think NK cells fit within sort of the B-cell lymphoma, DL-BCL landscape, I think there's lots of opportunity here.

We feel really confident about our ability to re dose and I'm certainly demonstrated our ability to re dose safely with tolerability up to six doses over a 45 day period.

With respect to where we think NK cells fit within sort of the b cell lymphoma, <unk> PCL landscape.

There's lots of opportunity here I mean, clearly we've started out in a position where we are.

Operator: I mean, clearly, we've started out in a position where we are, you know, you can think of it as sort of a third line where patients have failed multiple lines of rituximab. We're really excited about what we've seen in that setting where we've combined FT-516, for instance, with rituximab in patients that have either relapsed or failed rituxima We think there's a great opportunity there given the response rates that we're seeing with FT-516. And additionally, like we discussed, we actually think if the product candidate really does synergize effectively with rituximab, and if it really does continue to show a different...

You can think about it as sort of third line.

Where patients have failed multiple lines of Rituximab and we're really excited about what we've seen in that setting where we've combined ft 516 for instance, with rituximab in patients that have either relapsed or failed rituximab.

We think there's a great opportunity there given the response rates that we're seeing with ft 516.

And Additionally, like we discussed we actually think if the product candidate really does synergize effectively with Rituxan and if it really does continue to show a difference.