Q3 2021 Fate Therapeutics Inc Earnings Call

November 4, 2021

Irrigation Reform Act of 1995 these.

Unnamed Speaker: Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements.

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 factor.

Unnamed Speaker: 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 September 30, 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 the 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.

<unk> included in our Form 10-Q for the quarter ended September 32021 that was filed with the SEC today.

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

Except as required by law say therapeutics disclaims any obligation to update these forward looking statements to reflect future information events or circumstances.

Unnamed Speaker: Joining me on today's call are Dr. Wayne Chu, our Senior Vice President of Clinical Development; Ed Dulac, our Chief Financial Officer; and Dr. Bob Valamehr, our Chief Research and Development Officer. Today, we will highlight our clinical progress over the past several months with our off-the-shelf IPSC-derived NK-Cell program and discuss our plans to share clinical and preclinical data from certain of these programs in connection with the Society for Immunotherapy of Cancer annual meeting in mid-November and the American Society of Hematology annual meeting in mid-December. Beginning with our B-cell malignancy franchise. Autologous CAR T-cell therapies targeting CD19 have delivered remarkable results for patients with relapsed refractory B-cell lymphoma.

Joining me on today's call our Doctor weighing shoe, our senior Vice President of clinical development.

Do lock, our Chief Financial Officer.

And Doctor, Bob <unk>, our Chief Research and development Officer.

Today, we will highlight are clinical progress over the past several months with our off the shelf Ips C derived and queso programs.

And discuss our plans to share clinical and preclinical data from certain of these programs in connection with the society for immunotherapy of cancer annual meeting in mid November and the American Society of Hematology annual meeting in mid December.

Beginning with our B cell malignancy franchise.

Autologous car T cell therapies targeting CD 19 have delivered remarkable results for patients with relapsed refractory b cell lymphomas how're.

Unnamed Speaker: However, there remains a significant need to develop off-the-shelf, cell-based cancer immunotherapies that can bring transformative outcomes to more patients. Over the past several months, we have made significant clinical progress in advancing our FT-516 and FT-596 product candidates, including expanding clinical investigation of these off-the-shelf IPS-derived NK cell programs to broader patient populations. We continue to be very pleased with the early clinical data we have observed from our Phase I studies of FT516 and FT596 in relapsed refractory B-cell lymphoma, where interim clinical data have shown the potential to drive response rates that are comparable to those achieved with autologous CAR T-cell therapy while maintaining a substantially differentiated safety profile that not only supports administration in an outpatient setting without requiring hospitalization but may FT596 is our off-the-shelf, iPSC-derived, CAR and K-cell product candidate designed to target multiple B-cell antigens, both through its CD19-targeted chimeric antigen receptor and through its high-affinity, non-cleavable CD16FC receptor in combination with tumor-targeting antibodies.

However, there remains a significant need to develop off the shelf cell based cancer immunotherapies that can bring transformative outcomes to more patients.

Over the past several months, we have made significant clinical progress in advancing our F. T 516, and FTE 596 product candidates, including expanding clinical investigation of these off the shelf Ips derived NK sell programs to broader patient populations.

We continue to be very pleased with the early clinical data we have observed from our phase one studies of FTE 516 ft 596 in relapsed refractory b cell lymphoma.

Unnamed Speaker: In our dose-escalating phase one study, FT596 is being assessed as monotherapy, as well as in combination with rituximab, a multi-antigen targeting approach that we believe may hold best-in-class potential in addressing tumor heterogeneity and antigen escape. In August, we announced that as of the data cutoff date of June 25, 2021, 10 of 14 patients treated with a single dose of FT-596 achieved an objective response, including seven patients that achieved a complete response in the second and third dose cohorts of 90 million cells and 300 million cells, respectively. Importantly, four of these 14 patients had previously been treated with autologous CD19 CAR T-cell therapy, two of whom achieved a complete response with a single dose of FT-596 in combination with rituximab.

With a single dose of F. T 596 in combination with Rituxan that.

Unnamed Speaker: Treatment with FT596 was well tolerated and showed a differentiated safety profile to that commonly observed with CAR T cell therapy, with only two reported low-grade adverse events of cytokine release syndrome, and no reported adverse events of immune effects or cell-associated neurotoxicity or graft-versus-hospitality. We have now enrolled approximately 30 total patients in the second, third, and fourth single-dose cohorts of 90 million cells, 300 million cells Earlier today, we announced that updated clinical data from our FT-596 Phase I study will be featured in an oral presentation at ASH on Monday, December 13.

Treatment with FTE 596 was well tolerated and showed a differentiated safety profile to that commonly observed with car T cell therapy with only two reported low grade adverse events of cytokine released syndrome, and no reported adverse events of.

Immune effector sell associated neurotoxicity or graft versus host disease.

We have now enrolled approximately 30 total patients and the second third and fourth single dose cohorts of 90 million cells 300 million cells and 900 million cells respectively.

Earlier today, we announce that updated clinical data from our FTE 596 Phase one study will be featured in an oral presentation at ash on Monday December 13.

Unnamed Speaker: The presentation is expected to cover safety and Duration of Response for all patients treated through the third single-dose cohort of 300 million cells as monotherapy and in combination with rituximab. In addition, we plan to hold an investor event on Tuesday, December 14 to further supplement the ASH presentation, where we expect to present safety and tumor response data for those patients treated in the fourth single-dose cohort of 900 million cells.

The presentation is expected to cover safety tumor.

Tumor response.

And duration of response for all patients treated through the third single dose cohort of 300 million cells as mono therapy and in combination with rituxan them.

In addition, we plan to hold an investor event on Tuesday December 14 to further supplement the ash presentation, where we expect to present safety and tumor response data for those patients treated in the fourth single dose cohort of 900 million cells.

Unnamed Speaker: We continue to believe that one significant advantage of off-the-shelf cell therapy is the potential to deliver multiple doses over multiple cycles and that such a treatment paradigm will confer best-in-class outcomes for patients. To that end, having observed that a single-dose treatment cycle of FT-596 was well-tolerated with no dose-limiting toxicity, we have now increased the frequency of FT-596 dosing and initiated enrollment in a two-dose treatment, with FT-596 administered on day one and day 15 at 300 million cells per dose with the potential to dose escalate to 900 million cells per dose. Patients showing clinical benefit following the first two-dose treatment cycle are eligible to receive a second two-dose treatment cycle.

We continue to believe that one significant advantage of off the shelf cell therapy has the potential to deliver multiple doses over multiple cycles and that such a treatment paradigm will confirm best in class outcomes for patients.

To that end, having observed that a single dose treatment cycle of FTE 596 was well tolerated with no dose limiting toxicities.

We have now increased the frequency of FTE 596, dosing and initiate enrollment of a two dose treatment cycle with F. T 596 administered on day, one and day 15 at 300 million cells per dose with the potential to dose escalate to 900.

Unnamed Speaker: Additionally, based on the positive interim clinical data we have observed with FT596 in relapsed refractory B-cell lymphoma, we have broadened our clinical investigation of FT596 to include treatment of other B-cell malignancies in our ongoing Phase I study. I'm pleased to announce that we have initiated enrollment of FT-596 in combination with abinituzumab for the treatment of patients with relapse Turning to FT-516.

Unnamed Speaker: In August, we also announced positive interim clinical data, as of the data cutoff date of July 7, 2021, from our dose-escalating Phase I study of FT516 in combination with rituximab for the treatment of relapsed refractory B-cell lymphoma. 8 of 11 patients achieved an objective response, including six patients that achieved a complete response, in the second and third multi-dose cohorts of 90 million cells per dose and 300 million cells per dose, on day 29 of the second FT-516 treatment.

Unnamed Speaker: Five of the 11 patients maintained their response without further therapeutic intervention, with follow-up ongoing at between 4.6 and 9.5 months, indicating that FT516 has the potential to drive durable responses. The observed safety profile of FT-516 was favorable and is differentiated from that of T-cell based therapy. No FT-516-related serious adverse events or FT-516-related grade 3 or greater adverse events were observed, and no events of any grade of cytokine release syndrome, immune effect, or cell-associated neurotoxicity, or graft-versus-host disease were reported.

Bring up between four six and nine five months, indicating that FTE $5 16 has the potential to drive durable responses.

The observed safety profile of FTE $5 16 was favorable and is differentiated from that of T cell based therapies.

No FTE $5 16 related serious adverse events or FTE $5 16 related grade three or greater adverse events were observed.

And no events of any grade of cytokine release syndrome immune effector cell associated neurotoxicity or.

Graft versus host disease were reported.

Unnamed Speaker: We have now completed the dose escalation stage of our FT516 Phase 1 study, having enrolled seven patients in the fourth multi-dose cohort of 900 million cells per dose. Earlier today, we announced that updated clinical data from our FT516 Phase I study will be featured in a poster presentation at ASH on Monday, December 13. The presentation is expected to cover safety.

We have now completed the dose escalation stage of our FTE $5 16 phase one study.

Having enrolled seven patients in the fourth multi dose cohort of 900 million cells per dose.

Earlier today, we announced that updated clinical data from our FTE $5 16 Phase one study will be featured in a poster presentation at ash on Monday December 13.

The presentation is expected to cover safety.

Unnamed Speaker: Tumor response and duration of response for all 18 patients treated at the 2nd, 3rd, and 4th multidose COVID. In addition, we plan to further supplement the ASH presentation with updated FT516 data at our investor event on Tuesday, December 14th. After completing dose escalation, we have now initiated dose expansion, at 900 million cells per dose, to further assess the clinical activity of FT516, and are intending to enroll patients into three disease-specific cohorts, including one for third-line diffuse large B-cell lymphoma in patients that are naive to autologous CD19 CAR T-cell therapy.

Tumor response and duration of response for all 18 patients treated at the second third and fourth multi dose cohorts in.

In addition, we plan to further supplement the ash presentation with updated FTE $5 16 data at our Investor event on Tuesday December 2014.

Having completed dose escalation, we have now initiated dose expansion.

At 900 million cells per dose to further assess the clinical activity of FTE $5 16.

And are intending to enroll patients into three disease specific cohorts, including one.

Third line.

Fuse large b cell lymphoma, and patients that are naive to autologous CD 19 car T cell therapy.

Unnamed Speaker: Number two, third-line folliculum, in patients that are naive to autologous CD19 CAR T-cell therapy. And three, patients with relapsed refractory B-cell lymphomas whose disease has progressed following autologous CD19 CAR-T cell therapy. We believe assessing the clinical activity of FT-516 in patients whose disease has progressed following autologous CD19 CAR T-cell therapy addresses a growing market segment with significant unmet need and may offer a potential fast-to-market development opportunity. In addition, because FT-516 may be administered in the outpatient setting and given its favorable safety profile observed to date, we have also initiated dose expansion of FT-516 in combination with benda Importantly, in these four dose expansion cohorts, we intend to include sites that serve patients in the community.

Two third line Follicular lymphoma in patients that are naive to autologous CD 19 car T cell therapy.

And three patients with relapsed refractory b cell lymphomas, whose disease has progressed following autologous CD 19 car T cell therapy.

Unnamed Speaker: Turning to our Multiple Myeloma Disease Franchise, I'm pleased to announce that we have treated the first patient in our dose-escalating Phase 1 study of FT538 in combination with the CD38-targeted monoclonal antibody, Daratumab. Our FT-538 product candidate builds off of our FT-516 backbone and is engineered with three functional components to optimize innate immunity. In addition to a novel, high-affinity, non-cleavable CD16FC receptor, FT-538 incorporates an IL-15 receptor fusion and the deletion of the CD38 gene.

In combination with CD 38 targeted monoclonal antibody Dara tune them.

Our FTE $5 38 product candidate builds off of our FTE $5 16 backbone.

And is engineered with three functional components to optimize innate immunity and.

In addition to our novel high affinity non cleavable CD 16 FC receptor FTE $5 38 incorporates an IL 15 receptor fusion and the deletion of the CD 38 <unk>.

In preclinical studies recently published in the peer reviewed journal cell stem cell, we showed that FTE $5 38 exhibits enhanced serial killing antibody dependent cellular cytotoxicity and functional persistence compared to peripheral blood NK cells.

Unnamed Speaker: In preclinical studies recently published in the peer-reviewed journal Cell Stem Cell, we showed that FT538 exhibits enhanced serial killing, antibody-dependent cellular cytotoxicity, and functional persistence compared to peripheral blood encases. The superior anti-tumor activity of FT538 is attributable to the biological effect of Increased Resistance to Oxidative Stress, which induces a protein expression program that enhances NK cell The Phase I study of FT538 is designed to assess three once-weekly doses of FT538 in combination with Daratumab for the treatment of relapsed refractory multiple myeloma. The first patient was treated with 100 million cells per dose.

The superior anti tumor activity of FTE $5 38 was attributable to the biological effects of its novel IL 15 receptor fusion and CD 38 knockout, which were shown to improve metabolic fitness.

Increased resistance to oxidative stress.

And induces a protein expression program that enhanced NK cell activation and inspector function.

Unnamed Speaker: Similar to our approach in lymphoma, where we are developing FT-516 and FT-596, we have further modified our FT-538 product candidate to create FT-57s, our off-the-shelf, IPS-derived, car-in-case cell product candidate designed to target multiple antigens both through its high-avidity BCMA-targeted chimeric antigen receptor and its high-affinity, non We have initiated enrollment in our dose-escalating Phase 1 study of FT576 to assess both single-dose and multi-dose treatment registries, as monotherapy, as well as in combination with Dar-2-Met, an approach that enables targeting of both BCMA and CD38 anti-cancers, which we believe may hold best-in-class potential for the treatment of multiple myeloma. Patient dosing will begin with FT-576 as monotherapy in the single-dose treatment cohort at a dose of 100 million cells. Turning to our AML Disease Franchise.

38 programs, which are indicated that Ips derived NK cells are well tolerated and tenant do subjective responses with complete clearance of leukemic blasts from the bone marrow importantly, these clinical outcomes were achieved with Ips derived NK cells administer off the shelf and in the <unk>.

Outpatient setting.

Over the past three months, we have made significant strides in opening our dose escalating phase one study of FTE 538 at additional clinical sites and our rate of enrollment has accelerated accordingly, we have now enrolled approximately 10 patients with relapsed refractory AML.

Unnamed Speaker: We continue to be excited about the potential of IPS-derived and K-cell therapies to play a foundational role in the treatment of patients with AML. We are encouraged by our initial Phase I clinical data from our FT-516 and FT-538 programs, which have indicated that iPS-derived NK cells are well tolerated and can induce objective responses with complete clearance of leukemic blasts from the bone marrow. Importantly, these clinical outcomes were achieved with iPS-derived NK cells administered off the shelf and in the outpatient setting.

In the first and second multi dose cohorts of 100 million cells per dose and 300 million cells produce respectively.

No dose limiting toxicities have been reported and treatment with FTE $5 38 continues to be well tolerated.

We've also commenced enrollment in an investigator initiated phase one clinical trial that T 538.

In combination with Dara <unk>.

And patients with relapsed refractory AML.

A therapeutic strategy designed to exploit the product candidates proprietary high affinity non cleavable, CD 16 receptor and CD 38 knockout to recognize bind and kill leukemic blasts expressing CD 38 through antibody dependent cellular cytotoxicity.

Unnamed Speaker: Over the past three months, we have made significant strides in opening our dose-escalating Phase 1 study of FT538 at additional clinical sites, and our rate of enrollment has accelerated accordingly. We have now enrolled approximately 10 patients with relapsed refractory AML in the first and second multi-dose cohorts of 100 million cells per dose and 300 million cells per dose, respectively. No dose-limiting toxicities have been reported, and treatment with FT538 continues to be well-tolerated.

We have also completed the dose escalation stage of our FTE 516 phase one study in relapsed refractory ammo.

Having enrolled seven patients in the third multi dose cohort of 900 million cells per dose.

The maximum tolerated dose of FTE 516 was not established and treatment with FTE 516 was well tolerated.

Unnamed Speaker: We've also commenced enrollment in an investigator-initiated Phase I clinical trial of FT538, in combination with Dara Tumamab in patients with relapsed refractory AML. A therapeutic strategy designed to exploit the product candidates' proprietary high-affinity non-cleavable CD16 receptor and CD38 knockout to recognize, bind, and kill leukemic blasts expressing CD38 through antibody-dependent We have also completed the dose escalation stage of our FT-516 phase one study in relapsed refractory AML, having enrolled seven patients in the third multi-dose cohort of 900 million cells per dose. The maximum tolerated dose of FT-516 was not established, and treatment with FT-516 was well tolerated.

We will look to provide an update on our FTE 516, and up to 538 programs in relapsed refractory AML as we generate additional dose escalation data with FTE 538, including duration of response. So we were able to fully compare the safety anti leukemic activity activities.

Unnamed Speaker: We will look to provide an update on our FT5-16 and FT5-38 programs in relapsed refractory AML as we generate additional dose escalation data with FT5-38, including duration of response, so we're able to fully compare the safety, anti-leukemic activity, and durability of response of both programs. Now, turning to our Solid Tumor Franchise.

Unnamed Speaker: We are looking forward to the CITSE conference next, where our FT-536 CAR and K-Cell program will be featured in an oral presentation. FT536 is our off-the-shelf, multiplexed-engineered, IPS-derived NK-cell product candidate that incorporates a novel CAR targeting the Alpha 3 domain of the Pan-Tumor Associated Stress Antigens, MIC-A and MIC IND-enabling preclinical data for FT536 will be presented on Saturday, November 13, and will highlight the novel binding domain of FT536, which is specifically designed to overcome tumor escape mechanisms mediated by loss of MHC class 1 expression and by shedding of MYC-A1.

That our product candidates seek to exploit and attacking solid tumors.

Our proprietary multiplexed engineering and single Ips C selection platform as well as new innovative features and functionality that we are currently assessing for integration into our solid tumor product candidates.

Unnamed Speaker: We expect to submit an IND application for FT536 in the fourth quarter of 2021 for the treatment of advanced solid tumors, including in combination with monoclonal antibody therapy to exploit multi-antigen targets. In addition, on Monday, November 5th... We intend to host a virtual 90-minute investor event to highlight our emerging pipeline of off-the-shelf, multiplexed-engineered, IPS-derived NK and T- During the investor event, we plan to discuss the following, which are multiplexed engineered preclinical candidates for which we intend to submit IND applications during the next 18 months.

Or multiple multi arm phase one study of FTE 538 in solid tumors, where.

Where we have initiated an enrollment of FTE 538 in combination with checkpoint inhibitor therapy and patients with resistance to checkpoint inhibitor and in combination with tumor targeting monoclonal antibody therapy, including those that target the tumor associated antigens egfr her too and.

<unk>.

Unnamed Speaker: The unique mechanisms of action that our product candidates seek to exploit in attacking solid tumors. Our proprietary multiplexed engineering and single IPSC selection platform, as well as new innovative features and functionality that we are currently assessing for integration into our solid tumor product candidates, our multi-arm phase one study of FT538 in solid tumors, where we have initiated enrollment of FT538 in combination with checkpoint inhibitor therapy in patients with resistance to checkpoint inhibitor and in combination with tumor targeting monoclonal antibody therapy, including those that target the tumor associated antigens EGFR, HER2, and PD-L1.

Unnamed Speaker: And we also plan to disclose clinical data from our first generation product candidates for solid tumors in patients that have progressed or failed checkpoint inhibitor therapy. Our Phase 1 study of FT500 enrolled approximately 10 patients in dose expansion at 300 million cells per dose and includes heavily pre-treated patients with non-small cell lung cancer or classical Hodgkin lymphoma that have progressed or failed PD-1, PD-L1 checkpoint inhibitor therapy. Our phase one study of FT516 has enrolled approximately 12 patients in dose escalation, ranging from 90 million cells per dose to 900 million cells per dose, and primarily includes heavily pre-treated patients with stage four melanoma that have progressed or failed PD-1 and PD-L1 checkpoint inhibitors. I would now like to turn the call over to Ed to highlight our third quarter financial results.

And our G&A expenses was attributable primarily to an increase in employee head count and compensation, including share based compensation and an office and computer supplies, including software licenses.

Total operating expenses for the third quarter of 2021 were $55 $3 million net of $13 $5 million and noncash share based compensation expense.

Unnamed Speaker: Scott, I'm turning to our financial results.

Unnamed Speaker: Revenue was $14.2 million for the third quarter of 2021, compared to $7.6 million for the same period last year. Revenue in the current quarter was derived from our collaborations with Janssen,

Note that in connection with the treatment of the first patient with our off the shelf Ips derived car T cell product candidate FTE $8 19, we achieve the clinical milestone set forth in our amended license agreement with Memorial Sloan Kettering Cancer Center.

This clinical milestone triggered a first milestone payment in the amount of $20 million to EMS, K, which we plan to pay in the fourth quarter.

Unnamed Speaker: Jansen, and Ono Pharmaceutical.

Unnamed Speaker: Research and development expenses for the third quarter of 2021 were $53.1 million, compared to $30.7 million for the same period last year. The increase in our R&D expenses was attributable primarily to an increase in employee headcount and compensation, including share-based compensation, and in expenses.

Up to two additional milestone payments may be owed to MSA based on subsequent trading values of the company's common stock ranging from 100 to $150 per share.

Unnamed Speaker: Associated with Third-Party Professional Consultants and Clinical Trials

Unnamed Speaker: General and administrative expenses for the third quarter of 2021 were $15.7 million, compared to $8.3 million for the second quarter of 2021.

Unnamed Speaker: for the same period last

Unnamed Speaker: The increase in our G&A expenses was attributable primarily to an increase in employee headcount and compensation, including share-based compensation, and in office and computer supplies, including software licenses. Total operating expenses for the third quarter of 2021 were $55.3 million, net of $13.5 million in non-cash, share-based compensation expense. Note that in connection with the treatment of the first patient with our off-the-shelf IPSC-derived CAR T-cell product candidate FT819, we achieved the clinical milestone set forth in our amended license agreement with Memorial Sloan Kettering Cancer Center.

Obviously, you've already presented in 596 data show would we be able to get a pretty good picture about how that shaping up at ash given 596 and also higher doses. That's question. One and then question two I think you just laid out some nice commentary around you.

Unnamed Speaker: This clinical milestone triggered a first milestone payment in the amount of $20 million to MSK, which we plan to pay in the fourth quarter. Up to two additional milestone payments may be owed to MSK based on subsequent trading values of the company's common stock, ranging from $100 to $150 per share. We assess the fair value of the contingent milestone payments, currently valued at $24.6 million, on a quarterly basis. In the third quarter, we recorded a non-cash, $11 million non-operating benefit associated with the change in fair value.

Your solid tumor update I know these are super heavily pretreated patients how should we put that type of data you will present into context. I mean responses are good what would you expect to see and what's the read through thank you so much.

Sure. So with respect to your first question with respect to durability of 516 versus 596, yes, I think at Ash, we will be able to do a first look at comparing durability of both $5 <unk> and $5 96, we plan to present.

When lane plots for both $5 16, and 596, if you recall from our lymphoma update in August we did present, a swim lane plot for $5 16.

Unnamed Speaker: The company ended the third quarter with $804 million of cash, cash equivalents, and investments. Our common stock outstanding was 95 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 data cut for that I think was late July or sorry. It was probably late June early July will be able now to fast forward that swim lane.

As well as that as well as add patients that were dosed at 900 million cells and I believe I had mentioned there were seven patients dosed at 900 million cells with ft 516.

With respect to FTE 596 recall, we had 10 of 14 patients that had responded.

Operator: Ladies and gentlemen, if you have a question at this time, please press star, then the number 1 on your telephone keypad. If your question has been answered or you wish to remove yourself from the queue, please press the pound key. Once again, that's star, then the number 1 on your telephone keypad.

In the second and third dose level.

We will now be able to present duration of response.

On those 14 patients.

Including adding a couple additional patients that were dosed at the 300 million cell level as backfill.

Operator: Your first question comes from the line of Michael Yee.

Michael Jonathan Yee: Michael Yee from Jeffries, Urlana.

We've also now I mentioned I think we've treated about 30 total patients including.

Scott: Hey Scott, thanks for the updates. I had two questions. One is about the updates coming later this year at ASH, and obviously, the abstracts are out today. Can you compare and contrast how you think durability would play out for 5.1.6 versus 5.9.6?

Michael Jonathan Yee: Obviously, you've already presented some 5.9.6 data, so would we be able to get a pretty good picture about how that's shaping up at ASH given 5.9.6 and also higher doses? That's question one. And then question two, I think you just laid out some nice commentary on your solid tumor update. I know these are in super heavily pre-treated patients. How should we put that type of data you'll present into context? I mean, responses are good.

Scott: What would you expect to see, and what's the read-through? Thank you so much. Sure.

Scott: So, with respect to your first question, with respect to durability of 516 versus 596, yes, I think at ASH we will be able to do a first look at comparing durability of both 516 and 596. We plan to present swim lane plots for both 516 and 596. If you recall from our lymphoma update in August, we did present a swim lane plot for 516. The data cut for that, I think, was late July or, sorry, probably late June or early July.

We'd be able to look at safety data will be able to look at.

Obviously clinical responses, but again your expectations should be pretty modest with these.

These first generation in case of product candidates.

Got it thank you very much.

Sure.

Your next question comes from the line of I'll see a young from Ken Toy Your line is open.

I'll see a young from Kandahar Your line is open.

Your next question comes from the lineup Michael Schmidt from Guggenheim Security. Your line is open.

Scott: We'll be able now to fast forward that swim lane as well as add patients that were dosed at 900 million cells. And I believe I mentioned there were seven patients dosed at 900 million cells with FT5. With respect to FT-596, recall that we had 10 of 14 patients that responded in the second and third dose levels. We will now be able to present duration of response on those 14 patients, including adding a couple additional patients that were dosed at the 300 million cell level as backfill.

Hey, this is calcium for Michael Thank you for taking our questions I think just the two from us.

First 596, I guess are are we still thinking about you know now that you're kind of moving from one cycle to cycle is there still need flexibility there to maybe increase that further or is that kind of where where do you think you'll end up and then kind of following up on that as he built out the solid tumor franchise I guess kind of what you based on what you've.

Scene with 500 and 516 is is you know, adding additional cycles for the upcoming Nexgen products is that something that you would consider or or are you still kind of thinking about three cycle about the Max Thank you.

Sure.

So with F. T 596, we have.

We have continued to dose.

One dose per cycle, and we now have the ability to give two cycles.

If you recall when we initially advanced R. F T 596 program.

We were gated on giving a second cycle.

Scott: But you'll be able to compare the swim plots and make inferences, is your point, and see what 596 is doing. That's correct. We will have a SWIM plot for FT-596.

With FTA consent.

So we're now able to give two cycles of F. T 596, without without going back to the F D a and.

And so we will continue to dose patients at one dose.

Scott: That is correct. Good. Okay.

Giving two cycles and now we will we will now add two doses in each cycle.

Scott: And then just quickly on solid tumors. Yeah, with respect to solid tumors, most of what we will present at CITSI will be a go-forward look at our R&D in the emerging pipeline. I think we've always maintained, at the end of the day, cracking the solid tumor nut, if you will, has proven to be much more difficult than treating hematologic malignancies. And I think that's consistent no matter what therapeutic modality you're looking at, whether it's small molecule biologics or cell therapy.

And continue to give two cycles.

Scott: And so, really, as we think about our solid tumor franchise, we're focused on multiplexed engineered product candidates that can attack the tumor from multiple different angles. We're looking at FT-500 and FT-516 literally as just a first experience with an IPS-derived NK cell therapy. You should have pretty modest expectations with respect to what we think these product candidates can drive on their own with respect to solid tumors. It's really just getting our feet under us with NK cell therapy in solid tumors.

Scott: And we think we've done that with FT-500 and FT-516. We'll certainly be able to look at safety data. We'll be able to look at, obviously, clinical responses. But, again, your expectations should be pretty modest with these first-generation NK cell products. Thank you very much.

Moving out FTE 596, we did not fully appreciate the therapeutic value of the CD 38 knockout.

Operator: Your next question comes from the line of Althea Yong from Cantor. Your line is open.

Operator: Your line is open. I'll see ya y'all from Cantor. Your line is open.

And initially we thought of CD 38 knockout as.

Step that we would take a functional step that we would add that would be unique for myeloma, knocking out CD 38 could prevent fracture side when delivering the therapy in combination with Dara two mab, obviously, we've come to appreciate and there's been publications on the therapeutics.

Operator: Your next question comes from the line of Michael Schmidt from Guggenheim Securities. Your line is open.

Kelsey Beatrice Goodwin: Thank you. Thank you. Thank you. Hey, this is Kelsey on behalf of Michael.

Kelsey Beatrice Goodwin: Thanks for taking our questions. I think you have just two from us. First, on 5.9.6, I guess, are we still thinking about, you know, now that you're kind of moving from one cycle to two cycles, is there still any flexibility there to maybe increase that further? Or is that kind of where you think you'll end up? And then kind of following up on that, as you build out the solid tumor franchise, I guess, kind of what you're thinking about, based on what you've seen with 500 and 5.1.6, is, you know, adding additional cycles for the upcoming next-gen products, is that something that you would consider? Or are you still kind of thinking about three cycles as the max? Thank you.

Evaluate the CD 38 knockout more broadly we certainly are incorporating that into all our product candidates on a go forward basis, including our product candidates for solid tumors and certainly.

We reserve the right obviously to continue to build off of $5 38 for lymphoma.

Got it that makes sense and then maybe just a quick follow up.

With respect to as you did a good job of outlining what to expect for 516 and $5 96, as well, but is there any other datasets that we should be focused on at ash.

So we're going to hold an investor event.

On Tuesday, we will spend most of the time I think on that Investor event discussing lymphoma, and I think I don't think thats going to be a significant focus of ash as well as the investor event.

Scott: So, with FT-596, we have continued to administer one dose per cycle, and we now have the ability to administer two cycles. If you recall, when we initially advanced our FT-596 program, we were gated on giving a second cycle with FDA consent. So we're now able to administer two cycles of FT-596 without going back to the FTP.

We're continuing to generate data across all our programs obviously.

We look forward to providing updates.

Got it thank you.

Your next question comes from the line of CEO Yung from Cantor. Your line is open hey, guys.

Thanks for taking my question, sorry, I was on mute.

I wanted to talk a little bit about 538, and your choice of using it in combination with <unk>, maybe versus some of the other maybe even though some of those other than just kind of your perspective, there on that kind of differentiation.

Scott: And so we will continue to dose patients at one dose, giving two cycles, and now we will add two doses in each cycle and continue to give it. We are planning on amending the protocol so that if patients relapse at some point, we could re-intervene with FT-595. And so right now, we're sticking to one or two doses per cycle, giving two cycles, and now adding the ability to reintervene if a patient later relapses. So that's where we're headed with FT5.

Sure Wayne do you want to take that question with respect to $5 38 in AML and thinking about.

Combining with our versus <unk>.

Sure.

Scott: With respect to our solid tumor franchise, very similar. We are giving multi-doses in a cycle. As an example, FT538 is a product candidate that we're now dosing with solid tumors in combination with monoclonal antibody. It's a multi-dose treatment, and we are giving multiple cycles, and we do, again, if a patient later relapses, we have the ability to re-intervene again. So we are now looking at the potential to withdraw patients upon progression.

Kelsey Beatrice Goodwin: Okay, great. Thank you so much.

Operator: Your next question comes from the line of Mike Ulz from Morgan Stanley. Your line is open.

Michael Eric Ulz: Hey guys, thanks for taking the question. Just a quick question on the CD38 knockout. You sort of highlighted that modification as providing some... Improved Metabolic Fitness, so I was just curious about 596. I notice you don't have that modification there, so I guess two questions: number one, why not? And number two, are you considering potentially adding that?

They see these are concepts that are continuing to be under consideration.

And.

At some point, we would consider opening up a clinical experiment that looks at combinations of ourselves with these other anti leukemic ages.

Scott: Sure, so for FT5, we've built out our platform over time in a very sort of methodical stepwise fashion. And at the time when we were building out FT596, we did not fully appreciate the therapeutic value of the CD38 knockout. And initially, we thought of CD38 knockout as a step that we would take, a functional step that we would add, that would be unique for myeloma. Knocking out CD38 could prevent fratricide when delivering the therapy in combination with daratumab.

Great. Thank you very much.

Sure.

Your next question comes from the line a fever last time from my place.

Hey, Thanks for thanks for taking the questions Uhm, so uhm multiple myeloma.

Scott: Obviously, we've come to appreciate, and there have been publications on the therapeutic value of the CD38 knockout more broadly. We certainly are incorporating that into all our product candidates on a go-forward basis, including our product candidates for solid tumors. And certainly, we've reserved the right, obviously, to continue to build off of 538 for lymphoma.

Scott: I got it. That makes sense.

Scott: And then maybe just a quick follow-up. With respect to Ash, you did a good job of outlining what to expect for 5.16 and 5.96 as well, but are there any other data sets that we should be focused on at ASH? So we're going to hold an investor event.

Scott: So we're going to hold an investor event on Tuesday. We'll spend most of the time, I think, at that investor event discussing lymphoma, and I think that's going to be a significant focus of ASH, as well as the investor event. We're continuing to generate data across all our programs, obviously, and we look forward to providing updates.

Operator: Your next question comes from the line of Althea Young from Cantor. Your line is open. Hey guys, thanks for taking my questions. Sorry I was on mute. Um, I wanted to talk a little bit about 538 and your choice of using...

Operator: When you can't pour, your line is open.

Wayne: Sure, Wayne, do you want to take that question with respect to 538 in AML and thinking about combining it with DARA versus venetoclax? Sure. So... Combinations of FT-538 and daratumumab in AML.

At some level. It's the first time keep in mind right. This first time of Ips derived NK cell therapies have been delivered in solid tumors.

So in the Ft, 500 dose escalation in 2016, or sorry dose expansion in ft, 516 dose escalation started sometime ago and so for success for US was just again demonstrating that we could deliver multiple doses of an non engineered NK cell.

Wayne: https://www.youtube.com And so, as...

Wayne: You know, as we've discussed, one of the engineering features of FTP.

Wayne: And so, given the availability of Daratumumab and given the data around CD38 expression in AML, it's a natural consequence that a clinical experiment would be

And then a first engineered NK cell in the setting of solid tumors and that they would the multiple dose paradigms multiple cycle paradigms would be safe and well tolerated and that we could potentially see some control of active.

Wayne: We tried to see whether or not combining FT-538 with an ADCC-competent monoclonal antibody against an antigen that is known to be expressed on AML cells, you know, is an experiment moving forward. And that is something that's being done as part of our IIT collaboration with the University of Minnesota. As far as combinations of 538,

Tumor tumor tumor activity and that we would be able to look at translational data that we can continue to build off of as we.

Build a multiplexed engineered pipeline.

Okay.

Thank you so much thanks for taking the question.

Sure.

Wayne: https://www.youtube.com

Wayne: And, you know, at some point, we would consider it.

Operator: Your next question comes from the line of Peter Lawson from Barclays. Your line is open.

Operator: Lawson, from Mark Clay, your line is open. Thanks for taking the questions.

Peter Richard Lawson: What do you think we'll see at ASH and what's the appropriate buy, you think, and is it current Cartes? And, yeah, just...

Scott: 538 versus 5.

Scott: Sure. So, again, you know, I'll make a comment. We've continued to build out our pipeline in a very methodical way and build off of, you know, multiplexed engineered backbones to add additional features, which we believe will add incremental therapeutic value. So, building off of IFT538, we built 576, adding a CAR against BCMA, which again, in combination with Daratumab, we believe allows for multi-antigen targeting against both CD38 and BCMA. So, much like lymphoma, where we think 596 is a best-in-class product candidate, we believe the same for multiple myeloma and 576.

And the safety profile and the flexibility we have with our platform certainly reserve the right to continue to do a bit of exploration as part of our phase one studies, including with as I mentioned alternative conditioning regimens and earlier line combining with standard of care regimens.

Scott: Obviously, both statements need to play out in the clinic, but we're firm believers that multi-antigen targeting... will lead to the best responses, including durability of response, and that that kind of approach can absolutely overcome tumor heterogeneity that exists both in lymphoma and myeloma. Do you think we'll get enough data from Ash, or is this kind of end of twos and threes that we should be thinking about first?

With respect to.

How we characterize our master cell banks, and how we release our product candidates.

I'm not going to sort of get into any details around that other than to say.

We.

Assess for genetic abnormalities at multiple points.

Scott: Yeah, I think I mean, you know, I think I think it's, I think to for that to play out over time, multi antigen targeting best in class approach, you're not just looking at response rates, you're looking at durability of response. And obviously, it will take some time for the durability of response to mature, such that you know, we can be absolutely certain in our belief systems that we have based on preclinical, And then just a comment on one of the questions you asked about the modest expectations around, Solid tumors, is that a case that you kind of, you're not expecting to see any kind of responses or is it cytokine levels you're kind of looking at or influx of cells?

In the process of selecting our single cell.

Which we use to make a master cell bank.

And so again, our master cell bank is based on the selection of a single cell, which we do exquisite characterization around to select that single cell.

And then again use that to make a master cell bank.

That master cell bank goes through extensive testing and qualification in order for it to meet.

FDA sort of guidelines and recommendations for use as a master cell bank.

Scott: Well, what's a success for you for five hundred and five? Yeah, I mean, this is the first, at some level, it's the first time, keep in mind, right, this is the first time IPS-derived NK cell therapies have been delivered in solid tumors. So, you know, and the FT500 dose escalation in 516, or sorry, dose expansion in FT516 dose escalation started, you know, some time ago. And so, success for us was just, again, demonstrating that we could deliver multiple doses, of an unengineered NK cell and then a first engineered NK cell in the setting of solid tumors in that they would, the multiple dose paradigms, multiple cycle paradigms would be safe and well tolerated and that we could potentially see some control of tumor activity and that we would be able to look at translational data that we could continue to build off of as we build the multiplexed engineered pipeline.

Things that we focus on.

Again, we don't believe there's much value.

Daina Michelle Graybosch: And I wonder if you could speak to why at 900 and why not go higher?

And a long term persisting cell.

Daina Michelle Graybosch: And the second question is, can you discuss your rate of genetic abnormalities in an IPSC product simply from cell division and how that might compare to, let's say, a donor-derived product?

If the functional activity of that cell has significantly great. It.

There's no point in a cell persisting if it doesn't have functionality. So we focus on functional persistence and one of the ways to drive functional persistence is certainly through editing, although I'm not sure stealth editing to be fair is a way to drive functional persistence.

Scott: Sure. So, I'm chuckling at the second question.

Scott: With respect to going higher on doses, you know, look, we reserve the right to go higher on doses. Absolutely. And I'm not suggesting we won't continue to potentially explore higher doses and alternative dosing schedules because we do believe we have an incredibly flexible platform, to your point, that has proven to be, at least to date, very safe. So I do think it provides us with a lot of flexibility with respect to continuing to explore higher doses and alternative dosing schedules.

Multi dosing strategy is one way to create functional persistence, albeit through a multi dosing strategy I'll turn it over to Bob here to talk a little bit about sort of the three.

Three approaches we think about as it relates to maximizing functional persistence.

Sure. Thanks, Scott Robin So for Ash, we are presenting our one of our strategy and Scott mentioned, we have three.

Categorize them into cloak.

That's one second is eliminate and third attack and potentiate. So the cloaking strategy, which is a manuscript redrafting right now with Kelly Malburg focuses on complete disruption of the interaction between Tnn K cells with our products. So this is basically T or NK cells will not be able to recognize our products.

Scott: That said, I mean, we're quite pleased with what we're seeing, both with FT-516 and FT-596, with respect to response rates, including CR rates, as well as the durability of response. And so we do believe it is worthwhile, and we do think there's a significant development opportunity to move forward at the 900 million cell level in, for instance, expansions. And we plan on doing that.

I don't want to get into details with that I think I'm gonna respect kellys publication, but here. This goes beyond just thinking that one leg and on the cell will overcome to hundreds of inhibitory and activating receptors are found on NK cells as others are trying to do this is more about going to the heart of the interaction between Tnn case, though so that's cool.

Scott: But again, given the safety profile and the flexibility we have with our platform, we certainly reserve the right to continue to do a bit of exploration as part of our Phase I studies, including with, as I mentioned, alternative conditioning regimens and earlier lines, combined with standard of care regimens. With respect to how we characterize our master cell banks and how we release our product candidates, I'm not going to sort of get into any details around that other than to say we assess for genetic abnormalities at multiple points in the process of selecting our single cell, which we use to make a master cell bank.

Eliminate which is what's an ash is our unique strategy of using <unk> to a map to get rid of all the activate a TNA NK cells that are surrounding ourselves through the engagement of agents City 16 fund on ourselves with the anti C. D 38 map targa.

Targeting to activate itself that come nearby and keep in mind that because our product is 638 negative. This becomes a very unique lymph conditioning strategy, that's better than other strategies that are using maps for this because to a method.

Safe and only target activated alloreactive tnn queso. Unlike other strategies that may go into more progenitor populations to induce a nympho conditioning, therefore depletion and lastly, we're very excited about it attack and potentiate and so this is the idea of where to sell the product itself.

Scott: And so again, our master cell bank is based on the selection of a single cell, which we do exquisite characterization around to select that single cell. And then again, use that to make a master cell. That master cell bank goes through extensive testing and qualification in order for it to meet FDA guidelines and recommendations for use as a master cell provider.

Has the unique ability to not only target alloreactive cells that come near it but also to utilize that attack to cliff right in potentiate itself. So this is the strategy that has been published in nature biotech last year by Max where our defense receptor.

It's used to target one target the alloreactive cells and K R. T cells, but also through the signaling domain.

Daina Michelle Graybosch: Okay, thank you very much for both of those. Sure.

Additional signal to the product itself to Clifford. So this becomes a very unique timely and.

Operator: Your next question comes from the line of Robin Karnaskas from Truvis Securities. Your line is open.

Induction of propagation. So we can use a dr in situations such as the elimination of slight flu conditioning or creating space for our product.

Operator: Hey guys, this is Kirpan for Robin. Thank you so much for taking the time to answer my question.

On your second question with respect to the assays that we use I mean honestly, we develop the assays with a bunch of Kols with respect to how do you. How do you assess allo reactivity or rejection I'm happy to have a conversation with you offline based on the feedback you are getting versus the feedback we've gotten from our sale house that.

Kirpan: You have one poster at ASH that talks about modifications you're making to current K-cells to evade allo rejection. Can you talk about other strategies you may also be working on or considering to ensure that the cells stay in stealth mode? And a related question: with the current candidates that you have, you've talked about the absence or at least low levels of allo rejection you're seeing.

We've used to develop these assays.

It'd be great. Thank you I appreciate your color. Thank you very much.

Kirpan: At least within the time frame that you've observed, there seems to be, we've talked to a bunch of KOLs, and there seems to be a level of confusion in terms of how you show that there is no allorejection. Can you talk a little bit about what assays are used and what sort of feedback you have gotten from the KOL community in terms of the comfort level that there is little to no allergic action? Thank you. Sure, I mean, we're going to talk about this more...

Yep.

Your next question comes from the Lion F. Matt Siegler. Some open heimer your line is open.

Hey, guys.

I'll be quite just one for me just kind of a question on a less healed, but just wanted to get your thoughts on the use of the platform outside of oncology applications.

If there's any plans there I'm sure you've seen some recent data on a stem cell derived therapy for diabetes.

Pretty exciting, albeit early so just kind of one of your thoughts on that.

Scott: Sure. I mean, we're going to talk about this more, for instance, at our Solid Tumor Investor event. We'll certainly talk more about this at ASH. I think, you know, again, there's been a lot of discussion about the value of stealth engineering. I think one of the things that, you know, we focus on... Again, we don't believe there's much value in a long-term persisting cell if the functional activity of that cell has significantly degraded.

Sure absolutely.

We absolutely think we have a platform that can be broadly applicable we have certainly focused initially.

On cell based cancer Immunotherapies.

We certainly believe there is opportunity for the cell types, we make today, including NK cells and T cells that could be those could be used outside of oncology and we're doing some of that work internally at fate Therapeutics, we certainly don't talk about it publicly yet but certainly exploring.

Scott: There's no point in a cell persisting if it doesn't have functionality, so we focus on functional persistence. And one of the ways to drive functional persistence is certainly through editing, although I'm not sure stealth editing, to be fair, is a way to drive functional persistence. The multidosing strategy is one way to create functional persistence, albeit through a multidosing strategy. I'll turn it over to Bob here to talk a little bit about sort of the three approaches we think about as it relates to maximizing functional persistence. Thanks, Scott.

Use of NK cells and T cells in areas, where those could be leveraged outside of oncology I would also say just generally speaking, yes, I mean, we certainly closely watch the whole Ips drive cell therapy space, including with respect to areas that we would consider to be regenerative medicine type of applications.

Excited about all the opportunities that are emerging in Ips derives cell therapy, I think you and I've talked about it I think it's going to be the platform of the future for cell therapy, and certainly we will look to play.

Bob: Robin, so for ASH, we are presenting one of our strategies, and Scott mentioned we have three. Let's categorize them into CLOAK. That's one.

Broadly in those in the field of Ips derive cell therapy overtime.

Oh, great. Thanks, guys congrats.

Sure.

Your next question comes from the line and very Nixon Stifel. Your line is open.

Bob: Second is eliminate, and third is attack and potentiate. So the cloaking strategy, which is a manuscript we're drafting right now with Calais Malberg, focuses on complete disruption of the interaction between T and NK cells with our product. So this basically means that T or NK cells will not be able to recognize our product. I don't want to get into details about that.

Hello. This is Kevin <unk> been person I'm trying to remember Matt. Thank you for taking our question.

<unk> B cell lymphoma programs, you've mentioned in the past they need the that'd be pretty in a certain dose of sales to see activity weekday it can television 16 construct.

Bob: I think I want to respect Calais' publication. But here, this goes beyond just thinking that one ligand on the cell will overcome the hundreds of inhibitory and activating receptors that are found on NK cells, as others are trying to do. This is more about going to the heart of the interaction between T and NK cells. So that's cloak.

For how long would you expect to have N H, a tendency to 16 activity in combination with redox them up with other when Germany Easter.

596, 900 million sounds good nose.

Sure so.

We give a single dose of Rituxan ma'am.

And that single dose of Rituxan Mab, we think provides tumor targeting availability. If you look at for the traditional Rituxan Mab PK curves and receptor occupancy data with respect to Rituxan Mabin tumors, we think there's ability to engage a single dose of rituximab over more.

Bob: Eliminate, which is what's in ASH, is our unique strategy of using daratumumab to get rid of all the activated T and NK cells that are surrounding our cell through the engagement, targeting the activated cells that come nearby. And keep in mind that because our product is CD38 negative, this becomes a very unique lymphoconditioning strategy that's better than other strategies that are using MAPs for this because Darutumumab is safe and only targets activated alloreactive TNNK cells, unlike other strategies that may go into more progenitor populations to induce lymphoconditioning or lymphodepletion.

<unk> week period, let's call it three to four weeks.

Have certainly shown I think a little bit of data with respect to FTE 596 that FTE 596 has in a single dose essentially we've shown it has functional persistence over about a 14 to 21 day period.

We are certainly looking forward to giving a second dose of Rituxan lab, where we think that second dose can still engage rituximab during that multi week period to continue to add therapeutic benefit so for us we.

Bob: And lastly, what we're very excited about ATT&CK and potentiate. And so this is the idea where the cell, the product itself, has the unique ability to not only target alloreactive cells that come near it but also to utilize that ATT&CK to proliferate and potentiate itself. So this is the strategy that was published in Nature Biotech last year by MACs, where the allodefense receptor is used to target one, target the alloreactive cells, NK or T cells, but also, through the signaling domain, add additional signals to the product itself to proliferate. So this becomes a very unique, timely induction of propagation.

He started the experience with FTE 596, as a single dose.

We are certainly excited about adding a second dose of FTE 5961 day 14 to exploit that let's call. It that that second window of Rituxan maps availability in coding tumors.

And again I think this gets back to the point of we really look to focus we really focus on the idea of functional persistence and there's multiple ways to achieve functional persistence certainly through engineering approaches, but a multi dosing approach can really add functional persistence by.

Bob: So we can use ADR in situations such as elimination of CyFlu conditioning or creating space for our product. On your second question with respect to the assays that we use, I mean, honestly, we develop the assays with a bunch of KOLs with respect to how do you assess alloreactivity or rejection? I'm happy to have a conversation with you offline based on the feedback you're getting versus the feedback we've gotten from our KOLs that we've used to develop these assays. That would be great. Thank you.

Giving again second dose that can have a day one experience.

Understood. Thank you.

Sure.

Your next question comes from the lineup Marianne Goldstein for me do home your line is open.

Thank you very much maybe that's a bit of an oddball question, but with.

With respect to presentations at Ash a S T.

Hi, <unk> presentation.

It asks ash and a 5961 is an oral and one is a poster and should we read anything into that.

No Okay [laughter].

Kirpan: That'd be great. Thank you. I appreciate the color. Thank you very much.

Don't read anything under.

Alright, well I have to ask.

Yes.

Don't read anything into it.

Operator: Your next question comes from the line of Matt Biegler from Oppenheimer. Your line is open.

And then I wanted to ask any AML program. It just seems that perhaps that is evolving a little bit slower.

Matthew Cornell Biegler: Oh, guys. I'll be quick. Just one from me. Just kind of a question out of left field, but just wanted to get your thoughts on the use of the platform outside of oncology applications, if there are any plans there. I'm sure you've seen some recent data on a stem cell-derived therapy for diabetes that is pretty exciting, albeit early, so just kind of wanted your thoughts on that. Thanks.

Then the B cell lymphoma, maybe you can talk about that a little bit alright, yeah sure incorrect in my opinion.

No. That's fair. So we were I mean, we were a little delayed in getting out of the first dose level with FTE 538, and it wasn't because we saw any toxicity. We were only open at a single site and so and the single fight was the University of Minnesota. So we launched the FTE 538.

<unk> at.

At the University of Minnesota.

And we we.

We ran into some struggles early on.

Scott: Sure, absolutely. We absolutely think we have a platform that can be broadly applicable. We certainly focused initially on cell-based cancer immunotherapies, but we certainly believe there is opportunity for the cell types we make today, including NK cells and T cells, to be used outside of oncology. And we're doing some of that work internally at Fate Therapeutics. We certainly don't talk about it publicly yet, but we are certainly exploring the use of NK cells and T cells in areas where those could be leveraged outside of oncology. I would also say, just generally speaking, yes.

At that single slate with essentially.

Essentially patients meeting the enrollment criteria and we had a couple of screen failures in a row, which was just unfortunate. We've now open the study at multiple sites and we've seen significant pick up in activity, where I think we mentioned I mentioned, we've enrolled about 10 patients now with at 538 and AML. So we've seen significant pick up now that we've been.

We've been able to open at multiple sites.

Okay, Alright, and then if I could just ask since you're recognized summary.

Some revenue that's attributable to cancel collaboration maybe you can talk a little bit about where you are there and what we should be thinking about as potentially next public disclosure on that program.

Scott: I mean, we certainly closely watch the whole IPS-derived cell therapy space, including with respect to areas that we would consider to be regenerative medicine types of applications. And we are excited about all the opportunities that are emerging in IPS-derived cell therapy. You and I have talked about it. I think it's gonna be the platform of the future for cell therapy, and certainly we will look to participate broadly in the field of IPS-derived cell therapy over time. Thanks, guys. Congratulations.

Yeah. So I'm in the Jansen collaboration has continued to go very well and obviously as you can tell from the revenue that continues to increase we continue to increase the resources under the collaboration I think we've disclosed in the past that the collaboration started with two antigen targets one in hematologic malignancies, one in solid tumors.

A third antigen target has now been added to the collaboration.

Jansen reserves, the right to add a fourth target.

The collaboration so collaborations moving forward, we're really pleased with it.

It will be able to give a little bit of visibility on the first product candidate at the solid tumor day, although we may not be able to disclose the target quite yet.

Matthew Cornell Biegler: Agreed. Thanks, guys. Congratulations. Sure.

Okay. Thanks, a lot I appreciate time sharp.

Operator: Your next question comes from the line of Ben Burnett from Stifel. Your line is open. Hello, this is Carolina Ibanez-Dentoson for Dempur-Net. Thank you for taking our question. In your B-cell lymphoma programs, you've mentioned in the past the need for delivering a certain dose of cells to see activity with the HN-CD16 construct. For how long would you expect to have HN-CD16 activity in combination with rituximab or another when you administer 596 at 900 million cells?

Your next question comes from in the lineup Nick Abbot from Wells Fargo. Your line is open.

Hey, Thanks for taking my question and.

And it's getting late so I'll just ask one quick one during the call late cause I apologize that you provided some commentary on on 819, but.

You have dos and patience now.

Is it too early to comment on experience with that and how that compares to memorial so extensive experience with autologous products.

Yeah sure I can comment on it and you are the first one to ask about it. So no one had asked about it before the studies that the study is up and running I think we're up and running at three or four sites now we've certainly dose patients in.

Operator: [inaudible]

Carolina Ibanez: Sure. So.

Scott: We give a single dose of rituximab. And that single dose of rituximab, we think, provides tumor targeting availability. If you look at the traditional rituximab PK curves and receptor occupancy data with respect to rituximab in tumors, we think there's the ability to engage a single dose of rituximab over a multi-week period.

More than one disease area remember to three disease area studies, So we've dosed patient L. L. We've dose patients in lymphoma, we've not yet dose if I'm remembering correctly in.

So starting at 90 million cells.

Depending on what data sets you look at in the Allogeneic space Nine party cell space 90 million cells may be on the verge of being inactive dose. It's a little bit early we're still early dosing. The first couple of patients here, we've not yet escalated to the second dose level.

Scott: We have certainly shown, I think, a little bit of data with respect to FT-596, that FT-596 has, in a single dose, essentially, we've shown it has functional persistence over about a 14 to 21 day period. We are certainly looking forward to giving a second dose of rituximab, where we think that second dose can still engage rituximab during that multi-week period to continue So, for us, we started the experience with FT-596 as a single dose.

We're making good progress.

Hi, Thank you.

Sure.

Your next question comes from in the line of third stanza Piper Sandler Your line is open.

Great. Thank you Uhm, alright, Curtis mercenary curriculum, the premier Kirk familiar with <unk>.

And sort of what you're doing with two cells.

Is there any work being done looking.

Uhm medical seizures or anything along those lines in terms of a kiss.

Hello. Thanks.

Scott: We're certainly excited about adding a second dose of FT-596 on day 14 to exploit that, let's call it, that second window of rituximab's availability in coding tumors. And again, I think this gets back to the point of, you know, we really look to focus on the idea of functional persistence. And there are multiple ways to achieve functional persistence, certainly through engineering approaches, but a multi-dosing approach can really add functional persistence by giving, again, a second dose that can have a day one experience.

Sure I'll turn that over to Bob Bob's, obviously, leading the effort on research and development and the exploration of alternative cell types in the hematopoietic lineage other than in Kmt.

Thanks, Scott I'll, just be quick and say that our our city 34 note is multi potent so it does give rise to not only and can T cells, but also the mildly lineages and so we're actively looking into other cell types within that.

Sub lineage and I think we're making great progress and we hope to give some updates when Scott allows us to do so [laughter].

Thanks, guys looking forward to all the data read out some of the different adventure planning.

Great. Thanks.

Your next question comes from the lineup from variance from H C. Wainwright Caroline is open.

Scott: Okay. Thank you. Sure. Your next question comes from the line of Mara Goldstein from Mizuho. Your line is open.

Hi, Thank you very much for the.

Update here.

As you've commented on presenting preclinical data in the past.

Operator: Thanks very much. Hey, maybe this is a bit of an oddball question, but with respect to presentations at ASH, you have a 516 presentation at ASH and a 596.

And that you will also show day Trek City.

Considering the incremental data regarding NK cells and solid tumors could.

Could you, perhaps clarify this transmitter slash investigation.

Shall pursuing solid tumors.

Mara Goldstein: One's an oral history, and one is a poster. And should we read anything into that? No. No. Okay. Don't. Don't.

Sure and solid tumors, we and we will talk about this there are certain mechanisms of action, where we think with at least with respect to in NK cells chassis, where NK cells can be advantaged.

Scott: Don't read anything into it. No. All right. Well, I had to ask. It's okay to ask.

Certainly looking at areas for instance, in non small cell lung cancer as an example, where we think NK cells can actually.

Mara Goldstein: Yeah, No. You don't need them.

Be valuable and be therapeutically relevant in patients that have progressed are filled checkpoint inhibitor therapy.

Scott: Don't read anything into it. All right. And then I wanted to ask about the AML program. It just seems that perhaps that is evolving a little bit slower than B-cell lymphoma.

Now treating those patients with an an engineered NK cell may not be the optimal approach, but certainly patients that have progressed or failed checkpoint inhibitor therapy. There are definitely challenges and mechanisms of resistance, where T cells may no longer be effective and some of those mechanisms of.

Scott: Maybe you can talk about that a little bit or if I'm incorrect in my assumption. Yeah. Yeah. Sure. Oh, no.

Scott: No, that's fair. So we were, I mean, we were a little delayed in getting out of the first dose level with FT-538. And it wasn't because we saw any toxicity. We were only open at a single site. And so, and the single site was the University of Minnesota. So we launched the FT-538 experience at the University of Minnesota. And, you know, we ran into some struggles early on at that single site with essentially patients meeting the enrollment criteria. And we had a couple screen failures in a row, which was just unfortunate.

<unk> two T cells are opportunities to engage those tumors for instance, with an <unk> as an example, one of the mechanisms of resistance and non small cell lung cancer is downregulation of MHC class one.

That is a cell type that in case, so can absolutely recognize target and kill.

Another example for instance in.

Array of solid tumors is when.

Rumors are undergoing escape mechanisms associated with T cells. There is often times up regulation of stress log ins like Mick MC B, which is which is <unk>, which is for instance expressed on many solid tumors are 536 product candidate has a car engine.

Scott: We've now opened the study at multiple sites, and we've seen a significant pickup in activity where I think I mentioned we've enrolled about 10 patients now with FT-538 and AML. So we've seen a significant pickup now that we've been able to open at multiple sites.

Heard Intuit, obviously, which key key on the MC game Mcbee receptors. So we're looking at certain mechanisms, where we think.

Scott: Okay, alright. And then if I could just ask, since you recognized some revenue that's attributable to the Johnson Collaboration, maybe you could talk a little bit about where you are there and what we should be thinking about as potentially the next public disclosure on that program?

NK cells may be advantaged, and where there are mechanisms of escape and play with respect to T cells.

Great. Thank you.

Sure.

This concludes our question and answer session I would now like to turn the conference back to our President and CEO got smaller scale.

Scott: Yeah, so the Janssen collaboration has continued to go very well, and obviously, as you can tell from the revenue that continues to increase, we continue to increase the resources under the collaboration. I think we've disclosed in the past that the collaboration started with two antigen targets, one in hematologic malignancies, and one in solid tumors. A third antigen target has now been added to the collaboration, and Janssen reserves the right to add a fourth target to the collaboration.

Thank you. Thank you for everyone for participating in today's call be well and we look forward to speaking with you at 60.

Take care.

Ladies and gentlemen. This concludes today's conference. Thank you for your participation in and have a wonderful day you may all disconnect.

[music].

Scott: So collaboration is moving forward. We're really pleased with it. I think we'll be able to give a little bit of visibility on the first product candidate at solid tumor day, although we may not be able to disclose the target quite yet. Okay.

Scott: Okay. Thanks a lot. I appreciate the time. Sure.

Operator: Your next question comes from the line of Nick Abbott from Wells Fargo.

Operator: From Wells Fargo: Your line is open.

Nick Abbott: Thanks for taking my question. I know it's getting late, so I'll just ask one quick one. During the call late, Scott, I apologize if you provided some commentary on 819, but you've dosed some patients now. Is it too early to comment on your experience with that and how that compares to...

Scott: as to, you know, memorials, and extensive experience with autologous products. Yeah, uh, sure, I-

Scott: Yeah, sure, I'd comment on it, and you're the first one to ask about it, so no one had asked about it before. The study's up and running. I think we're up and running at three or four sites now, and we've certainly dosed patients in more than one disease area. Remember, it's a three-drug area study, so we've dosed a patient in ALL. We've dosed patients in lymphoma. We've not yet dosed them in CLL, if I'm remembering correctly.

Scott: So, starting at 90 million cells, which, depending on what data sets you look at in the allogeneic space, part T cell space, 90 million cells may be on the verge of being an active dose. It's a little bit early. We're still early dosing the first couple patients here. We've not yet escalated to the second dose level, but we're making good progress.

Operator: Your next question comes from the line by Ted Stanzoff from Piper Sandler.

Operator: This is a call from Piper Sandler. Your line is open.

Ted Stanzoff: Great, thank you. Actually, I think most of my questions have been answered, but maybe there was just one about 819 and sort of what you're doing with T-cells. And is there any work being done looking at macrophages or anything along those lines in terms of the IPSC cell line?

[music].

Bob: Thanks. I'll turn that over to Bob. Bob's obviously leading.

Bob: I'll turn that over to Bob. Bob is obviously leading the effort in research and development and the exploration of alternative cell types in the hematopoietic lineage other than NK and T. Thanks, Scott. I'll just be quick and say that our CD34 node is multipotent, so it does give rise to not only NK and T cells but also myeloid lineages. And so we're actively looking into other cell types within that sub-lineage, and I think we're making great progress.

Ted Stanzoff: Thanks, guys. I'm looking forward to all the data readouts and the different events you're planning.

Operator: Your next question comes from the line of Rob Burns from HC Wainwright. Your line is open.

Operator: Hi. Thank you very much for the update. As you commented on presenting preclinical data in the past, and that you'll also show data at SIPC. Considering the incremental data regarding, you know, NK cells and solid tumors. Could you perhaps clarify the strategy-slash-investigational route that you will pursue in Solid Tumors? Sure, in solid tumors, and we will talk about this, there are certain mechanisms of action where we think, at least with respect to an NK cell chassis, NK cells can be advanced.

Operator: We're certainly looking at areas, for instance, in non-small cell lung cancer, as an example where we think NK cells can actually be valuable and be therapeutically relevant in patients that have progressed or failed checkpoint inhibitor therapy. Now, treating those patients with an unengineered NK cell may not be the optimal approach, but certainly, patients that have progressed or failed checkpoint inhibitor therapy, there are definitely challenges and mechanisms of resistance where T cells may no longer be effective.

Operator: And some of those mechanisms of resistance to T cells are opportunities to engage those tumors, for instance, with an NK cell. For example, one of the mechanisms of resistance in non-small cell lung cancer is downregulation of MHC class I. That is a cell type that an NK cell can absolutely recognize, target, and kill. Another example, for instance, in an array of solid tumors is when tumors are undergoing escape mechanisms associated with T-cells, there's oftentimes an upregulation of stress ligands, like MYC-A and MYC-B, which is, for instance, expressed on many solid tumors.

Operator: Our 536 product candidate has a car engineered into it, obviously, which can key on the MYC-A and MYC-B receptors. So we're looking at certain mechanisms where we think NK cells may be advantaged and where there are mechanisms of escape in play with respect to T cells.

Scott: This concludes our question and answer session. I would now like to turn the conference back to our President and CEO, Scott Walsh. Thank you.

Scott: Thank you. Thank you everyone for participating in today's call. Be well, and we look forward to speaking with you at CITSE.

Operator: Ladies and gentlemen, this concludes today's conference. Thank you for your participation and have a wonderful day. You may all go now.

Operator: For a day, you may all disconnect.

Operator: ??? ??? Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music Music, ?? ?? ?? ?? ?? ?? ?? ?? ?? ?? ?? ?? ?? ?? ?? ?? ?? ?? ?? ?? ?? ?? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? If you have any questions or other problems, please post them in the comments. If you have any questions or other problems, please post them in the comments.

Operator: Welcome to the Fate Therapeutics 3rd quarter.

Operator: 2021 Financial Results Conference Call. At this time, all participants are in listen-only mode. This call is being webcast live on the Investor's website

Operator: section of Fate's website at fatetherapeutics.com.

Operator: As a reminder, today's call is being recorded. I would now like to introduce Scott Walshko, President and CEO of Fate Therapeutics.

Scott: Thank you. Good afternoon, and thanks, everyone, for joining us for the Fate Therapeutics third 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 September 30, 2021, was filed shortly thereafter, and can be found on the Investors section of our website under Financial Information.

[music].

Scott: 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: 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 September 30, 2021, that was filed with the SEC today. Undue reliance should not be placed on forward-looking statements, which speak only as of the date they are made, as the 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: Joining me on today's call are Dr. Wayne Chu, our Senior Vice President of Clinical Development; Ed Dulac, our Chief Financial Officer; and Dr. Bob Valamehr, our Chief Research and Development Officer. Today, we will highlight our clinical progress over the past several months with our off-the-shelf IPSC-derived NK-Cell program and discuss our plans to share clinical and preclinical data from certain of these programs in connection with the Society for Immunotherapy of Cancer annual meeting in mid-November and the American Society of Hematology annual meeting in mid-December. Beginning with our B-cell malignancy franchise. Autologous CAR T-cell therapies targeting CD19 have delivered remarkable results for patients with relapsed refractory B-cell lymphoma.

Scott: However, there remains a significant need to develop off-the-shelf, cell-based cancer immunotherapies that can bring transformative outcomes to more patients. Over the past several months, we have made significant clinical progress in advancing our FT-516 and FT-596 product candidates, including expanding clinical investigation of these off-the-shelf IPS-derived NK cell programs to broader patient populations. We continue to be very pleased with the early clinical data we have observed from our Phase I studies of FT516 and FT596 in relapsed refractory B-cell lymphoma, where interim clinical data have shown the potential to drive response rates that are comparable to those achieved with autologous CAR T-cell therapy while maintaining a substantially differentiated safety profile that not only supports administration in an outpatient setting without requiring hospitalization but may FT596 is our off-the-shelf, IPSC-derived CAR and K-cell product candidate designed to target multiple B-cell antigens, both through its CD19-targeted chimeric antigen receptor and through its high-affinity, non-cleavable CD16FC receptor in combination with tumor-targeting antibodies.

Scott: In our dose-escalating Phase 1 study, FT596 is being assessed as monotherapy, as well as in combination with rituximab, a multi-antigen targeting approach that we believe may hold best-in-class potential in addressing tumor heterogeneity and antigen escape. In August, we announced that as of the data cutoff date of June 25, 2021, 10 or 14 patients treated with a single dose of FT-596 achieved an objective response, including seven patients that achieved a complete response in the second and third dose cohorts of 90 million cells and 300 million cells, respectively. Importantly, four of these 14 patients had previously been treated with autologous CD19 CAR T-cell therapy, two of whom achieved a complete response with a single dose of FT-596 in combination with rituximab.

[music].

Scott: Treatment with FT596 was well tolerated and showed a differentiated safety profile to that commonly observed with CAR T-cell therapy, with only two reported low-grade adverse events of cytokine release syndrome, and no reported adverse events of immune effects or cell-associated neurotoxicity or graft-versus-hepatitis. We have now enrolled approximately 30 total patients in the second, third, and fourth single-dose cohorts of 90 million cells, Earlier today, we announced that updated clinical data from our FT-596 Phase I study will be featured in an oral presentation at ASH on Monday, December 13.

Welcome to the fate Therapeutics third quarter 2021 financial results conference call. At this time all participants are in listen only mode. This call is being webcast live on the investors section of its website at fate Therapeutics Dot com.

Scott: The presentation is expected to cover safety and Duration of Response for all patients treated through the third single-dose cohort of 300 million cells as monotherapy and in combination with rituximab. In addition, we plan to hold an investor event on Tuesday, December 14 to further supplement the ASH presentation, where we expect to present safety and tumor response data for those patients treated in the fourth single-dose cohort of 900 million cells.

As a reminder, today's call is being recorded.

I would now like to introduce Scott Walsh go President and CEO of fate Therapeutics.

Thank you good afternoon, and thanks, everyone for joining us for the fate Therapeutics third 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.

Scott: We continue to believe that one significant advantage of off-the-shelf cell therapy is the potential to deliver multiple doses over multiple cycles and that such a treatment paradigm will confer best-in-class outcomes for patients. To that end, having observed that a single-dose treatment cycle of FT-596 was well-tolerated, with no dose-limiting toxicity, we have now increased the frequency of FT-596 dosing and initiated enrollment in a two-dose treatment, with FT-596 administered on day one and day 15 at 300 million cells per dose with the potential to dose escalate to 900 million cells per dose. Patients showing clinical benefit following the first two-dose treatment cycle are eligible to receive a second two-dose treatment cycle.

In addition, our Form 10-Q for the quarter ended September 32021 was filed shortly thereafter and can be found on the investors section of our website 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 1995.

Scott: Additionally, based on the positive interim clinical data we have observed with FT596 in relapsed refractory B-cell lymphoma, we have broadened our clinical investigation of FT596 to include treatment of other B-cell malignancies in our ongoing Phase I study. I'm pleased to announce that we have initiated enrollment of FT-596 in combination with abinituzumab for the treatment of patients with relapse Turning to FT5-16.

<unk> included in our Form 10-Q for the quarter ended September 32021 that was filed with the SEC today.

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.

Lark, our chief Financial Officer.

Scott: In August, we also announced positive interim clinical data as of the data cutoff date of July 7, 2021 from our dose-escalating phase one study of FT516 in combination with rituximab for the treatment of relapsed refractory B-cell lymphoma. 8 of 11 patients achieved an objective response, including six patients that achieved a complete response, in the second and third multi-dose cohorts of 90 million cells per dose and 300 million cells per dose, on day 29 of the second FT516 treatment.

And Doctor bogged down there, our chief research and development Officer.

Today, we will highlight our clinical progress over the past several months with our off the shelf Ips derived NK cell programs.

Beginning with our B cell malignancy franchise.

Autologous car T cell therapies targeting CD 19 have delivered remarkable results for patients with relapsed refractory b cell lymphomas. However, there remains a significant need to develop off the shelf cell based cancer immunotherapies that can bring transformative outcomes to more patients.

Scott: Five of the 11 patients maintained their response without further therapeutic intervention, with follow-up ongoing at between 4.6 and 9.5 months, indicating that FT516 has the potential to drive durable responses. The observed safety profile of FT516 was favorable and is differentiated from that of T-cell based therapy. No FT-516-related serious adverse events or FT-516-related grade 3 or greater adverse events were observed, and no events of any grade of cytokine release syndrome, immune effectors, cell-associated neurotoxicity, or graft-versus-host disease were reported.

Over the past several months, we have made significant clinical progress in advancing our FTE $5 16, and FTE 596 product candidates, including expanding clinical investigation of these off the shelf Ips derived NK cell programs to broader patient.

Relations.

We continue to be very pleased with the early clinical data we have observed from our phase one studies of FTE $5 16, FTE $5 96 in relapsed refractory B cell lymphoma, where interim clinical data have shown the potential to drive response rates that are comparable to those achieved with all.

Scott: We have now completed the dose escalation stage of our FT516 Phase 1 study, having enrolled seven patients in the fourth multidose cohort of 900 million cells per dose. Earlier today, we announced that updated clinical data from our FT516 Phase I study will be featured in a poster presentation at ASH on Monday, December 13. The presentation is expected to cover safety, tumor response, and duration of response for all 18 patients treated at the second, third, and fourth multi-dose cohort. In addition, we plan to further supplement the ASH presentation with updated FT516 data at our investor event on Tuesday, December 14th.

Collagen car T cell therapies, while maintaining a substantially differentiated safety profile that not only supports administration in outpatient setting without requiring hospitalization, but may also enable combination with standard of care treatment regimens used in earlier.

In community settings.

FTE $5 96 is our off the shelf Ips derived car NK cell product candidate designed to target multiple b cell antigens, both through its CD 19 targeted chimeric antigen receptor and through its highest entity non cleavable CD 16 FC receptor <unk>.

Combination with tumor targeting antibodies.

In our dose escalating phase one study FTE 596 is being assessed as monotherapy as well as in combination with Rituximab, a multi antigen targeting approach that we believe may hold best in class potential in addressing tumor heterogeneity and antigen escape.

Scott: After completing dose escalation, we have now initiated dose expansion, at 900 million cells per dose, to further assess the clinical activity of FT516, and are intending to enroll patients into three disease-specific cohorts, including one third-line diffuse large B-cell lymphoma in patients that are naive to autologous CD19 CAR T-cell therapy. Number two, third-line folliculums, in patients that are naive to autologous CD19 CAR T-cell therapy. And three, patients with relapsed refractory B-cell lymphomas whose disease has progressed following autologous CD19 CAR-T cell therapy.

In August we announced that as of the data cutoff date of June $25 2021.

10 of 14 patients treated with a single dose of FTE 596 achieved an objective response, including seven patients that achieved a complete response in the second and third dose cohorts of 90 million cells and 300 million cells respectively.

Importantly, four of these 14 patients had previously been treated with autologous CD 19 car T cell therapy, two of whom achieved a complete response with a single dose of FTE 596 in combination with Rituximab.

Scott: We believe assessing the clinical activity of FT-516 in patients whose disease has progressed following autologous CD19 CAR T-cell therapy addresses a growing market segment with significant unmet need and may offer a potential fast-to-market development opportunity. In addition, because FT516 may be administered in the outpatient setting and given its favorable safety profile observed to date, we have also initiated dose expansion of FT516 in combination with bendamustine and rituximab, and without CyFlu chemotherapy, to explore its potential to combine with standard-of-care CD20-targeted regimens that are used in earlier-aligned community settings. Importantly, in these four dose expansion cohorts, we intend to include sites that serve patients in the community.

Treatment with Ft, 596 was well tolerated and showed a differentiated safety profile to that commonly observed with car T cell therapy.

With only two reported low grade adverse events of cytokine release syndrome, and no reported adverse events of immune effector cell associated neurotoxicity or graft versus host disease.

We have now enrolled approximately 30 total patients in the second third and fourth single dose cohorts of 90 million cells 300 million cells and 900 million cells respectively.

Earlier today, we announced that updated clinical data from our FTE 596 Phase one study will be featured in an oral presentation at ash on Monday December 13.

Presentation is expected to cover safety.

Scott: Turning to our Multiple Myeloma Disease Franchise, I'm pleased to announce that we have treated the first patient in our dose-escalating Phase 1 study of FT538 in combination with the CD38-targeted monoclonal antibody, Daratumab. Our FT-538 product candidate builds off of our FT-516 backbone and is engineered with three functional components to optimize innate immunity. In addition to a novel, high-affinity, non-cleavable CD16FC receptor, FT-538 incorporates an IL-15 receptor fusion and the deletion of the CD38 gene.

Tumor response and duration of response for all patients treated through the third single dose cohort of 300 million cells as mono therapy and in combination with Rituximab.

To that end, having observed that a single dose treatment cycle of FTE $5 96 was well tolerated with no dose limiting toxicities.

Scott: In preclinical studies recently published in the peer-reviewed journal Cell Stem Cell, we showed that FT538 exhibits enhanced serial killing, antibody-dependent cellular cytotoxicity, and functional persistence compared to peripheral blood encases. The superior anti-tumor activity of FT538 is attributable to the biological effects of its novel IL-15 receptor fusion and CD38 knockout, which were shown to improve metabolic fitness. Increased resistance to oxidative stress and induces a protein expression program that enhances NK cell activation and infector function.

We have now increased the frequency of FG 596, dosing and initiate enrollment of a two dose treatment cycle with ft 596 administered on day, one and day 15 at 300 million cells per dose with the potential to dose escalate to 900.

<unk> cells per dose.

Patients so showing clinical benefit following the first two dose treatment cycle are eligible to receive a second two dose treatment cycle.

Additionally, based on the positive interim clinical data, we have observed with FTE $5 96 in relapsed refractory B cell lymphoma, we have broadened our clinical investigation of FTE 596 to include treatment of other b cell malignancies in our ongoing phase one study.

Scott: The Phase I study of FT538 is designed to assess three once-weekly doses of FT538 in combination with Daratumab for the treatment of relapsed refractory multiple myeloma. The first patient was treated with 100 million cells per dose. Similar to our approach in lymphoma, where we are developing FT-516 and FT-596, we have further modified our FT-538 product candidate to create FT-57, our off-the-shelf, IPS-derived, car- and K-cell product candidate designed to target multiple antigens both through its high-avidity BCMA-targeted chimeric antigen receptor and its high-affinity, non-

I am pleased to announce that we have initiated enrollment of FTE 596 in combination with <unk> for the treatment of patients with relapsed refractory CLO and have treated the first patient at 30 million cells per dose.

Turning to FTE $5 16.

In August we also announced positive interim clinical data.

As of the data cutoff date of July seven 2021 from our dose escalating phase one study of FTE $5 16 in combination with Rituximab for the treatment of relapsed refractory b cell lymphoma.

Eight of 11 patients achieved an objective response.

Including six patients that achieved a complete response in the second and third multi dose cohorts of 90 million cells per dose and 300 million cells per dose on day 29 of the second FTE $5 16 treatment cycle.

Scott: We have initiated enrollment in our dose-escalating Phase 1 study of FT576 to assess both single-dose and multi-dose treatment registries, as monotherapy, as well as in combination with Dar-Tu-Meh, an approach that enables targeting of both BCMA and CD38 anti-cancer, which we believe may hold best-in-class potential for the treatment of multiple myeloma. Patient dosing will begin Turning to our AML Disease Franchise.

Five of the 11 patients maintained their response without further therapeutic intervention with follow up ongoing up between four six and nine five months, indicating that FTE $5 16 has the potential to drive durable responses the <unk>.

<unk> safety profile of <unk> 16 was favorable and is differentiated from that of T cell based therapies.

No FTE $5 16 related serious adverse events or FTE $5 16 related grade three or greater adverse events were observed.

No events of any grade of cytokine release syndrome immune effector cell associated neurotoxicity or graft versus host disease were reported.

Scott: We continue to be excited about the potential of IPS-derived and K-cell therapies to play a foundational role in the treatment of patients with AML. We are encouraged by our initial Phase I clinical data from our FT516 and FT538 programs, which have indicated that iPS-derived NK cells are well-tolerated and can induce objective responses with complete clearance of leukemic blasts from the bone marrow. Importantly, these clinical outcomes were achieved with iPS-derived NK cells administered off the shelf and in the outpatient setting.

We have now completed the dose escalation stage of our FTE $5 16 phase one study.

Having enrolled seven patients in the fourth multi dose cohort of 900 million cells per dose.

Earlier today, we announced that updated clinical data from our FTE $5 16 Phase one study will be featured in a poster presentation at ash on Monday December 13.

The presentation is expected to cover safety.

Tumor response and duration of response for all 18 patients treated at the second third and fourth multi dose cohorts.

Scott: Over the past three months, we have made significant strides in opening our dose-escalating Phase 1 study of FT538 at additional clinical sites, and our rate of enrollment has accelerated accordingly. We have now enrolled approximately 10 patients with relapse-refractory AML in the first and second multi-dose cohorts of 100 million cells per dose and 300 million cells per dose, respectively. No dose-limiting toxicities have been reported, and treatment with FT538 continues to be well-tolerated.

In addition, we plan to further supplement the ash presentation with updated FTE $5 16 data at our Investor event on Tuesday December 2014.

Having completed dose escalation.

We have now initiated dose expansion at 900 million cells per dose to further assess the clinical activity of FTE $5 16.

And are intending to enroll patients into three disease specific cohorts, including one.

Third line.

Fuse large b cell lymphoma in patients that are naive to autologous CD 19 car T cell therapy.

Scott: We've also commenced enrollment in an investigator-initiated Phase I clinical trial of FT538, in combination with Daratumumab in patients with relapsed refractory AML. A therapeutic strategy designed to exploit the product candidates' proprietary high-affinity non-cleavable CD16 receptor and CD38 knockout to recognize, bind, and kill leukemic blasts expressing CD38 through antibody-dependent cellular We have also completed the dose escalation stage of our FT-516 phase one study in relapsed refractory AML, having enrolled seven patients in the third multi-dose cohort of 900 million cells per dose. The maximum tolerated dose of FT-516 was not established, and treatment with FT-516 was well tolerated.

Number two third line Follicular lymphoma in patients that are naive to autologous CD 19 car T cell therapy.

And three patients with relapsed refractory b cell lymphomas, whose disease has progressed following autologous CD 19 car T cell therapy.

We believe assessing the clinical activity of <unk> hundred 16 in patients whose disease has progressed following autologous CD 19 car T cell therapy addresses a growing market segment with significant unmet need and may offer a potential fast to market development opportunity.

In addition, because FTE $5 16 may be administered in the outpatient setting and given its favorable safety profile observed to date. We have also initiated dose expansion of FTE $5 16 in combination with Bendamustine and Rituximab.

Scott: We will look to provide an update on our FT5-16 and FT5-38 programs in relapsed refractory AML as we generate additional dose escalation data with FT5-38, including duration of response, so we're able to fully compare the safety, anti-leukemic activity, and durability of response of both programs. Now, turning to our Solid Tumor Franchise.

And without Cy flew chemotherapy conditioning.

To explore its potential to combine with standard of care CD 20 targeted regimens that are used in earlier lines community settings.

Importantly in these four dose expansion cohorts, we intend to include sites that serve patients in the community setting.

Turning to our multiple myeloma disease franchise.

Scott: We are looking forward to the CITSE conference next, where our FT-536 CAR and K-Cell program will be featured in an oral presentation. FT536 is our off-the-shelf, multiplexed-engineered, IPS-derived, NK-cell product candidate that incorporates a novel CAR targeting the Alpha 3 domain of the Pan-Tumor Associated Stress Antigens, MIC-A and IND-enabling preclinical data for FT536 will be presented on Saturday, November 13, and will highlight the novel binding domain of FT536, which is specifically designed to overcome tumor escape mechanisms mediated by loss of MHC class 1 expression and by shedding of MYC-A-MYC.

I'm pleased to announce that we have treated the first patient in our dose escalating phase one study of FTE $5 38 in combination with CD 38 targeted monoclonal antibodies Dara tune them.

Our FTE $5 38 product candidate builds off of our FTE $5 16 backbone and.

And is engineered with three functional components to optimize innate immunity and.

In addition to our novel high affinity non cleavable <unk> FC receptor FTE $5 38 incorporates an IL 15 receptor fusion and the deletion of the CD 38 <unk>.

Scott: We expect to submit an IND application for FT536 in the fourth quarter of 2021 for the treatment of advanced solid tumors, including in combination with monoclonal antibody therapy to exploit multi-antigen targets. In addition, on Monday, November... We intend to host a virtual 90-minute investor event to highlight our emerging pipeline of off-the-shelf, multiplexed-engineered, IPS-derived NK and T-cell product During the investor event, we plan to discuss the following, which are multiplexed engineered preclinical candidates for which we intend to submit IND applications during the next 18 months.

The superior anti tumor activity of FTE $5 38 was attributable to the biological effects of its novel IL 15 receptor fusion and CD 38 knockout, which were shown to improve metabolic fitness.

Increased resistance to oxidative stress.

And induces a protein expression program that enhanced NK cell activation and inspector function.

The phase one study of FTE $5 38 is designed to assess three once weekly doses in combination with Dara to map for the treatment of relapsed refractory multiple myeloma.

The first patient was treated at 100 million cells per dose.

Scott: The unique mechanisms of action that our product candidates seek to exploit in attacking solid tumors, our proprietary multiplexed engineering and single IPSC selection platform, as well as new innovative features and functionality that we are currently assessing for integration into our solid tumor product candidates, our multi-arm phase one study of FT538 in solid tumors, where we have initiated enrollment of FT538 in combination with checkpoint inhibitor therapy in patients with resistance to checkpoint inhibitor therapy and in And we also plan to disclose clinical data from our first-generation product candidates for solid tumors in patients that have progressed or failed checkpoint inhibitor therapy.

Similar to our approach in lymphoma, where we are developing FTE $5 16, an FTE 596, we are further modified our FTE $5 38 product candidate to create FTE 576.

Our off the shelf Ips derived car NK cell product candidate designed to target multiple antigens, both through its high avidity be CMA targeted chimeric antigen receptor.

And its high affinity non cleavable <unk> FC receptor.

We have initiated enrollment in our dose escalating phase one study of FTE 576 to assess both single dose.

And multi dose treatment regimens as monotherapy as well as in combination with Dara two mab.

And approach that enables targeting of both be CMA and CD 38 antigens.

Which we believe may hold best in class potential for the treatment of multiple myeloma.

Patient dosing will begin with FTE $5 seven six as monotherapy in the single dose treatment cohort at a dose of 100 million cells.

Scott: Our Phase 1 study of FT500 has enrolled approximately 10 patients in dose expansion at 300 million cells per dose and includes heavily pretreated patients with non-small cell lung cancer or classical Hodgkin lymphoma that have progressed or failed PD-1, PD-L1 checkpoint inhibitor therapy. Our phase one study of FT516 has enrolled approximately 12 patients in dose escalation, ranging from 90 million cells per dose to 900 million cells per dose, and primarily includes heavily pre-treated patients with stage four melanoma that have progressed or failed PD-1 and PD-L1 checkpoint inhibitors. I would now like to turn the call over to Ed to highlight our third quarter financial report.

Turning to our AML disease franchise.

We continue to be excited about the potential of Ips derived NK cell therapies to play a foundational role in the treatment of patients with AML. We are encouraged by our initial phase one clinical data from our FTE $5 16, an FTE $5 38 programs, which are indicated that Ips derived NK cells are well tolerated.

And Ken induced objective responses with complete clearance of leukemic blast from the bone marrow importantly, these clinical outcomes were achieved with Ips derived NK cells administered off the shelf and in the outpatient setting.

Over the past three months, we have made significant strides in opening are dose escalating phase one study of FTE $5 38 at additional clinical sites and our rate of enrollment has accelerated accordingly, we have now enrolled approximately 10 patients with relapsed refractory AML.

Ed: Thank you, Scott. Turning to our financial results, revenue was $14.2 million for the third quarter of 2021, compared to $7.6 million for the same period last year.

In the first and second multi dose cohorts of 100 million cells per dose and 300 million cells per dose respectively.

Ed: Revenue in the current quarter was derived from our collaborations with Janssen and Ono Pharmaceuticals. Research and development expenses for the third quarter of 2021 were $53.1 million, compared to $30.7 million for the same period last year. The increase in our R&D expenses was attributable primarily to an increase in employee headcount and compensation, including share-based compensation, and in expenses associated with third-party professional services.

No dose limiting toxicities have been reported and treatment with FTE $5 38 continues to be well tolerated.

We've also commenced enrollment in an investigator initiated phase one clinical trial of <unk> $5 38.

Combination with Dara two mab in patients with relapsed refractory AML.

Ed: Third-Party Professional Consultants and Clinical Trials

Ed: General and administrative expenses for the third quarter of 2021 were $15.7 million, compared to $8.3 million for the same period last year. The increase in our G&A expenses was attributable primarily to an increase in employee headcount and compensation, including share-based compensation, and in office and computer supplies, including software licenses. Total operating expenses for the third quarter of 2021 were $55.3 million, net of $13.5 million in non-cash, share-based compensation expense. Note that in connection with the treatment of the first patient with our off-the-shelf IPSC-derived CAR T-cell product candidate, FT819, we achieved the clinical milestone set forth in our amended license agreement with Memorial Sloan Kettering Cancer Center.

We have also completed the dose escalation stage of our FTE $5 16 phase one study in relapsed refractory AML.

Having enrolled seven patients in the third multi dose cohort of 900 million cells per dose.

The maximum tolerated dose of FTE <unk> 16 was not established and treatment with FTE $5 16 was well tolerated.

We will look to provide an update on our FTE $5 16, an FTE $5 38 programs in relapsed refractory AML as we generate additional dose escalation data with FTE $5 38, including duration of response. So we are able to fully compare the safety anti leukemic activity.

<unk> and durability of response of both programs.

Turning to our solid tumor franchise, we are looking forward to the Citi Conference next week, where our FTE 536 car NK cell program will be featured in an oral presentation.

FTE 536 is our off the shelf multiplexed engineered Ips derived NK cell product candidate that incorporates a novel car targeting the alpha three domain of the pan tumor associated stress antigens maguey and mcbee.

Ed: This clinical milestone triggered a first milestone payment in the amount of $20 million to MSK, which we plan to pay in the fourth quarter. Up to two additional milestone payments may be owed to MSK based on subsequent trading values of the company's common stock, ranging from $100 to $150 per share. We assess the fair value of the contingent milestone payments, currently valued at $24.6 million, on a quarterly basis. In the third quarter, we recorded a non-cash $11 million non-operating benefit associated with the change in fair value.

IND, enabling preclinical data for FTE 536 will presented on Saturday November 13, and will highlight the novel binding domain of FTE 536, which is specifically designed to overcome tumor escape mechanisms mediated by loss of MHC class One X.

Pression and by shedding of Mccain Mcbee.

We expect to submit an IND application for FTE $5 36 in the fourth quarter of 2021 for the treatment of advanced solid tumors, including in combination with monoclonal antibody therapy to exploit multi antigen targeting.

Ed: The company ended the third quarter with $804 million of cash, cash equivalents, and investments. Our Common Stock Outstanding was 95 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.

In addition on Monday November 15, we intend to host a virtual 90 minute investor event to highlight our emerging pipeline of off the shelf multiplexed engineered.

Yes, derived NK and T cell product candidates for solid tumors.

During the Investor event, we plan to discuss the following.

Our multiplexed engineered preclinical candidates for which we intend to submit IND applications. During the next 18 months.

The unique mechanisms of action that our product candidates seek to exploit and attacking solid tumors.

Our proprietary multiplex engineering and single Ips C selection platform as well as new innovative features and functionality that we are currently assessing for integration into our solid tumor product candidates.

Operator: Hey Scott, thanks for the updates. I had two questions.

Michael Jonathan Yee: I have two questions. One is about the updates coming later this year at ASH, and obviously, the abstracts are out today. Can you compare and contrast how you think durability would play out for 5.1.6 versus 5.9.6?

Our multiple multi arm phase <unk> study of FTE 538 in solid tumors.

Where we have initiated enrollment of FTE $5 38 in combination with checkpoint inhibitor therapy in patients with resistance to checkpoint inhibitor and in combination with tumor targeting monoclonal antibody therapy, including those that target the tumor associated antigens Egfr hurt too.

Michael Jonathan Yee: Obviously, you've already presented some 5.9.6 data, so would we be able to get a pretty good picture about how that's shaping up at ASH given 5.9.6 and also higher doses? That's question one. And then question two, I think you just laid out some nice commentary around your solid tumor update. I know these are in super heavily pre-treated patients. How should we put that type of data you'll present into context? I mean, responses are good.

PDL one.

And we also plan to disclose clinical data from our first generation product candidates for solid tumors in patients that have progressed or failed checkpoint inhibitor therapy.

Our phase one study of Ft, 500 has enrolled approximately 10 patients in dose expansion at 300 million cells per dose and includes heavily pretreated patients with non small cell lung cancer or classical hodgkin lymphoma that have progressed or failed PD one PDL.

Scott: What would you expect to see, and what's the read-through? Thank you so much. Sure. So, with respect to your first question with respect to durability of 516 versus 596, yes, I think at ASH we will be able to do a first look at comparing the durability of both 516 and 596. We plan to present swim lane plots for both 516 and 596. If you recall from our lymphoma update in August, we did present a swim lane plot for 516. The data cut for that I think was late July, or sorry, it was probably late June or early July.

<unk> checkpoint inhibitor therapy.

Our phase one study of <unk> hundred 16 has enrolled approximately 12 patients in dose escalation ranging from 90 million cells per dose pen 900 million cells per dose and.

And primarily includes heavily pretreated patients with stage four melanoma that have progressed or failed PD, one PDL one checkpoint inhibitor therapy.

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

Thank you Scott turning to our financial results revenue was $14 2 million for the third quarter of 2021 compared to seven 6 million for the same period last year revenue.

Scott: We'll be able now to fast forward that swim lane as well as add patients that were dosed at 900 million cells. And I believe I mentioned there were seven patients dosed at 900 million cells with FT5. With respect to FT-596, recall that we had 10 of 14 patients that had responded to the second and third dose levels. We will now be able to present duration of response on those 14 patients, including adding a couple additional patients that were dosed at the 300 million cell level as backfill.

Revenue in the current quarter was derived from our collaborations with Janssen and Ono pharmaceutical.

Research and development expenses for the third quarter of 2021 were $53 1 million compared to $30 7 million for the same period last year. The increase in our R&D expenses was attributable primarily to an increase in employee head count and compensation.

<unk> share based compensation and in expenses associated with third party professional consultant and clinical trials.

General and administrative expenses for the third quarter of 2021 were $15 7 million compared to $8 3 million for the same period last year the.

Scott: We've also now, I mentioned, I think we've treated about 30 total patients, including probably about 12 to 15 patients at the 900 million cell level. We will at least be able to give a response, first response, to those patients, although durability may not yet be meaningful, just given how immature the patient is. But you'll be able to compare the swim blocks and make inferences, is your point, and see what 596 is doing. That's correct. We will have a SWIM plot for FT596. That is correct. Good. Okay.

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

Total operating expenses for the third quarter of 2021 were $55 $3 million net.

Net of $13 5 million in noncash share based compensation expense.

Note that in connection with the treatment of the first patient with our off the shelf Ips derived car T cell product candidate FTE $8 19, we achieved the clinical milestone set forth in our amended license agreement with Memorial Sloan Kettering Cancer Center.

This clinical milestone triggered a first milestone payment in the amount of $20 million to MSA, which we plan to pay in the fourth quarter.

Scott: And then just quickly on solid tumors. Yeah, with respect to solid tumors, most of what we will present at CITSE will be a go-forward look at our R&D in the emerging pipeline. I think we've always maintained, at the end of the day, cracking the solid tumor nut, if you will, has proven to be much more difficult than treating hematologic malignancies. And I think that's consistent no matter what therapeutic modality you're looking at, whether it's small molecule biologics or cell therapy.

Up to two additional milestone payments may be owed to MSA based on subsequent trading values of the company's common stock ranging from 100 to $150 per share.

We assessed the fair value of these contingent milestone payments currently valued at $24 6 million on a quarterly basis.

In the third quarter, we recorded a noncash $11 million non operating benefit associated with the change in fair value.

Scott: And so, really, as we think about our solid tumor franchise, we're focused on multiplexed engineered product candidates that can attack the tumor from multiple different angles. We're looking at FT500 and FT516 literally as just a first experience with an IPS-derived NK cell therapy. You should have pretty modest expectations with respect to what we think these product candidates can drive on their own with respect to solid tumors. It's really just getting our feet under us with NK cell therapy in solid tumors.

The company ended the third quarter with $804 million of cash cash equivalents and investments.

Our common stock outstanding was 95 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.

Ladies and gentlemen, if you have a question at this time. Please press Star then the number one on your telephone keypad.

My question has been answered or you wish to remove yourself from the queue. Please press the bounty once again Thats Star then the number one on your telephone keypad.

Scott: And we think we've done that with FT500 and FT516. We'll certainly be able to look at safety data. We'll be able to look at, obviously, clinical responses. But, again, your expectations should be pretty modest with these first-generation NK cell products. Thank you very much.

Your first question comes from the line of Michael Yee from Jefferies. Your line is open.

Hey, Scott Thanks for the updates.

I had two questions. One is on the updates coming later this year at Ash, obviously, the abstracts are out today can you.

Operator: Your next question comes from the line of Althea Yong from Cantor. Your line is open.

Compare and contrast, how you think durability would play out for $5 six versus 596, obviously, you've already presented some 596 data show would we be able to get a pretty good picture about how that shaping up at ash given 596 and also higher doses. That's question. One and then question two I think you just laid out.

Operator: Althea Yong from Cantor, your line is open. I'll see ya y'all from Cantor. Your line is open.

Operator: Your next question comes from the line of Michael Schmidt from Guggenheim Security.

Operator: Your line is now disconnected. Hey, this is Kelsey on behalf of Michael.

Some nice commentary around.

Your solid tumor update I know these aren't super heavily pre treated patients how should we put that type of data you will present into context. I mean responses are good what would you expect to see in which the retail. Thank you so much.

Kelsey Beatrice Goodwin: Thanks for taking our questions. I think you have just two from us. First on 5.9.6, I guess, are we still thinking about, you know, now that you're kind of moving from one cycle to two cycles, is there still any flexibility there to maybe increase that further? Or is that kind of where you think you'll end up? And then kind of following up on that, as you build out the solid tumor franchise, I guess kind of what you're doing based on what you've seen with 500 and 5.1.6 is, you know, adding additional cycles for

Sure. So with respect to your first question with respect to durability of 516 versus 590, <unk>, Yes, I think at Ash, we will be able to do a first look at comparing durability of both 516 and 596, we plan to present.

<unk> Lane plots for both $5 16, and 596, if you recall from our lymphoma update in August we did present, a swim lane plot for $5 16.

The data cut for that I think was late July or sorry. It was probably late June early July will be able now to fast forward that swim lane.

Operator: https://www.youtube.com

Operator: Thank you.

As well as that as well as add patients that were dosed at 900 million cells and I believe I had mentioned there were seven patients dosed at 900 million cells with ft 516.

Scott: So with FT-596, we have continued to do, at one dose per cycle, and we now have the ability to give two cycles. If you recall, when we initially advanced our FT-596 program, we were gated on giving a second cycle with FDA consent. So we're now able to give two cycles of FT-596 without going back to the FDA.

With respect to FTE $5 96 recall, we had 10 of 14 patients that had responded.

In the second and third dose level.

We will now be able to present duration of response.

On those 14 patients.

Scott: And so we will continue to dose patients at one dose, giving two cycles, and now we will add two doses in each cycle and continue to give it. We are planning on amending the protocol so that if patients relapse at some point, we could re-intervene with FT594. And so right now, we're sticking to one or two doses per cycle, giving two cycles, and now adding the ability to reintervene if a patient later relapses. So that's where we're headed with FT5.

Including adding a couple additional patients that were dosed at the 300 million cell level as backfill.

We've also now I mentioned I think we've treated about 30 total patients including.

Probably about 12 page 12 to 15 patients at the 900 million cell level.

We will at least be able to give.

<unk> response first response on those patients, although durability may not yet meaningful.

Just given how immature the patients are.

But youll be able to compare this one plots of making for instance, as your appointment and see what <unk> is doing that your point.

Scott: With respect to our solid tumor franchise, very similar, but we are giving multiple doses in a cycle. As an example, FT538 is a product candidate that we're now dosing with solid tumors in combination with monoclonal antibody. It's a multiple dose treatment, and we are giving multiple cycles, and we do, again, if a patient later relapses, we have the ability to re-intervene again. So we are now looking at the potential to withdraw patients upon progression.

That's correct, we will have a swimmer plot for FTE 590, <unk> that is correct.

Okay, and then on just quick or solid tumors with respect to solid tumors with respect to solid tumors. I mean, most of what we will presented Citi will be go forward look at R&D and emerging pipeline I think we've always maintained at the end of the day cracking the solid tumor not if you will.

<unk> has proven to be much more difficult than treating hematologic malignancies, and I think thats consistent no matter, what therapeutic modality or looking at whether it's small molecule biologic or cell therapy, and so really as we think about our solid tumor franchise. We're focused on multiplexed engineered product candidates that can attack the tumor from <unk>.

Kelsey Beatrice Goodwin: Okay, great. Thank you so much.

Operator: Your next question comes from the line of Mike Ulz from Morgan Stanley. Your line is open.

Well different angles, we're looking at <unk> 500, and FTE $5 16, literally is just a first experience within Ips derived NK cell therapy, you should have pretty modest expectations.

Operator: Hey guys, thanks for taking the question. Just a quick question on the CD38 knockout. You sort of highlighted that modification as providing some... Improved Metabolic Fitness. Why not? And number two, are you considering potentially adding that?

With respect to what we think these product candidates can drive.

On their own with respect to solid tumors.

It is really just getting our feet under our under us within NK cell therapy in solid tumors, and we think we've done that with ft $5 to $195 16 will certainly be able to look at safety data, we'll be able to look at.

Michael Eric Ulz: Sure, so for FT5, we've built out our platform over time in a very sort of methodical stepwise fashion. And at the time when we were building out FT596, we did not fully appreciate the therapeutic value of the CD38 knockout. And initially, we thought of CD38 knockout as a step that we would take, a functional step that we would add, that would be unique for myeloma. Knocking out CD38 could prevent fratricide when delivering the therapy in combination with daratumab.

Obviously clinical responses, but again your expectation should be pretty modest with these.

These first generation NK cell product candidates.

Got it thank you very much.

Sure.

Yes.

Your next question comes from the line of.

Young from Cantor Your line is open.

Ophelia young from <unk>.

Ken Your line is open.

Your next question comes from the line of Michael Schmidt from Guggenheim Securities. Your line is open.

Hey, this is kelsey on for Michael Thanks for taking our questions I think just two from us.

Michael Eric Ulz: Obviously, we've come to appreciate, and there have been publications on the therapeutic value of the CD38 knockout more broadly. We certainly are incorporating that into all our product candidates on a go-forward basis, including our product candidates for solid tumors. And certainly, we've reserved the right, obviously, to continue to build off of 538 for lymphoma.

Alright.

596, I guess are we still thinking about now that you're kind of moving from one cycle to cycle is there still any flexibility there to maybe increase that further or is that kind of where where do you think you'll end up and then kind of following up on that as you build out the solid tumor franchise I guess kind of what you based on what you've seen with <unk>.

505, one is adding.

Adding additional cycles for the upcoming next Gen products is that something that you would consider or are you still kind of thinking about the recycle about the Max Thank you.

Scott: Got it. That makes sense.

Sure.

So with Ft 596, we have.

We have continued to dose.

One dose per cycle, and we now have the ability to give two cycles.

If you recall when we initially advanced our FTE $5 96 program.

We were <unk>.

<unk> on giving a second cycle.

With FDA consent.

So we're now able to give two cycles of FTE $5 96.

Scott: So we're gonna hold an investor event on Tuesday. We'll spend most of the time, I think, at that investor event discussing lymphoma. And I think that's going to be a significant focus of ASH as well as the investor event. We're continuing to generate data across all our programs, obviously, and we look forward to providing updates.

Without without going back to the FDA.

And so we will continue to dose patients at one dose.

Giving two cycles and now we will we will now add two doses in each cycle.

And continue to give two cycles.

We are planning on amending the protocol so that if patients relapse at some point, we could re intervene with FTE 596.

Operator: Your next question comes from the line of Althea Young from Cantor. Your line is open. Hey, guys. Thanks for taking my questions. Sorry, I was on mute. I wanted to talk a little bit about 538 and your choice of using it in common...

And so right now we're sticking to one or two doses per cycle, giving two cycles and now adding the ability to re intervene if a patient later relapses. So that's where we're headed with ft 596.

With respect to our solid tumor franchise very some very similar we are giving multi doses in a cycle. As an example, FTE $5 38 is a product candidate that we're now dosing with solid tumors in combination with monoclonal antibody.

Operator: For more, your line is open. Hey guys, thanks for taking my questions.

Mull Pi dose treatment, and we're giving multiple cycles and we do again, if a patient later relapses, we have the ability to re intervene again. So we are now looking at the potential to retreat patients upon progression.

Wayne: Sure, Wayne, do you want to take that question with respect to 538 in AML and thinking about combining it with DARA versus venetoclax? Sure. So... Combinations of FT-538 and Dar-2-1.

Okay, great. Thank you so much.

Sure.

Your next question comes from the line of Mike.

From Morgan Stanley Your line is open.

Operator: www.cdc.gov.au And so, as we've discussed, one of the engineered features of FT538 is the high-affinity, non-cleavable CD16. And so, given the availability of daratumumab and given the data around CD38 expression in AML, it's a natural consequence that a clinical experiment would try to see whether or not combining FT538 with an ADCC-competent monoclonal antibody against an antigen that

Hey, guys. Thanks for taking the question.

Just a quick question on on the CD 38 knockout you sort of highlighted that.

Modification is providing some improved metabolic fitness so I was.

Just curious for $5 96, I notice you don't have that modification there. So I guess two questions number one.

Why not and number two are you considering potentially adding that in the future.

Sure. So for FG five I mean, we build out our platform over time in a very sort of methodical stepwise fashion and at the time. When we were building out FTE $5 96, we did not fully appreciate the therapeutic value of the CD 38 knockout and initially we thought of CD 38 knockout as.

Wayne: is known to be expressed on AML cells.

<unk>.

Wayne: is an experiment moving forward, and that is something that's being done as part of our IIT collaboration with the University of Minnesota.

Wayne: As far as combinations of 538 with other agents, like Minnesota...

Wayne: We remain very interested, you know, in those combinations, obviously not in the context of ADCC, but, you know, understanding really more about how combinations of things with BCL2 inhibitors can have an impact on our cells in the context of these diseases. And so these are concepts that are continuing to be under consideration, and, you know, at some point, we would consider opening up a clinical trial that looks at combinations of our cells with these other anti-leukemic agents.

Due of the CD 38 knockout more broadly we certainly are incorporating that into all our product candidates on a go forward basis, including our product candidates for solid tumors.

And certainly.

We reserve the right obviously to continue to build off of $5 38 for lymphoma.

Got it that makes sense and then maybe just a quick follow up.

With respect to as you did a good job of outlining what to expect for 516 and $5 96, as well, but is there any other datasets that we should be focused on at ash.

So we're going to hold an investor event.

On Tuesday, we will spend most of the time I think on that Investor event discussing lymphoma, and I think I don't think thats going to be the significant focus of ash as well as the investor event.

Operator: Your next question comes from the line of Peter Lawson from Barclays. Your line is open.

Operator: Peter Lawson from Barclays, Utah. Thanks for taking the questions. So, on multiple myeloma...

We're continuing to generate data across all our programs obviously.

And we look forward to providing updates.

Peter Richard Lawson: How much data could we see at ASH and what's the appropriate value, you think, and is it current CAR T's? And yeah, just details around that and how you think about... 538 versus 576 in that. Sure.

Got it thank you.

Your next question comes from the line of <unk> Yang from Cantor. Your line is open hey.

Hey, guys. Thanks for taking my question, sorry, I was on mute.

I wanted double of about 538, and your choice of using it in combination with <unk>, maybe versus some of the other.

Have you been able to talk with some of those other than just kind of your perspective, there on that things kind of differentiated.

Scott: So, again, you know, I'll make a comment. We've continued to build out our pipeline in a very methodical way, building off of, you know, multiplexed engineered backbones to add additional features, which we believe will add incremental therapeutic value. So, building off of IFT538, we built 576, adding a CAR against BCMA, and again, in combination with Daratumab, we believe allows for multi-antigen targeting against both CD38 and BCMA. So, much like lymphoma, where we think 596 is a best-in-class product candidate, we believe the same for multiple myeloma and 576.

Sure Wayne do you want to take that question with respect to $5 38.

In AML and thinking about.

Comp combining with <unk> versus <unk>.

Sure.

No.

The combination of <unk> $5 38, and <unk> in AML was based on.

He bought being emerging evidence about CD 38 expression on AML on AML cells, and so as you know as we've discussed one of the engineered.

Engineered features of Ft 538 at the high affinity non cleavable, <unk> 16, and so given the availability of dollars tumor map and given the data around CD 38 expression in AML.

It's a natural consequence Nash.

Natural consequence that a clinical experiment with try to see whether or not combining FTE $5 38, with an ADC competent monoclonal antibody against an antigen that is known to be expressed on AML.

Scott: Obviously, both statements need to play out in the clinic, but we're firm believers that multi-antigen targeting will lead to the best responses, including durability of response, and that kind of approach can absolutely overcome tumor heterogeneity that exists both in lymphoma and myeloma. Do you think we'll get enough data from Ash, or is this kind of end of twos and threes that we should be thinking about first?

AML cells.

The experiment moving forward in that and that is something that's being done.

As part of our collaboration with the University of Minnesota as far as combination of $5 38 with other agents like <unk>, we remained very interested.

In those combinations.

Obviously, not in the context of ADC, but.

Scott: Yeah, I think I mean, you know, I think I think it's, I think to for that to play out over time, multi antigen targeting best in class approach, you're not just looking at response rates, you're looking at durability of response. And obviously, it will take some time for the durability of response to mature, such that, you know, we can be absolutely certain in our belief systems that we have based on preclinical, And then just a comment on one of the questions you asked about the modest expectations around, Solid tumors, is that a case that you kind of, you're not expecting to see any kind of responses or is it cytokine levels you're kind of looking at or influx of cells?

Understanding really more about how combinations of things with Bcl two inhibitors.

Can have an impact on ourselves in the context of these diseases and so.

These are concepts that are continuing to be under consideration.

<unk>.

At some point.

We would consider opening up a clinical experiment that looks at combinations of ourselves with these other anti leukemic ages.

Great. Thank you very much.

Okay.

Sure.

Your next question comes from the line of Peter Lawson from Barclays. Your line is open.

Hey, thanks, Thanks for taking the questions.

So and multiple myeloma.

Just how much data could we see at ash and what's the appropriate by you think is it current car Ts.

Scott: What's a success for you for $505,000? Yeah, I mean, this is the first it's at some level, it's the first time, keep in mind, right, this first time IPS derived NK cell therapies have been delivered in solid tumors. So, you know, and the FT 500 dose escalation and 516 are sorry, dose expansion and FT 516 dose escalation started, you know, some time ago. And so for success for us was just, again, demonstrating that we could deliver multiple doses, of an unengineered NK cell, and then a first engineered NK cell in the setting of solid tumors in that they would, the multiple dose paradigms, multiple cycle paradigms would be safe and well tolerated, and that we could potentially see some control of tumor activity, and that we would be able to look at translational data that we could continue to build off of as we build the multiplexed engineered pipeline.

And yes just.

Details around that.

How do you think about.

<unk> hundred three eight versus.

570 seats.

In that space.

Sure. So again I'll make a comment we can see we've continued to build out our pipeline in a very methodical way and building off of.

Multiplexed engineered backbones to add additional features which we can which we believe will add incremental therapeutic value. So building off of our FTE $5 38, we built 570, <unk>, adding a car against the CMA and again in combination with Dara to map, we believe allows for multi.

Antigen targeting against both CD 38, <unk>, so much like lymphoma, where we think 596 as a best in class product candidate. We believe the same four for multiple myeloma and $5 seven six obviously, both statements need to play out in the clinic, but we're firm believers that multi antigen target.

Operator: Your next question comes from the line of Daina Graybosch from SVP Lyrinc. Your line is open. Thanks. I, too, have two questions. The first is, it seems like you're expanding a lot of your products in the 900... [inaudible] And the second question is, can you discuss your rate of genetic abnormalities in an IPSC product simply from cell division and how that might compare to, let's say, a donor-derived product?

<unk>.

Yes.

Will lead to best responses, including durability of response and that that kind of approach can absolutely overcome tumor heterogeneity that exists both in lymphoma and myeloma.

Do you think we get enough data by Ash or is this kind of ends of twos and threes that we should be thinking about.

Yes, I think I mean, I think I think it's I think too for that to play out.

Operator: Sure. So, I'm chuckling at the second question.

Over time multi antigen targeting best in class approach, you're not just looking at response rates Youre looking at durability of response and obviously it will take some time for the durability of response to mature such that we can be absolutely certain and our belief systems that we have based on preclinical data.

Got you and then just a comment on one of the questions.

The modest expectations around.

Solid tumors is that the case that you've kind of euronext.

I can see any kind of responses or is it.

So that's the kind of levels, you're kind of looking at all in.

Influx of sales.

Well, it's a success for you for 505 Homesites.

Yeah. I mean this is the first is at some level. It's the first time keep in mind right. This first time of Ips derived NK cell therapies have been delivered in solid tumors.

So in the Ft, 500 dose escalation and $5 16, or sorry dose expansion in ft, 516 dose escalation started sometime ago and so for success for US was just again demonstrating that we could deliver multiple doses.

And on engineered NK cell and then a first engineered NK cell in the setting of solid tumors and that they would the multiple dose paradigms multiple cycle paradigms will be safe and well tolerated and that we could potentially see some control of activity.

Tumor tumor tumor activity and that we would be able to look at translational data that we can continue to build off of as we.

Build the multiplexed engineered pipeline.

Okay.

Thank you so much thanks for taking the question.

Sure.

Your next question comes from the line of Diana <unk> from SVP Leerink. Your line is open.

Thanks, I have two questions. The first is it seems like you're expanding a lot of your products in the 900.

We will dose range, whereas other NK cell companies are giving multiple billions of doses and I Wonder if you could speak to why at 900 and why not go higher.

Scott: And so again, our master cell bank is based on the selection of a single cell, which we do exquisite characterization around to select that single cell. And then again, use that to make a master cell back. That master cell bank goes through extensive testing and qualification in order for it to meet FDA guidelines and recommendations for use as a master cell.

Its just that youre not seeing any maximum tolerated doses.

And the second question is could you discuss your rate of genetic abnormalities.

<unk> product.

Simply from cell division, and how that might compare to let's say a donor derived product.

Sure so.

Im chuckling on the second question.

Scott: Okay, thank you very much.

With respect to going higher on doses look we reserve the right to go higher on doses, absolutely and I'm not suggesting we won't continue to potentially explore higher doses and alternative dosing schedules because we do believe we have an incredibly flexible platform to your point that has proven to be at least to date.

Operator: Your next question comes from the line of Robin Karnaskhan.

Operator: This is Carolina's Costs from Truvis Securities. Your line is open.

Operator: Hey guys, this is Kirpan for Robin. Thank you so much for taking my question. You have one poster at ASH that talks about modifications you're making to current K-cells to evade allo rejection. Can you talk about other strategies you may also be working on or considering to ensure that the cells stay in stealth mode?

Very safe.

So I don't think it provides us a lot of flexibility with respect to continuing to explore higher doses and alternative dosing schedules that said I mean, we are quite pleased with what we're seeing both with FTE $5 16, an FTE $5 96 with respect to response rates, including CR rates.

As well as the durability of response and so we do believe it is worthwhile.

And we do think there's significant development opportunity to move forward at the 900 million cell level.

Operator: And a related question:

Operator: [inaudible]

Operator: The time frame that you've observed, there seems to be, we've talked to a bunch of KOLs, and there seems to be a level of confusion.

In for instance, expansions and we plan on doing that but again, given the safety profile and the flexibility we have with our platform certainly reserve the right to continue to do a bit of exploration as part of our phase one studies, including with as I mentioned alternative conditioning regimens.

Operator: in terms of how you show that there is no allorejection. Can you talk a little bit about what assays are used and what sort of feedback you have gotten from the KOL community in terms of the comfort level that there is little to no allergic action?

Operator: Thank you. Sure. I mean, we're going to talk about this.

And earlier line, combining with standard of care regiments.

With respect to.

How we characterize our master cell banks, and how we release our product candidates.

I'm not going to sort of get into any details around that other than to say.

We.

Assess for genetic abnormalities at multiple points.

In the process of selecting our single cell.

Which we use to make a master cell bank.

And so again, our master cell bank is based on the selection of a single cell, which we do exquisite characterization around to select that single cell.

And then again use that to make a master cell bank.

That master cell bank goes through extensive testing and qualification in order for it to meet.

FDA sort of guidelines and recommendations for use as a master cell bank.

Okay. Thank you very much for Bucks sure.

Sure.

Your next question comes from the line of Robyn <unk>.

Scott from Covid Securities. Your line is open.

Hey, guys. This is <unk> on for Robyn. Thank you so much for taking my question.

Bob: Robin, so for ASH, we are presenting one of our strategies, and Scott mentioned we have three. Let's categorize them into CLOAK. That's one.

You have one poster at ash that talks about modifications youre, making too.

T cells to evade allo rejection.

Bob: Second is eliminate, and third is attack and potentiate. So the cloaking strategy, which is the manuscript we're drafting right now with Calais Malberg, focuses on complete disruption of the interaction between T and NK cells with our product. So this basically means that T or NK cells will not be able to recognize our product. I don't want to get into details about that.

Can you talk about other strategies you may also be working on.

Or considering to ensure that the cells.

Stay in stealth mode.

And related question.

Hi.

The candidates that you have you talked about the absence or at these low levels of Ala rejection you're seeing.

At least within the timeframe that you've observed.

We've talked to a bunch of Kols and there seems to be a level of confusion.

In terms of how.

You show that there is no allo rejection.

Can you talk a little bit about what assays are used and what what kind of feedback have you gotten from the KOL community in terms of the comfort level that there is little to no allo rejection. Thank you.

Bob: Eliminate, which is what's in ASH, is our unique strategy of using daratumumab to get rid of all the activated T and NK cells that are surrounding our cell through the engagement, targeting the activated cells that come nearby. And keep in mind that because our product is CD38 negative, this becomes a very unique lymphoconditioning strategy that's better than other strategies that are using MAPs for this, because Darutumumab is safe and only targets activated alloreactive TNNK cells, unlike other strategies that may go into more progenitor populations to induce lymphoconditioning or lymphodepletion.

Sure I mean, we're going to talk about this more for instance at solid to at our solid tumor Investor event, we'll certainly talk more about this at Ash I think.

Again, there's been a lot of discussion about the value of Delta Engineering, I think one of the things that we focus on.

Again, we don't believe there is much value.

And our long term persisting cell.

If the functional activity of that cell has significantly degrade it.

There is no point in a cell persisting if it doesn't have functionality.

So we focus on functional persistence and one of the ways to drive functional persistence is certainly through editing, although I'm not sure stealth editing to be fair is a way to drive functional persistence multi dosing strategy is one way to create functional persistence.

Bob: And lastly, what we're very excited about ATT&CK and potentiate. And so this is the idea where the cell, the product itself, has the unique ability to not only target alloreactive cells that come near it but also to utilize that ATT&CK to proliferate and potentiate itself. So this is the strategy that was published in Nature Biotech last year by MACs, where the allodefense receptor is used to, one, target the alloreactive cells and KRT cells, but also, through the signaling domain, add additional signals to the product itself to proliferate.

Albeit through a multi dosing strategy I'll turn it over to Bob here to talk a little bit about sort of the three approaches we think about as it relates to maximizing functional persistence.

Sure. Thanks, Scott.

Robyn so for Ash, we are presenting our one of our strategies and Scott mentioned, we have three.

Categorize them into cloak.

That's one second is eliminate and third attack and potentiate. So the cloaking strategy, which is a manuscript redrafting right now with Kelly Malburg focuses on complete disruption of the interaction between T and NK cells with our products. So this is basically T or NK cells will not be able to recognize our product.

Bob: So this becomes a very unique, timely induction of propagation. Thus, we can use ADR in situations such as the elimination of CyFlu conditioning or creating space for our product. On your second question, with respect to the assays that we use, I mean, honestly, we develop the assays with a bunch of KOLs. With respect to how you assess alloreactivity or rejection, I'm happy to have a conversation with you offline based on the feedback you're getting versus the feedback we've gotten from our KOLs that we've used to develop these assays. That'd be great. Thank you.

I don't want to get into details with that respect <unk> publication, but here. This goes beyond just thinking that one ligand on the cell will overcome to hundreds of inhibitory and activating receptors that are found on NK cells as others are trying to do this is more about going to the heart of the interaction between <unk> NK cells. So thats clear.

<unk> eliminate which is what's in ash is our unique strategy of using data to a map to get rid of all the activated T and NK cells that are surrounding our sell through the engagement of <unk> 16 found on ourselves with the anti CD 38 Mab.

Targeting to activate the cells that come nearby and keep in mind that because our product is $3 38 negative. This becomes a very unique lymphoid conditioning strategy, that's better than other strategies that are using maps for this because dark from a method safe and only target activated allo reactive T and NK cells. Unlike other strategies that may go.

Operator: That'd be great. Thank you. I appreciate the color. Thank you very much.

Operator: Your next question comes from the line of Matt Biegler from Oppenheimer. Your line is open.

<unk> into more progenitor populations to induce in lymphoseek conditioning of therefore depletion and lastly, we're very excited about it attack and potentiate and so this is the idea of where to sell the product itself has the unique ability to not only target allo reactive cells that come near it but I'll.

So to utilize that attack to proliferate and potentiate itself. So this is the strategy. That's been published in nature biotech at last year by Max where our defense receptor hits.

It's used to target to one target to allo reactive cells NK or T cells, but also through the signaling domain.

Scott: Sure, absolutely. We absolutely think we have a platform that can be broadly applicable. We certainly focused initially on cell-based cancer immunotherapies, but we certainly believe there is opportunity for the cell types we make today, including NK cells and T cells, that could be used outside of oncology, and we're doing some of that work internally at Fate Therapeutics. We certainly don't talk about it publicly yet, but we are certainly exploring the use of NK cells and T cells in areas where those could be leveraged outside of oncology.

Additional signal to the product itself to proliferate. So this becomes a very unique.

<unk> and.

Induction of propagation. So we can use ADR and situations such as elimination of psi fluid conditioning or creating space for our product.

On your second question with respect to the assays that we use I mean honestly, we develop the assays with a bunch of Kols with respect to how do you how do you assess allo reactivity or rejection.

Happy to have a conversation with you offline based on the feedback youre getting versus the feedback we've gotten from our scale house that we've used to develop these assays.

That'd be great. Thank you I appreciate.

Asia color. Thank you very much.

Sure.

Your next question comes from the line of Matt Biegler from Oppenheimer. Your line is open.

Hey, guys.

I'll be quick just one for me.

Scott: I would also say, just generally speaking, yes, we certainly closely watch the whole IPS-derived cell therapy space, including with respect to areas that we would consider to be regenerative medicine types of applications. And we are excited about all the opportunities that are emerging in IPS-derived cell therapy. I think, you know, I've talked about it. I think it's going to be the platform of the future for cell therapy, and certainly, we will look to participate broadly in the field of IPS-derived cell therapy over time. Thanks, guys. Congratulations.

I had a question out of left field, but just wanted to get your thoughts on the use of the platform outside of oncology applications.

If there is any plans there I'm sure you've seen some recent data on our stem cell derived therapy for diabetes.

Pretty exciting, albeit early so I'm just kind of wanted your thoughts on that thanks.

Sure absolutely.

We absolutely think we have a platform that can be broadly applicable we have certainly focused initially.

On cell based cancer Immunotherapies we.

Matthew Cornell Biegler: Agreed, thanks guys, congrats.

Operator: Your next question comes from the line of Ben Burnett from Stifel. Your line is open. Hello, this is.

The use of NK cells and T cells in areas, where those could be leveraged outside of oncology I would also stages generally speaking, yes, I mean, we certainly closely watched the whole Ips derived cell therapy space.

Operator: Your line is open.

Operator: In your B-cell lymphoma programs, you've mentioned in the past the need to deliver a certain dose of cells to see activity with the HN-CD16 construct. For how long would you expect to have HN-CD16 activity in combination with rituximab or

Including with respect to areas that we would consider to be regenerative medicine type of applications.

Excited about all the opportunities that are emerging in Ips derived cell therapy, I think you and I have talked about it I think it's going to be the platform of the future for cell therapy and <unk>.

Operator: 596 at 900 million cells per dose.

Scott: Sure. So.

Scott: We give a single dose of rituximab, and that single dose of rituximab, we think, provides tumor targeting availability. If you look at traditional rituximab PK curves and receptor occupancy data with respect to rituximab in tumors, we think there's the ability to engage a single dose of rituximab over a multi-week period. Let's call it three to four weeks.

Certainly we will look to play.

Late in the faith in the field of Ips derived cell therapy over time.

Oh, great. Thanks, guys congrats.

Sure.

Your next question comes from the line of Ben Burnett from Stifel. Your line is open.

Hello. This is kind of Eni and perform for example, Matt. Thank you for taking our question.

On your B cell lymphoma programs, you've mentioned in the past have been me, though that he put in a certain dose of cells to see activity with.

Scott: We have certainly shown, I think, a little bit of data with respect to FT-596, that FT-596 has, in a single dose, essentially, we've shown it has functional persistence over about a 14- to 21-day period. We are certainly looking forward to giving a second dose of rituximab, where we think that second dose can still engage rituximab during that multi-week period So, for us, we started the experience with FT-596 as a single dose.

Hey, Tien TV 16 construct.

But how long would you expect to have.

<unk> 2016 activity in combination with Rituximab, but other Wyndham Easter.

90, <unk> 900 million Pik notes.

Sure so.

We give a single dose of Rituximab and.

And that single dose of Rituximab, we think provides tumor targeting availability. If you look at the traditional rituximab PK curves and receptor occupancy data with respect to Rituximab in tumors. We think there is ability to engage a single dose of rituximab over <unk>.

Weak period, let's call it three to four weeks.

Certainly shown I think a little bit of data with respect to FTE $5 96 that FTE $5 96 has in a single dose essentially we've shown it has functional persistence over about a 14% to 21 day period.

We are certainly looking forward to giving a second dose of Rituximab, where we think that second dose.

Can still engage rituximab during that multi week period to continue to add therapeutic benefit so for us we.

We started the experience with ft 596, as a single dose.

We're certainly excited about adding a second dose of FTE $5 96, one day 14 to exploit that let's call. It that that second window of rituximab availability in coding tumors.

Scott: Understood. Thank you. Sure. Your next question comes from the line of Mara Goldstein from Mizuho. Your line is open. Thank you very much.

And again I think this gets back to the point of we really look to focus we really focus on the idea of functional persistence and theres multiple ways to achieve functional persistence certainly through engineering approaches, but a multi dosing approach can really add functional persistence by.

Operator: Thanks very much. Hey, maybe this is a bit of an oddball question, but with respect to presentations at ASH, you have a 516 presentation at ASH and a 596.

Giving again, a second dose that can have a day one experience.

Operator: One's an oral exam and one is a poster, and should we read anything into that? No. Okay, don't do it. Don't read anything into it. It's not like that. All right, well, I had to ask. That's okay to ask. Don't read anything into it. All right. And then I wanted to ask about the AML program. It just seems that perhaps that is evolving a little bit slower than B-cell lymphoma. Maybe you can talk about that a little bit, or am I incorrect in my assumption?

Understood. Thank you.

Sure.

Your next question comes from the line of Mara Goldstein from Mizuho. Your line is open.

Thanks very much.

Maybe it's a bit of an oddball question, but.

With respect to presentations at ash of FTE.

516 presentation.

Ash and a 5961 is an oral and one is a poster and should we read anything into that.

Okay.

Don't read anything into it.

I had to ask.

Yes.

Don't read anything into it.

Okay, and then I wanted to ask on the AML program. It just seems that perhaps that is evolving a little bit slower.

Then b cell lymphoma, maybe you can talk about that a little bit our yes, youre correct in my assumption.

Sure. So we were.

We were a little delayed in getting out of the first dose level with FTE $5 38, and it wasn't because we saw any toxicity. We were only opened at a single site and so and the single site was the University of Minnesota. So we launched the ft 538 experience.

At the University of Minnesota.

And yes, we are.

Ran into some struggles early on.

At that single flight with essentially.

Essentially patients meeting the enrollment criteria and we had a couple of screen failures in a row, which was just unfortunate. We've now opened the study at multiple sites and we have seen significant pickup in activity, where I think we mentioned I mentioned, we've enrolled about 10 patients now with FTE $5 38 in AML. So we've seen significant pick up now that we have been.

Scott: We've now opened the study at multiple sites, and we've seen a significant pickup in activity where I think we've enrolled about 10 patients now with FT-538 and AML. So we've seen a significant pickup now that we've been able to open at multiple sites.

It enable to open at multiple sites.

Scott: Okay. All right. And then, if I could just ask, since you recognized some revenue that's attributable to the Johnson Collaboration, maybe you can talk a little bit about where you are there and what we should be thinking about as potentially the next public disclosure on that program.

Okay, Alright, and then if I could just ask since you recognized so far.

Revenues attributable to the Janssen collaboration maybe you can talk a little bit about where you are there and what we should be thinking about as potentially next public disclosure on that program.

Yeah. So I mean, the Janssen collaboration has continued to go very well and obviously as you can tell from the revenue that continues to increase we continue to increase the resources under the collaboration I think we've disclosed in the past that the collaboration started with two antigen targets one in hematologic malignancies and solid tumors.

A third antigen target has now been added to the collaboration and.

And Janssen reserves, the right to add a fourth target to the collaboration so collaborations moving forward, we're really pleased with it.

Scott: So collaborations moving forward, we're really pleased with it. I think we'll be able to give a little bit of visibility on the first product candidate at solid tumor day, although we may not be able to disclose the target quite yet. Okay.

I think we'll be able to give a little bit of visibility on the first product candidate at the solid tumor day, although we may not be able to disclose the target quite yet.

Scott: Okay. Thanks a lot. I appreciate your time. Sure. Your next question comes from the line of Nick Abbott from...

Okay. Thanks, a lot I appreciate time sure.

Your next question comes from the line of Nick Abbott from Wells Fargo. Your line is open.

Operator: Abbott from Wells Fargo, your line is open.

Hey, guys. Thanks for taking my question.

Operator: Thanks for taking my question. I know it's getting late, so I'll just ask one quick one. Chewing the call late, Scott. I apologize if you provided some commentary on 819, but you've dosed some patients now. Is it too early to comment on your experience with that and how that compares?

And it's getting late so I'll just ask one quick one joined the call late Scotts I apologize that you provided some commentary on eight or nine but <unk>.

<unk> dosing patients now is it too early to comment on experience with that and how that compares to memorial and extensive experience with autologous products.

Nick Abbott: and how that compares to, you know, Memorial's extensive experience with autologous products. Yeah, uh, sure, I-

Yeah sure I can comment on it in your <unk>.

Scott: Yeah, sure, I'd comment on it, and you're the first one to ask about it, so no one had asked about it before. The study's up and running. I think we're up and running at three or four sites now, and we've certainly dosed patients in more than one disease area. Remember, it's a three-drug area study, so we've dosed patients in ALL, we've dosed patients in lymphoma, but we have not yet dosed patients in CLL, if I'm remembering correctly.

Just wanted to ask about it so no one had asked about it before.

Studies, the studies up and running I think we're up and running at three or four sites now we've certainly dosed patients in.

More than one disease area or members at three disease areas study. So we've dosed patient now al al we dose patients in lymphoma, we've not yet dosed, if I'm remembering correctly in CLO, so starting at 90 million cells, which depending on what data set.

Scott: So, starting at 90 million cells, which, depending on what data sets you look at in the allogeneic space, CAR-T cell space, 90 million cells may be on the verge of being an active dose. It's a little bit early, we're still early, dosing the first couple patients here. We've not yet escalated to the second dose level, but we're making good progress.

You look at in the Allogeneic space 90 car T cell space 90 million cells may be on the verge of being an active dose so a little bit early we're still early dosing. The first couple of patients here, we've not yet escalated to the second dose level.

We're making good progress.

Operator: Your next question comes from the line by Ted Stenzel from...

Alright, thank you.

Sure.

Your next question comes from the line of Ted <unk> from Piper Sandler Your line is open.

Operator: This is Ed Stanzoff from Piper Sampler. Your line is open.

Ted Stanzoff: Great, thank you. Actually, I think most of my questions have been answered, but maybe there was just one about 819 and sort of what you're doing with C-cells, and is there any work being done looking at macrophages or anything along those lines in terms of IPS C-cell lines? Thanks.

Yeah.

Great. Thank you.

Mercury quicker Premier group from everywhere.

It was lower than sort of what youre doing with T cells.

<unk>.

Is there any work being done.

King.

Medical sensors or anything along those lines in terms of I guess so.

Bob: I'll turn that over to Bob. Bob is obviously leading the effort in research and development and the exploration of alternative cell types in the hematopoietic lineage other than NK and T.

Thanks.

Sure ill turn that over to Bob Bob's, obviously, leading the effort on research and development and the exploration of alternative cell types in the hematopoietic lineage other than NK and T.

Bob: Thanks, Scott. I'll just be quick and say that our CD34 node is multipotent, so it does give rise to not only NK and T cells but also myeloid lineages. And so we're actively looking into other cell types within that sub-lineage, and I think we're making great progress.

Thanks, Scott I'll, just be quick and say that are our CD 34 node is multi potent so it does give rise to not only NK and T cells, but also the myeloid lineage isn't so we're actively looking into other cell types within that.

Lineage and I think we're making great progress and we hope to give some updates when Scott allows us to do so.

Ted Stanzoff: Thanks, guys. I'm looking forward to all the data readouts and the different events you're planning.

Thanks, guys looking forward to all the data read out some of the different events for planning.

Great. Thanks.

Operator: Your next question comes from the line of Rob Burns from HC Wainwright. Your line is open.

Your next question comes from the line of Rob <unk> from H C. Wainwright. Your line is open.

Operator: Hi, thank you very much for the update here. As you commented on, you know, presenting preclinical data in the past, and that you'll also show data at 50. Considering the incremental data regarding, you know, NK cells and solid tumors, could you perhaps clarify the strategy-slash-investigational route that you will pursue in Solid Tumors? Sure, in solid tumors, and we will talk about this, there are certain mechanisms of action where we think, at least with respect to an NK cell chassis, NK cells can be advanced.

Alright, Thank you very much for the update here.

As you've commented on presenting preclinical data in the past.

Youll also showed data at 60.

Considering the incremental data regarding NK cells and solid tumors.

Could you, perhaps clarify the strategy slash investigation.

Pursuing solid tumors.

Sure in solid tumors, we will talk about this there are certain mechanisms of action, where we think with at least with respect to an NK cell chassis, where NK cells can be advantaged.

Operator: We're certainly looking at areas, for instance, in non-small cell lung cancer, as an example where we think NK cells can actually be valuable and be therapeutically relevant in patients that have progressed or failed checkpoint inhibitor therapy. Now treating those patients with an unengineered NK cell may not be the optimal approach, but certainly, patients that have progressed or failed checkpoint inhibitor therapy, there are definitely challenges and mechanisms of resistance where T cells may no longer be effective.

Certainly looking at areas for instance, in non small cell lung cancer as an example, where we think NK cells can actually.

Be valuable and be therapeutically relevant in patients that have progressed or failed checkpoint inhibitor therapy.

Now treating those patients with an <unk> engineered NK cell may not be the optimal approach, but certainly patients that have progressed or failed checkpoint inhibitor therapy. There are definitely challenges of mechanisms of resistance, where T cells may no longer be effective and some of those mechanisms of resistance.

Operator: And some of those mechanisms of resistance to T cells are opportunities to engage those tumors, for instance, with an NK cell. For instance, one of the mechanisms of resistance in non-small cell lung cancer is downregulation of MHC class 1. That is a cell type that an NK cell can absolutely recognize, target, and kill. Another example, for instance, in an array of solid tumors is when tumors are undergoing escape mechanisms associated with T-cells, there's oftentimes an upregulation of stress ligands, like MYC-A and MYC-B, which is, for instance, expressed on many solid tumors.

<unk> two T cells are opportunities to engage those tumors for instance, with an NK cell as an example, one of the mechanisms of resistance in non small cell lung cancer is downregulation of MHC class one.

That is a cell type that an NK cell can absolutely recognize target and kill.

Another example for instance in.

And array of solid tumors.

Is when.

Tumors are undergoing escape mechanisms associated with T cells. There is often times up regulation of stress ligands like Mick <unk>, B, which is <unk>, which is <unk>, which is for instance expressed on many solid tumors or $5 36 product candidate has a car engine.

And here at Intuit, obviously, which can key on the <unk> receptors. So we're looking at certain mechanisms, where we think.

NK cells may be advantaged, and where there are mechanisms of escape in play with respect to T cells.

Scott: This concludes our question and answer session.

Okay.

Great. Thank you.

Sure.

This concludes our question and answer session I would now like to turn the conference back to our President and CEO Scott <unk>.

In this answer session, I would now like to turn the conference back to our President and CEO, Scott Walsh. Thank you.

Thank you. Thank you everyone for participating in today's call. Be well, and we look forward to speaking with you at CITSE.

Thank you. Thank you for everyone for participating in today's call B, well and we look forward to speaking with you at Citi.

Ladies and gentlemen, this concludes today's conference. Thank you.

Take care.

Ladies and gentlemen. This concludes today's conference. Thank you for your participation and have a wonderful day you may all disconnect.

Thank you for your participation, and have a wonderful day!

The Bulletproof Executive, 2013

Q3 2021 Fate Therapeutics Inc Earnings Call

Request a DemoDemo

FATE

Fate Therapeutics

Earnings