Q1 2020 Earnings Call
[music].
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I would now like the hand, the conference over to your speaker today, Melissa forced or go partners. Thank you. Please go ahead now.
Operator: BF-WATCH TV 2021, Ladies and gentlemen, thank you for standing by and welcome to the Syndax First Quarter 2020 conference. At this time, all lines are in a listen-only mode.
Thank you operator, welcome and thank you to those if he joining us on the line and the webcast. This afternoon for if he wants indexes first quarter 2020 financial and operating result.
Operator: After the speaker's presentation, there will be a question and answer session. If you have a question during the session, you will need to press star 1 on your telephone. Please be advised today's conference is being recorded. If you require any further assistance, please press star zero. I would now like to hand the conference over to your speaker today, Melissa Forst with Argo. Thank you. Please go ahead.
I'm most of course with our partners and with me. This afternoon to discuss the results and provide an update on the company's progress are Dr. Briggs Morrison, Chief Executive Officer, and Rick Shea Chief Financial Officer.
Also joining us on the call for the question answer session is Michael Metzger, President and COO Dr., Michael Myers, Chief Medical Officer, and Dr., Peter or does like Chief Scientific Officer.
Melissa Forst: Thank you, operator. Welcome and thank you to those of you joining us on the line and the webcast this afternoon for a review of Syndax's first quarter 2020 financial and operating results. I'm Melissa Force with Argo Partners, and with me this afternoon to discuss the results and provide an update on the company's progress are Dr. Brakes Morrison, Chief Executive Officer, and Rick Shea, Chief Financial Officer. Also joining us on the call for the question and answer session is Michael Metzger, President and COO, Dr. Michael Myers, Chief Medical Officer, and Dr. Peter Ordentlich, Chief Scientific Officer. This call is being accompanied by a slide deck that has been posted to the company's website, so I'd ask that you please turn to the forward-looking statements on slide two.
This call is being accompanied by a slide deck that it's been posted to the company's website Oh I got you. Please please turn to the forward looking statements on slide two.
Before we begin I'd like turn might use that any statements made during this call that are not historical are considered to be forward looking statements within the meaning of private Securities Litigation Reform Act of 1995.
Actual results may differ materially from those indicated by these statements as a result of various important factors, including those discussed in the risk factor section in the company's most recent quarterly report on form 10-Q, as well as other reports filed with the FCC.
<unk> looking statements represent the company's viewed as of today may seven only [noise].
Melissa Forst: Before we begin, I'd like to remind you that any statements made during this call that are not historical are considered to be forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these statements as a result of various important factors, including those discussed in the risk factors section of the company's most recent quarterly report on Form 10-Q, as well as other reports filed with the SEC. And the following statements represent the company's views as of today, May 7th only. Our replay of the call will be available on the company's website at syndax.com after the call. And with that, I'm pleased to turn the call over to Dr. Briggs Morrison, Chief Executive Officer.
A replay of the call will be available on the company's website at <unk> index Dot com after the call and with that I'm. Please to turn the call over to Dr. Briggs Morrison Chief Executive Officer.
Thank you very much Melissa. Thank you everyone joining us on today's call and webcast.
Before we get started I'd like to take a moment to acknowledge that we are actively monitoring the ongoing coping 19 pandemic to assess any potential impacts to our business.
Number one priority is of course to health and safety of our employees as well for patients and medical professionals involved our ongoing clinical programs.
At this time, we do not anticipate any interruption or delays to our ongoing clinical programs, nor do we expect any impact on our financial guidance.
Briggs Morrison: Thank you very much, Melissa, and thank you to everyone joining us on today's call and webcast. Before we get started, I'd like to take a moment to acknowledge that we are actively monitoring the ongoing COVID-19 pandemic to assess any potential impacts on our business.
We will continue to monitor is evolving situation and will provide updates.
Briggs Morrison: Our number one priority is, of course, the health and safety of our employees, as well as the patients and medical professionals involved in our ongoing clinical program. At this time, we do not anticipate any interruption or delays to our ongoing clinical programs, nor do we expect any impact on our financial guidance. We will continue to monitor the evolving situation and will provide updates as necessary. Now, let us turn to slide three, which provides a high-level summary of our current corporate priorities as we strive to realize a future in which people with cancer live longer and better than ever before. As we had anticipated, 2020 is turning out to be a tremendously exciting and transformative year for our company.
Sorry.
Let's now turn to slide three which provides a high level of summary of our current corporate priorities as we strive to realize a future in which people with cancer with longer better than ever before.
As we had anticipated 2020 is turning out to be a tremendously exciting and transformative year for our company.
Since our last call in March this year, we've presented the first clinical evidence that inhibition of the amended MLL one interaction by Dx 50, 613, our amended inhibitor can induce response in patients with MLL R. Acute leukemias and we announced the successful addition for approximately 100 million Don.
Collars to our balance sheet under attractive terms.
Moreover, the final overall survival read out a V 21, 12 will occur this quarter, bringing us closer to a potential near term FDA filing approval and launch hormone receptor positive.
Briggs Morrison: Since our last call in March of this year, we have presented the first clinical evidence that inhibition of the Menin-MLL1 interaction by SNDX5613, our Menin inhibitor, can induce responses in patients with MLLR acute leukemias, and we announced the successful addition of approximately $100 million to our balance sheet under Attractive Terms. Moreover, the final overall survival readout of E2112 will occur this quarter, bringing us closer to a potential near-term FDA filing, approval, and launch for hormone receptor-positive metastatic breast cancer. And finally, we continue to collect data that will further clarify the potential of our anti-CSF1R antibody, axitilumab, to treat chronic graft-versus-host disease. So let's review each of these opportunities in greater detail.
Positive metastatic breast cancer.
Finally, we continue to collect data that will further clarify the potential of our anti CSF, one our antibody [laughter] telematics to treat chronic graft versus host disease.
So let's review each of these opportunities in greater detail.
Slide four summarizes the design of the phase three trial up into the stat hormone receptor positive hertwo negative breast cancer.
Trials randomized 600 nave patients to exit methane placebo <unk> versus ex investing plus and 10 stat.
The focus of this trial is now on the final overall survival analysis.
Final analysis will be conducted once there are 410 events.
Which based on our modeling and recent discussions with the Cogs, We believe will occur before the end of June this year.
Positive outcome would allow us to file for regulatory approval, the United States based upon the terms of our breakthrough therapy designation in hormone receptor positive metastatic breast cancer and our special protocol assessment would have to yet.
Briggs Morrison: Slide 4 summarizes the design of the Phase 3 trial of Intenistat in hormone receptor-positive HER2-negative breast cancer. The trial randomized 608 patients to eczemastaine plus placebo versus eczemastaine plus antennastat, and the focus of this trial is now on the final overall survival analysis. The final analysis will be conducted once there are 410 events, which, based on our modeling and recent discussions with ECOG, we believe will occur before the end of June this year.
Team is prepared to submit a regulatory finally should the trabi positive within about six months of receiving the data for me Cock, which would set us up to launch into the stat in 2021.
The trial that 80% power to protect hazard ratio of 0.75, and the Maxim hazard ratio that would yield is statistically significant positive trial, it's approximately 22.
Briggs Morrison: The positive outcome would allow us to file for regulatory approval in the United States based upon the terms of our breakthrough therapy designation for hormone receptor positive metastatic breast cancer and our special protocol assessment with FDA. Our team is prepared to submit a regulatory filing, should the trial be positive, within about six months of receiving the data from ECOC, which would set us up to launch Intendostat in 2021. The trial has 80% power to detect a hazard ratio of 0.75, and the maximum hazard ratio that would yield a statistically significant positive trial is approximately 0.82. Based upon the design assumptions, if E2112 achieved a hazard ratio of 0.82, that would indicate that patients receiving the combination had about a five month improvement in median overall survival.
Based upon the design assumptions, if he 21 12 achieved hazard ratio of pointing to that would indicate that patients receiving she was a combination had about a five month improvement in median overall survival.
Slide five emphasizes the potential for the into the set next semester in regimen to be the preferred agent. After a first line Herrmann takes inhibitor, which is typically given either as a single agent or in combination with the CDK for six inhibitor.
Our current estimate is that between 30 and 50% of patients need 21, 12, well have received a CDK for six inhibitor prior to entering the trial.
Yes, we should have a highly relevant dataset to the post CDK for six patient population.
In our opinion the rapid adoption of CDK for six inhibitors, such as high brand in the first line setting underscores the desire of physicians and patients to approve the outcomes associated with anti estrogen therapies.
Briggs Morrison: Slide 5 emphasizes the potential for the antenniset-examestane regimen to be the preferred agent after a first-line hermitase inhibitor, which is typically given either as a single agent or in combination with a CDK4-6 inhibitor. Our current estimate is that between 30% and 50% of patients in E2112 will have received a CDK4-6 inhibitor prior to entering the trial. Thus, we should have a highly relevant data set in the post-CDK46 patient population. In our opinion, the rapid adoption of CDK4-6 inhibitors, such as Ibrance, in the first-line setting underscores the desire of physicians and patients to improve the outcomes associated with anti-estrogen therapy. In the setting of a positive E2112 result, we would expect Intenistat to achieve similar widespread use. This population of patients is substantial, with an estimated 34,000 patients in the U.S. each year who go on to receive hormone therapy after failing first-line therapy and who could, therefore, be eligible to receive Intensistat. Importantly, we will be prepared to launch AntennaSTAT in the U.S. on our own.
In this setting of a positive Etwenty 112 result, we would expect antenna stat to achieve similar widespread use.
This population of patients is substantial with an estimated 34000 patients in the U.S. each year, Google on to receive hormone therapy. After failing first line therapy, and who could therefore be eligible to receive the interest at regimen.
Importantly, we'll be prepared to launch into the stat in the U.S. on around.
Actively building out our internal commercial team to ensure we are well positioned for the potential launch of into the stat in 2021, well currently entering into discussions with potential rest of world commercial partners.
Slide six emphasizes the clinical potential of into the stat hormone receptor positive breast cancer.
In preparation for launching it to the stat, we have conducted qualitative market research with community physicians and breast cancer experts.
We tested a conservative profile.
Actually the minimum benefit that could provide a positive Pos result in 21 12.
Briggs Morrison: We are actively building out our internal commercial team to ensure we are well-positioned for the potential launch of AntennaSTAT in 2021, while currently entering into discussions with potential rest-of-world commercial partners. Slide 6 emphasizes the clinical potential of antennastat in hormone receptor-positive breast cancer. In preparation for launching antennastat, we have conducted qualitative market research with community physicians and breast cancer experts. We tested a conservative profile, essentially the minimum benefit that could provide a positive OS result in E2112. We consistently heard from both groups of physicians that there is a high need for novel agents in hormone receptor positive breast cancer and that they find the potential ability of Intinacet to resensitize patients to endocrine therapy to be a very attractive feature of Intinacet.
We consistently heard from both groups of physicians that there's a high need for novel agents hormone receptor positive breast cancer and that they find a potential ability of intend to set to lease sensitize patients to enter current therapy to be at very attractive feature I've been Tennessee.
Not surprisingly the uniformly so overall survival. That's the most important efficacy endpoint and believe that an agent that could extend survival and lakes in patients time on hormone therapy with minimal impact to the quality of life made it very compelling profile.
We remain confident the potential for a few 20 myself to be a positive trial in are eager to bring this potentially important new medicine to patients.
Let me now turn to slide seven and Sdx 50, 613 hard genetically targeted agent.
On our last call we highlighted two premier publications, one in cancer cell and one in science that provide the scientific rationale in pre clinical validation of our ongoing clinical trial.
Briggs Morrison: Not surprisingly, they uniformly saw overall survival as the most important efficacy endpoint and believed that an agent that could extend survival and lengthen a patient's time on hormone therapy with minimal impact on their quality of life had a very compelling profile. We remain confident in the potential for E2112 to be a positive trial and are eager to bring this potentially important new medicine to patients. Let me now turn to slide 7 in SNDX5613, our genetically targeted ADH. On our last call, we highlighted two premier publications, one in Cancer Cell and one in Science, that provide the scientific rationale and preclinical validation for our ongoing clinical trial. Those publications did not involve the use of our development candidate, SNDX5613. Therefore, we were quite excited to be selected to present the preclinical profile of SNDX5613 at the AACR New Drugs on the Horizon session last month. I will not review the details of that presentation; it is available on our website; but I will summarize a few key points.
Those publication this did not involve the use of our development candidate and Dx 50 613.
Therefore, we were quite excited to be selected to present, the preclinical profile of Sdx 56, and her team at the HCR new drugs on the horizon session last month.
Well not review the details of that presentation is available on our website, but I will summarize a few key points.
First our molecule is a potent and specific inhibitor of the men MLL interaction.
The only off target activity of note because it's relatively weak binding to the herd channel.
And second of clinical relevance.
Yes, and Dx 50, 613 is metabolized by situated for.
On slide eight summarized the detail experiments that were conducted to derive a model. The plasma exposures, we think will be needed in patients to drive efficacy.
We were of course pleased that as shown on slide nine second patient in the trial and the first patient in the trial with an M.L.R.. We arrangement had plasma exposures that exceeded the levels, we anticipated would be required for efficacy and indeed went on to achieve a complete response.
Briggs Morrison: First, our molecule is a potent and specific inhibitor of the menin-MLL interaction. The only off-target activity of note is its relatively weak binding to the HERD chain. Second, of clinical relevance, SNDX 5613 is metabolized by CYP3A4.
Importantly, clinical activity was observed rapidly by day 28 of therapy, no dose limiting toxicities were observed.
Briggs Morrison: On slide 8, we summarized the detailed experiments that were conducted to derive a model of the plasma exposures we think will be needed in patients to drive FDA approval. We were, of course, pleased that, as shown on slide 9, the second patient in the trial and the first patient in the trial with an MLLR rearrangement had plasma exposures that exceeded the levels we anticipated would be required for efficacy and indeed went on to achieve a complete response. Importantly, clinical activity was observed rapidly by day 28 of therapy, no dose-limiting toxicities were observed, and the only treatment-related adverse experience was a grade 2 QTC prolongation. Of note, this patient was on a concomitant medication that inhibits the activity of CYP3A4, which may account for the disproportional PK exposure relative to what we had anticipated.
Only treatment related adverse experience with a great to Q Tc prolongation.
Of note. This patient was on concomitant medications that inhibits the activity of Sip three four which may account for the disproportional PK exposure relative to what we had anticipated.
Full details on additional patients are included in the CR presentation, that's available on our website.
The updated first in human trial in the accelerated understanding of men inhibition or augment program is the augment one on one trial and has shown schematically on slide 10.
Just first in human clinical trials as a combined phase one in phase two trial.
Phase one portion is a dose escalation trial designed to identify the maximum tolerated dose and a recommended phase two dose of Aesynt Dx 50, 613 in two independent cohorts of patients with relapsed or refractory leukemia.
Briggs Morrison: Full details on additional patients are included in the AACR presentation that's available on our website. The updated first-in-human trial in the Accelerated Understanding of Menin Inhibition, or AUGMENT, program is the AUGMENT 101 trial and is shown schematically on slide 10. This first in human clinical trial is a combined phase one and phase two trial. The phase 1 portion is a dose escalation trial designed to identify the maximum tolerated dose and a recommended phase 2 dose of SNDX5613 in two independent cohorts of patients with relapsed or refractory leukemia. Arm A enrolls patients who are not on a strong CYP3A4 inhibitor, and Arm B enrolls patients who are on a strong CYP3A4 inhibitor at the time of enrollment. The first 28 days of dosing serve as the period in which safety is evaluated for determining dose escalation.
Our eight can rules patients who are not on a strong shipped through a four inhibitor and harm be enrolls patients who are on a strong sifthree for inhibitor at the time of enrollment.
The first 28 days of dosing serves as the period in which safety is evaluated for determining dose escalation.
As required by the FDA patients do not need to have a supposed specific genetic abnormality to enroll in the phase one toward a study.
As of the time of the HCR presentation, we have completed our evaluation of cohorts, one and two in arm, a and are evaluating a single patient dose level three.
No dose limiting for gray to toxicities had been observed to date.
And as his time of the HCR presentation in RMB, we've had no dose limiting toxicities kind of expanded two or three plus three design given one great to toxicity.
Briggs Morrison: As required by the FDA, patients do not need to have a specific genetic abnormality to enroll in the Phase 1 study. As of the time of this AACR presentation, we have completed our evaluation of Cohorts 1 and 2 in Arm A and are evaluating a single patient at Dose Level 3. No dose-limiting or grade 2 toxicities have been observed to date.
Our intent is to find a recommended phase two dose for each cohort.
Once the recommended phase two doses are established the phase two trial will proceed to enroll three distinct expansion cohorts each of which consists of a specific genetically defined relapsed or refractory acute leukemia.
The three cohorts are adults with MLL R acute lymphocytic leukemia or AOL.
Briggs Morrison: And as of the time of the AACR presentation, in R&B, we've had no dose limiting toxicities and have expanded to a 3 plus 3 design, given one grade 2 toxicity. Our intent is to define a recommended phase 2 dose for each cohort. Once the recommended Phase II doses are established, the Phase II trial will proceed to enroll three distinct expansion cohorts, each of which consists of a specific, genetically defined relapse or refractory acute leukemia, The three cohorts are adults with MLLR acute lymphoid leukemia or ALL, adults with MLLR acute myeloid leukemia or AML and adults with NPM1 mutant AML, Our intent is to have specified dosing guidelines for patients in Phase 2 derived from the two cohorts in Phase 1.
Adults with MLL R acute myeloid leukemia, or AML and adults with and PMN one.
You know.
Our intent is to have specified dosing guidelines for patients in phase two derived from the two cohorts in phase one.
Phase two portion will further characterize the safety of Aesynt Dx 50, 350, 613 and will provide initial estimate of the complete response rate as the primary measure therapeutic benefit.
Additional updates from the phase one portion of the argument one or one trial our anticipated in the fourth quarter of this year at a medical conference.
But do not anticipate any further updates before the fourth quarter.
In addition, we are eager to advance this molecule into the pediatric population is a key component of our overall strategy. We will have more to say about the details of the pediatric timing and approach on a future call.
Briggs Morrison: The Phase 2 portion will further characterize the safety of SNDX5613 and will provide an initial estimate of the complete response rate as the primary measure of therapeutic benefit. Additional updates from the Phase 1 portion of the Augment 101 trial are anticipated in the fourth quarter of this year at a medical conference. Do not anticipate any further updates before the fourth quarter.
We know pediatric leukemias with MLL R rearrangements represent a significant unmet medical need we're eager to work with the pediatric oncology community to bring Aesynt Dx 50, 60, 50 613 to their patients.
Let me now turn to slide 11 enacted telematics formally known as Sdx 63, 52, our potential best in class monoclonal antibody therapy targeting the CSF one receptor.
Briggs Morrison: In addition, we are eager to advance this molecule into the pediatric population, which is a key component of our overall strategy. We will have more to say about the details of the pediatric timing and approach on a future call. We know pediatric leukemias with MLLR rearrangements represent a significant unmet medical need, and we are eager to work with the pediatric oncology community to bring SNDX5613 to their patients.
Self from the multiple eighth ascending dose trials exploring actually telematic alone and in combination with Durvalumab in patients with solid tumors were presented last week during the virtual HCR meeting.
These results demonstrated the tolerability and robust pharmacodynamic biomarker modulation of exits and tell them that.
Briggs Morrison: Let me now turn to slide 11, an acetilumab, formerly known as SNDX6352, our potential best-in-class monocle antibody therapy targeting the CSF1 receptor. Results from the multiple ascending dose trials exploring axotilumab alone and in combination with drivalumab in patients with solid tumors were presented last week during the virtual AACR meeting. These results demonstrated the tolerability and robust pharmacodynamic biomarker modulation of X-Tilamab and underscored its ability to promote rapid and sustained depletion of circulating pro-inflammatory monocytes at all dose levels tested. As you know, we initiated a trial testing Actilimab as monotherapy in chronic graft-versus-host disease, and the rationale for using a CSF1R inhibitor against this disease is shown on slide 12. Chronic GVHD is a frequent complication of hematopoietic stem cell transplantation, wherein donor-derived immune cells contribute to the initiation and development of fibrosis and the myriad manifestations of the disease. In Preclinical Models, blocking the CSF1-CSF1R pathway with an anti-CSF1R antibody can result in the depletion of donor macrophages, thereby preventing and reducing chronic graft-versus-host disease. We believe chronic GVHD represents an important clinical opportunity.
[laughter] underscored its ability to promote rapid and sustained depletion of circulating pro inflammatory monocytes at all dose levels tested.
As you know we initiated a trial testing has told them out as monotherapy in chronic graft versus host disease and the rationale for using a CSF one our inhibitor against this disease as shown on slide 12.
[noise] chronic gvhd say frequent complication of hematopoietic stem cell transplantation, wherein donor derived immune cells contribute to the initiation and development of fibrosis and the myriad manifestations of the disease.
Preclinical models blocking blocking the CSF, one CSF, one heart pathway with an anti CSF one our antibody Henry's salt is it the depletion of donor macrophages, thereby preventing and reducing chronic graft versus host disease.
We believe chronic gvhd represents an important clinical opportunity.
Last year, we released the initial data from our phase one trial, which is diagrammed on slide 13.
Phase one portion is a dose escalation trial designed to identify the maximum tolerated dose and they recommended phase two dose I've asked to tell them that for the treatment of chronic graft versus host disease.
We have released data from the first five patients enrolled in the first three cohorts and if now modified the trial to include a phase two cohort at the one milligram per kilogram dose.
We will continue the phase one trial to formally defined the recommended phase two dose and May open one or more additional phase two.
Rick Shea: Last year, we released the initial data from our Phase 1 trial, which is diagrammed on slide 13. The Phase 1 portion is a dose escalation trial designed to identify the maximum tolerated dose and a recommended Phase 2 dose of acetilumab for the treatment of chronic graft-versus-host disease. We've released data from the first five patients enrolled in the first three cohorts and have now modified the trial to include a phase two cohort at the one milligram per kilogram dose. We will continue the Phase 1 trial to formally define the recommended Phase 2 dose and may open one or more additional Phase 2 cohorts, Finally, slide 14 summarizes the transactions that led to the acquisition of the Mennon MLR and Axitelimat programs.
Dose cohorts as well.
Finally, slide 14 summarizes the transactions that led to the acquisition of the men in MLL R and after telematic programs. We believe that we will be able to continue to expand our pipeline through the acquisition or in licensing of quality differentiated assets.
We believe we have the necessary skill to evaluate and identify high quality assets and the clinical development experience to bring these compounds through valuable inflection point.
We expect to remain among preferred partners such transactions.
I'll now turn the call over to Rick to review our financial results.
Yeah.
Thank you Greg.
Rick Shea: We believe that we will be able to continue to expand our pipeline through the acquisition or in-licensing of quality differentiated assets. We believe we have the necessary skill to evaluate and identify high-quality assets and the clinical development experience to bring these compounds through valuable inflections. We expect to remain among preferred partners in such transactions. I'll now turn the call over to Rick to review our financial results.
The results of our operations for the first quarter 2020.
The comparisons to the prior year quarter.
Included in our press release, two I will repeat them and these remarks additional financial details will be available in our first quarter form 10-Q, which will be filed today.
I would like to point out that our operating loss for the first quarter was $15.2 million.
But a noncash charge of $3.9 billion was recorded in the quarter due to the adjustment of the strike price on our series one series to warrants, bringing our reported net loss attributable to shareholders $19.1 million.
Rick Shea: Thank you, Briggs. The results of our operations for the first quarter of 2020, in comparison to the prior year's quarter, are included in our press release, though I won't repeat them in these remarks. Additional financial details will be available in our first quarter Form 10-Q, which will be filed today. However, I would like to point out that our operating loss for the first quarter was $15.2 million. But a non-cash charge of $3.9 million was recorded in the quarter due to the adjustment of the strike price on our Series 1 and Series 2 warrants, bringing our reported net loss attributable to shareholders to $19.1 million. This is described more fully in our 10-Q. Turning to slide 15, we ended the first quarter with $99 million in cash and 36.1 million shares in pre-funded warrants. It was outstanding.
And this is described more fully in our 10-Q.
Turning to slide 16.
We ended the first quarter with $99 million and cashing 36.1 million shares in pre funded warrants outstanding.
This cash balance included the proceeds from 35 million dollar equity offering and a 20 million dollar term loan we closed in February.
Earlier this week, we closed on another equity offering of 5.6 million shares at $18 with net proceeds of $93.7 million. Following this recent equity offering.
The total number of common shares in pre funded warrants is now 41.7 million.
Looking ahead I'd like to provide financial guidance for the second quarter 2020.
Rick Shea: The cash balance included the proceeds from a $35 million equity offering and a $20 million term loan we closed in February. Earlier this week, we closed on another equity offering of 5.6 million shares at $18, with net proceeds of $93.7 million, and following this recent equity offering, the total number of common shares and pre-funded warrants is now 41.7 million.
Our financial guidance for the second half of 2020 will be issued after we get the result of the 21 12 study.
We expect our operating expenses for the second quarter 2020 to increase over the first quarter 2020, R&D expenses for the second quarter will increase primarily due to increased development activities for SMB X 50, 613, our men and inhibitor.
Second quarter DNA expenses are expected to be similar to the first quarters DNA.
Rick Shea: Looking ahead, I'd like to provide financial guidance for the second quarter of 2020. Financial guidance for the second half of 2020 will be issued after we get the results of the E2112 study. We expect our operating expenses for the second quarter of 2020 to increase over the first quarter of 2020. R&D expenses for the second quarter will increase primarily due to increased development activities for S&DX 5613, our menin inhibitor. Second quarter G&A expenses are expected to be similar to the first quarter's G&A. For the second quarter of 2020, we expect R&D expenses to be $12 to $14 million, and Total Operating Expenses to be $18 to $20 million, including approximately 1.
The second quarter of 2020.
We expect R&D expenses to be $12 million to $14 million.
And total operating expenses to be $18 million to $20 million.
Including approximately $1.5 million.
Noncash stock compensation expense.
Given our cash from the recent equity offering.
And our operating expense guidance.
We expect and the second quarter of 2020.
With approximately $175 million a cash.
Which gives us the financial flexibility to take advantage of key development milestones well into 2021.
Now I'd like turn the call.
He brings.
Thanks, very much Rick.
Rick Shea: $1,000,000 of non-cash stock compensation expense. We've given our cash from the recent equity offering and our Operating Expense Guide. We expect to end the second quarter of 2020 with approximately $175 million of cash, which gives us the financial flexibility to take advantage of key development milestones well into 2021.
As I hope you have appreciated from my prepared remarks 2020, it's a busy year for syndax with several very important and exciting data readouts close at hand.
We believe that a positive Oh, EPS result, and he 21 12 would be transformative for syndax create significant shareholder value.
We anticipate a final read out very soon.
We also believe that Essen Dx 50, 613, our amended MLL R. Inhibitor is now significantly de risked we have many questions to answer, but we believe we have the skills and resources needed to advance the program potentially enable early regulatory clarity.
Briggs Morrison: Now, I'd like to turn the call back over to Briggs.
Operator: Thanks very much, Rick. As I hope you have appreciated from my prepared remarks, 2020 is a busy year for Syndax with several very important and exciting data readouts coming up. We believe that a positive O.S. result in E2112 would be transformative for Syndax and create significant shareholder value. We anticipate a final readout very soon. We also believe that SNDX5613, our amended MLR inhibitor, is now significantly de-risked. We have many questions to answer, but we believe we have the skill and resources needed to advance the program and potentially enable early regulatory clarity. And finally, we are excited about the early results we are seeing with hexatillumab in chronic graft-versus-host disease and look forward to presenting updated data from this program at the end of the year.
And finally, we are excited about the early results we are seeing what's actually tell them that.
In chronic graft versus host disease and look forward to presenting updated data from this program at the end of year.
With our recent highly successful financing we are comfortable that we have the financial resources to get us through these key upcoming milestones.
Finally, we are optimistic that we will continue to identify and bringing novel molecules to deepen our portfolio.
You have a proven track record of delivering on this pillar of our strategy and I believe this is a core strength of our company.
As always I'd like to think the wonderfully talented team here at Syndax, our collaborators and most importantly, the patients trial sites and investigators involved with our clinical programs.
Operator: With our recent, highly successful financing, we are comfortable that we have the financial resources to get us through these key upcoming milestones. Finally, we are optimistic that we will continue to identify and bring in novel molecules to deepen our portfolio. You have a proven track record of delivering on this pillar of our strategy, and I believe this is a core strength of our company. As always, I'd like to thank the wonderful talented team here at Syndax, our collaborators, and, most importantly, the patients, trial sites, and investigators involved with our clinical program. In addition, I'd like to thank our committed long-term investors who are helping us build this great company and to welcome the new investors who have joined in that effort with our recent findings. With that, I'd like to open the call to questions. Operator
In addition, I'd like to thank our committed long term investors, who are helping us build this great company and to welcome to new investors, who joined in that effort with our recent financing.
With that I'd like to open the call for questions.
Operator.
As a reminder to ask the question you want me to press Star one on your telephone.
I would throw your question press the pound Q.
Please stand by Bill, we compile the human a roster.
Operator: As a reminder, to ask a question, you will need to press star 1 on your telephone. To withdraw your question, press the pound key. Please stand by while we compile the Q&A roster. Your first question comes from the line of David Libel. Thank you very much for taking my question. Going into the Mennon Phase I studies, did you anticipate that the CYP, CYP34K4 inhibitors would impact the PK of the therapy, and I guess when you're moving towards the second stage, at some point, will you be bifurcating doses dependent upon whether or not the patients are on these inhibitors?
Your first question comes from a line of David Lebowitz.
Thank you very much for taking my question I'm going into the men in Phase. One study did you anticipate that Uh huh.
The see why <unk> to see why P.
See why he meaningful eight or editor would impact the PK of of the therapy and I guess, when you're moving towards the second stage at some point.
I will you bifurcated in dose is dependent upon.
Whether or not the patients are on these inhibitors.
Hi, David Yeah. Thanks for your question.
So we did indeed anticipate that.
The combination of 50 613 with a drug that is known to win hibbett strongly inhibit 64 would lead to higher plasma exposures in preclinical models are preclinical assay. The drug is primarily metabolized by substrate for so that.
Was anticipated.
We obviously have to characterize that in patients in terms of its magnitude and that's what we're doing carefully now with the army RMB.
Briggs Morrison: Hi David. Yeah, thanks for your question. So we did indeed anticipate that, uh... The combination of 5613 with a drug that is known to strongly inhibit CYP3A4 would lead to higher plasma exposures in preclinical models or preclinical assays. The drug is primarily metabolized by CYP3A4, so that was anticipated. We obviously have to characterize that in patients in terms of its magnitude, and that's what we're doing carefully now with the arm A, arm B separation. In terms of what we would do in phase two with regard to dose, after we finish the dose escalations in arms A and arm B, if it turns out that the magnitude of the increase due to CYP3A4 inhibition is rather modest, then we may say there's just one recommended dose. If that increase in exposure is more notable, then we may have a dose that we recommend for phase two and a dose adjustment if patients are on a strong inhibitor. An approach that's not uncommon for drugs that are metabolized by CYP3A4.
Separation.
In terms of what we would do in phase two in.
With regard to dose.
After we finish the dose escalations in arm a in RMB. If it turns out that the magnitude of the increased due to three or four inhibition is rather modest then we may say theres just a recommended one recommended dose.
If that increasing exposure is a more notable then we may have a dose that we recommend for phase two and a dose adjustment if patients are on.
Strong inhibitor.
And approach, it's not uncommon for drugs that are metabolized by six ray for.
[noise] makes sense and general these patients what is their prognosis versus.
Isn't that don't have these mutations.
Well so the if you take patients with acute myeloid leukemia, who have MLL R. Rearrangements that tends to be a bad prognostic group of patients.
They are generally aggressively treated as aggressively as the physician can treat them because they know they have a and a bad prognosis and unfortunately, even with that aggressive therapy.
Briggs Morrison: That makes sense. And in general, these patients, what is their prognosis versus patients that don't have these mutations?
They they still do worse than your average patient with AML.
Patients who have NPM one mutations.
Briggs Morrison: Well, if you take patients with acute myeloid leukemia who have MLLR rearrangements, that tends to be a bad prognostic group of patients. They are generally treated as aggressively as a physician can treat them because they know they have a bad prognosis, and unfortunately, even with that aggressive therapy...
Briggs Morrison: They still do worse than your average patient with AML. Patients who have NPM1 mutations, there's a spectrum. Some patients have only an NPM1 mutation with no other mutation, and those patients tend to do somewhat better than your average patient with AML. And then there are patients who have an NPM1 mutation with additional mutations, and those patients tend to do, again, worse than your average patient with AML.
Briggs Morrison: Thank you for that. Thanks for taking my question. Your next question is from the line of Christopher Marianora. Hi, good afternoon. Thanks for taking the time to answer the question. Chris Mirai from Nomura. I was wondering if you could perhaps elaborate on the opportunity in NPM AML with respect to this menin inhibitor. Obviously, you've got some pretty good data in the fusion setting, but I'm wondering how you expect that to kind of map out as you go into the NPM1 mutants and then, secondarily, as you think about sort of the registration path forward for the agent to expect NPM1 AML to be sort of a separate registration path from the rearranged patients.
Briggs Morrison: Hi Chris, thanks for your question. First, in terms of the NPM1 population, if we look at our preclinical data, we see a robust anti-leukemic effect both in the MLLR population and in the NPM1 population. If you will, the negative control for that is, for example, BCR-ABL and ALL, where we don't see any activity. But we do think there's good evidence from the preclinical data that the drug should also work in NPM1. We have not enrolled, as you saw at the AACR presentation; there was not an NPM1 patient enrolled yet. We believe that the investigators participating have been, many of them have a particular interest in MLLR, and so I think that's where that enrichment has come from. But we do hope to get patients with NPM1, and if nothing else, the Phase 2 portion, of course, has a dedicated NPM1 cohort. In terms of the registration path, it's uncertain at this point whether the path would be for a broad label for a variety of lesions or if there were different labeling language for patients with MLLR versus NPM1. I think our base assumption is that there will be labeling for MLLR and NPM1.
Briggs Morrison: Okay, that's helpful. And then, just with respect to your dose escalation trial, it seems you got higher than anticipated exposures due to SIP inhibition.
Briggs Morrison: in some patients.
Briggs Morrison: and where you are in that dose escalation phase. And you know how
Briggs Morrison: Any more dose levels?
Briggs Morrison: to reach similar exposures without... You know, patients with the SIP inhibition augmented exposure. Thank you.
Briggs Morrison: Arm A of the trial is patients who are not on a strong CYF3A4 inhibitor, and as I mentioned in my prepared comments, we've cleared dose levels 1 and 2, and we're now on dose level 3. If you look at the plasma exposures for patient number two, who was on dose level two but had sort of a disproportionate exposure relative to the first patient, we could sort of maybe hypothesize that dose levels four or five might be equivalent exposures in the absence of a strong inhibitor. What dose level might be getting close to a recommended phase two dose?
Briggs Morrison: It could be the level we're at. It could be four. It could be five. On the arm with the CYP3A4 inhibitor, again, at the time of the ACR presentation, we had not seen any dose-limiting toxicities, so we will continue to dose-escalate there. We, of course, in that second patient, saw very nice exposure, so we may not have as many steps to go up there, but time will tell.
Briggs Morrison: Thank you. I appreciate the color.
Said just be distinguished from Port six nine in ways that you will hypothesize may translate something in the clinic, which recognizes a challenging transitional question about it anyway.
Briggs Morrison: Your next question is from the line of Chris Shibutani. Great. Thank you very much, Briggs. Again, congratulations on the AACR data update. I have two questions. One, you make clear that the preclinical data that's been shared so far has been on the tool compound 469. Can you give us a sense for, number one, whether we'll be seeing some preclinical data on 3613 and how you would characterize 3613's profile to be distinguished from 469 in ways that you will hypothesize may translate to something in the clinic, which I recognize is a challenging translational question in Boston anyway?
Right. So Christie as you as you pointed out the publications have all been with 469 50 613 is in the same structural class as poor six nine and was chosen from a variety of molecules because of its biopharmaceutical properties.
The first portion of the A.C.R. presentation was our a fairly detailed description of the preclinical profile for our development candidate for 50 613 that was really why we were excited about being able to present. So I think there you can get a a pretty good view or the preclinical profiles of <unk>.
Briggs Morrison: Right, so Christy, as you pointed out, the publications have all been with 469. 5613 is in the same structural class as 469 and was chosen from a variety of molecules because of its biopharmaceutical properties. The first portion of our AACR presentation was a fairly detailed description of the preclinical profile of our development candidate for 5613. That was really why we were excited about being able to present. So I think there you can get a pretty good view of the preclinical profile of the molecule. And as I said, I think the thing that differentiated from our point of view preclinically was really the biopharmaceutical properties. And thus far, at least 5613 is turning out to have the biopharmaceutical properties that we predicted.
And as I said, I think that thing that differentiated from our point of view Preclinically was really the the biopharmaceutical properties and and thus far at least 50 613 is turning out to have their biopharmaceutical properties that we predicted.
Great and then turning to you know where we aren't today your line about skill and resources are on at hand to enable quote early regulatory clarity, having the sort of maybe greater confidence the resources that you do have on him out, particularly on the balance sheet.
Specific ways in which movie you're changing or modifying are thinking differently about all the level of aggression that you pursue chronicled you don't like 50, 613 and goes out on all change as a result of the 21 close outcome.
Briggs Morrison: And then turning to, you know, where we are today, your line about skill and resources is at hand to enable, quote, early regulatory clarity. Having the sort of maybe greater confidence in the resources that you do have on hand now, particularly on the balance sheet, Are there specific ways in which maybe you're changing or modifying or thinking differently about the level of aggression that you pursue clinical development with 5613? And does that at all change as a result of the E2112 outcome?
[noise], yeah. So I wouldn't say that are I think we've tried to be appropriately aggressive on the development of that men inhibitor we were.
You know we thought it had a very attractive preclinical profile, we've tried to move to trial along quickly.
Because I mentioned, we are in the process of of working with pediatric on colleges to try to put together a pediatric plan. So I I don't think the plan has changed I think.
Obviously, the the financial resources to make sure that plan gets executed are now you know a bit more stable and nor do I think that that plan changes dramatically based upon the results of 21 12, obviously, if 21 12 is positive.
Briggs Morrison: Yeah, so I wouldn't say that our, I think we've tried to be appropriately aggressive in the development of the Meden inhibitor. We were, you know, thought it had a very attractive preclinical profile, and we tried to move the trial along quickly.
There's a there's a tremendous focus of the management team to get ready for the filing and the launch.
But that will not detract from the team who's committed to the men in program. If Perchance 21, 12 is not positive you know I do think the company isn't very good shape, having both men in program manager G.P.H.D. program, which we find both of those programs quite promising.
Briggs Morrison: As I mentioned, we are in the process of working with pediatric oncologists to try to put together a pediatric plan, so I don't think the plan has changed. I think, obviously, the financial resources to make sure that plan gets executed are now, you know, a bit more stable. And nor do I think that that plan will change dramatically based upon the results of 2112. Obviously, if 2112 is positive, there's a tremendous focus on the management team to get ready for the filing and the launch. But that will not detract from the team who's committed to the Mennon Program. If, perhaps, 2112 is not positive, you know, I do think the company is in very good shape having both the Mennon Program and the GVHD Program, which we find both of those programs quite promising, and the resources we have would be dedicated to those programs.
And.
Versus rehab would be dedicated to those programs.
And then finally on the glosses host you anticipate that the data that we're hoping to have at the end of the year. We'll put you in a position to make it go versus no go decision I think historically you guys have had very good disciplined about being able to make those planes in the citizens given the opportunity that resources your home. Thanks.
Yeah. Thanks for our <unk> I I, we do hopes that by the end of the your data we have will allow us to make a decision or whether we want to go into a registration trial for for Gvhd.
But as you point out, we'll just try to be try to be pretty disciplined and looking at the data in deciding whether it works further development.
Briggs Morrison: And then finally, on the graph versus host, do you anticipate that the data that we're hoping to have at the end of the year will put you in a position to make a go versus no-go decision? I think historically, you guys have had very good discipline about being able to make those kinds of decisions, given the opportunity set and resources you have.
Right. Thanks for the epic.
The next question if from a line of Joel Beatty.
Briggs Morrison: Yeah, thanks for that comment, Chris. We do hope that by the end of the year, the data we have will allow us to make a decision about whether we want to go into a registration trial for GVHD. But, as you point out, we'll try to be pretty disciplined in looking at the data and deciding whether it warrants further development.
Oh, Yes. This is showing you can calling overdraw oh. Thank you for taking my question to suddenly today for phone 50, 613, I know the A.C.R. presentation of the thought of that I pediatric patients for Dos and you mentioned that you're you're looking to pursue that indicates as well I guess for.
Briggs Morrison: Thanks for the update.
Level from my scientific or genetic respective positive nieces fundamentally different between adults and children.
How's It also think about other potential working and it'd be different population and I don't follow football.
Briggs Morrison: Your next question is from the line of Joel Beatty. Hey guys, this is Sean Egan calling in for Joel. Thank you for taking my questions. There are two for me today. First on 5613, I know at the AACR presentation it was noted that five pediatric patients were dosed, and you mentioned that you're looking to pursue that indication as well. I guess from a high level, from a scientific or genetic perspective, are the diseases fundamentally different between adults and children, and how is it best to think about the potential of 5613 in the pediatric population? And I have a follow-up question as well.
[noise] Hi, Sean Thanks for the question [noise] so.
I think going into this we thought that the pediatric population might have a slightly higher probability of of the drug working simply because the M.L.L.R.
A.L.L. in particular in children tends to be.
Otherwise genetically silent you don't see a lot of other told mutations you just see the but we hypothesized was the M.L.R. driver. So if any thought it might have a slightly better chance of course older. Adults who've had other chemotherapy or have had.
Briggs Morrison: Hi Sean, thanks for the question. So we thought going into this that the pediatric population might have a slightly higher probability of the drug working simply because the MLLR, ALL, in particular in children, tends to be otherwise genetically silent. You don't see a lot of other co-mutations. You just see that what we hypothesized was the MLLR driver. So if any thought it might have a slightly better chance, of course, older adults who've had other chemotherapy or have had a chance for their tumor to develop other mutations may, in fact, be a little less likely. But, you know, time will tell. But I don't think we think of the pediatric population as being less likely than the adult population.
A chance for their tumor to develop other mutations may in fact be a little less likely but you know time will tell but but I don't think we think of the pediatric population is being less likely than the adult population.
Okay. That's helpful.
And then I put up with all of them, we remind us of what organ systems, you've observed that benefit in in in the longest duration of with Boston and you know they found Oregon systems are there already in place to be gained into what other indication that you could pursue <unk>.
Yeah. So again, it's only five patients and at the time that the data was released it we're only for patients had had made it through.
The evaluation period, so I think it's a little hard early on to say, which organ systems, we will it in which Oregon systems. We won't we've clearly seen Oregon's is a benefit in.
Briggs Morrison: Okay, that's helpful. And then on Exeterimab, can you remind us of what organ systems you've observed a benefit in, and for the longest duration of response? And, you know, based on the organ systems, are there any insights to be gained into what other indications you could pursue after chronic rapid heart disease? Yeah.
The gastrointestinal system I've had a T.V.H.D. and you may see you in our corporate deck very impressive benefit to patients, who x. skin graft versus host decent preclinical data would suggest that both skin and lung seemed to be particularly amenable.
Briggs Morrison: Yeah. So again, it's only five patients. And at the time that the data was released, there were only four patients that had made it through the evaluation period. So I think it's a little hard early on to say which organ systems we will and which organ systems we won't. We've clearly seen organ benefits in the gastrointestinal system, hepatic GVHD, and you may see in our corporate deck, the very impressive benefit to a patient who had skin grafts, and so these preclinical data would suggest that both skin and lung seem to be particularly amenable. But I think that that does relate to the earlier question of whether we'll be able to make a go or no go decision. Part of that will depend on which organ systems we see a benefit in and the durability of those. As you may know, in the GVHD world, the NIH consensus criteria for evaluating efficacy score efficacy at about six months after starting dosing. So one does need to see a good degree of durability, and your question about which organ systems will be used, you know, that's to be determined as we enroll more patients. Great, thank you so much.
I think that that does relate to the earlier question of you know, we'll be able to make a go no go decision part of that will read.
Depend on.
What Oregon systems, we see a benefit in and and you know at the durability of those as you may know into Gvhd world, the and H. consensus criteria for evaluating advocacy scores advocacy at about six months after starting dose.
So.
One does need to see a good degree of durability and your question about which Oregon systems, you know that that's to be determined as reenroll more patients.
[noise], great like it's a lot but.
The next question is from a lot of Peter <unk>.
Hi, Thanks to take my question, So Briggs just don't.
<unk>, which could potentially generate becca Africa's feel safety, when we think about M.L.A.L.A.L. versus.
And M.P. one.
<unk> be great.
Briggs Morrison: Great, thank you so much, folks. The next question comes from a lot of people. Hi, thanks for taking my question. 5613, just your thoughts around which arms could potentially generate better efficacy or safety when we think about AML and ALL versus NMP One. If you have any thoughts about that, that would be great.
[noise] right. So <unk>, we tend to the pre clinical data would suggest it it's really the M.L.R. translocation and whether it's a L.L.R.A.M.L.
Ah the time course of response and perhaps the type of response may vary a little bit between A.L. and M.L., but generally speaking we see benefit.
Ah independents really about the M.L.L.R., so I think thinking about M.L.R.A.L.L. versus M.L.R.A.M.L. I don't think we think again with time will tell we'd have to do the clock experiments, but I don't think we think of those as being two different.
Briggs Morrison: Right, so we tend to think that it's really the MLLR translocation and whether it's ALL or AML. The time course of response and perhaps the type of response may vary a little bit between ALL and AML, but generally speaking, we see benefit independent of the MLLR.
10, P.M., one I think.
You know I think to the question.
Valid questions still is does the drug work and N.P.M., one nobody has yet shown.
Like a c. in patients with N.P.M. one.
Mutant A.M.L. again are pretty Flamingo data suggest that we should but until we do that one is still I guess, one could say that's not validated in in that disease and you know, we'll we'll keep trying to [noise] find patients who weekend validated again based on pretty close.
Briggs Morrison: So I think thinking about MLLR-ALL versus MLLR-AML, I don't think we think, again, what time will tell, we have to do the clinical experiments, but I don't think we think of those as being too different. NPM1, I think, you know, I think the question, the valid question still is, does the drug work in NPM1. Nobody has yet shown efficacy in patients with NPM1 mutant AML. Again, our preclinical data suggests that we should, but until we do, that one is still, I guess one could say that's not validated yet in that. And, you know, we'll keep trying to find patients who we can validate it. Again, based on preclinical data, we would expect the efficacy to be comparable across all three arms in the phase two portion. However, your time will tell.
We would expect the advocacy to be comparable across all three arms and the phase two portion but.
Time hotel.
Great. Thank you and then just all the data we <unk>.
<unk>.
<unk> <unk> <unk> without a press releases that they throw to <unk> stages anything around timing or venues would be.
Do you think we could potentially have an M.P. or.
Patient weather.
So the one was guided is that it would be at a medical conference in the fourth quarter.
[noise] and there is a hematology conference that's typically held in a fourth quarter. If it's held this year virtually are alive. None of US you know know at this point, but that's sort of where I think most likely that would be an update whether we'll have it N.P.M. One patience is all by then is a little hard to tell.
Briggs Morrison: Great, thank you. And then just on the data we were expecting in 4Q from the program, I mean, would that be a press release? Is it data at a conference or an analyst? Just anything around timing or venues would be? And do you think we could potentially have an MP1 patient by then?
I I think there's a little bit of.
You know potential that new patients coming onto the trial at this point may actually be a little further enriched for M.L.R. since you've already seen advocacy there.
Briggs Morrison: So what we've guided is that it would be at a medical conference in the fourth quarter. And there is a hematology conference that's typically held in the fourth quarter. If it's held this year, virtually or live, none of us know at this point, but that's sort of where I think it's most likely there would be an update. Whether we'll have NPM1 patients enrolled by then is a little hard to tell. I think there's a little bit of..., and those patients don't have a lot of options. So, you know, we're speaking with our investigators and, you know, do hope to get patients with NPM1 mutations on, but there is the potential that, in fact, there'll be more enrichment for MLLR given the activity that's already been seen. Great, thank you so much. Thanks for taking the time to answer the question.
And those patients don't have a lot of options and so it you know we're we're speaking with our investigators and you know do hope to get patience with N.P.M. one mutations on but there is the potential that in fact, we you know they'll be more in Richmond for him at all are given the activity that's already.
<unk>.
Great. Thank as much thanks for taking the question.
Your next question isn't a line of my due tomorrow.
Hi, Thanks. This is Jack buying it from the do I never heard from the from the opening remarks, but Oh, there's like a covert I was wondering if your comment as to how the dose escalation of back to <unk> trials going.
Have you seen any affects their I guess.
I would say of of our three programs. That's the one that perhaps there's a little bit of an impact.
Briggs Morrison: Great. Thank you so much. Thanks for taking the question. Your next question is from the line of Madhu Kumar. Hi, thanks. This is Jack Donning from Nadeau.
They're not patients with acute leukemia, who need to be treated immediately.
We've been able to continue to enroll patience.
And our guidance that there'll be updates on you know completed phase one in the early data from phase two by the end of the year, we still very feel very comfortable with.
Briggs Morrison: I know you touched on this in your opening remarks, but with respect to COVID, I was wondering if you could comment as to how the dose escalation of the ActiKoimab trial is going? Have you seen any effects there, I presume?
But the the Roman may have slowed just a tad in that study.
[noise] awesome, but it's almost the same question.
Briggs Morrison: I would say of our three programs, that's the one that perhaps has a little bit of an impact. If they're not patients with acute leukemia who need to be treated immediately, we've been able to continue to enroll patients, and our guidance that there'll be updates on, you know, completed phase one and early data from phase two by the end of the year is something we feel very comfortable with. But enrollment may have slowed just a tad in that study.
Your next question is from a lot of bird has.
Okay.
<unk> all the progress just one of follow up on a little bit of discussion you were having earlier with regard to the expansion Oh, the patients and augment.
Brings do you think you would ever just focus the expansion on animal or patient specifically give it the video and save at U.M. One for for later time or or are you still committed to the the full expansion at all three groups.
Briggs Morrison: Awesome. Thank you so much for doing the questions. Your next question is from the line of Bert Hazard. Yeah, thanks.
[noise] Ah Yeah bird things for the question that just for the avoidance it out three arms run.
Briggs Morrison: Congratulations on all the progress. Just want to follow up on a little bit of the discussion you were having earlier with regard to the expansion of the patients in Augment. Briggs, do you think you would ever just focus the expansion on MLLR patients specifically, given the data you have, and save NTM1 for a later time, or are you still committed to the full expansion in all three groups?
Concurrently but independently.
So all three arms would be open.
We would be the aspect about filling all three as fast as possible if for whatever reason, one or the arms filled up more quickly and there was you know promising an exciting data in that arm.
<unk> It goes to one of the other questions that wouldn't preclude.
Potential regulatory path in.
Briggs Morrison: Thanks for the question; just for the avoidance of doubt, the three arms run concurrently but independently. So, all three arms would be open, uh, and we would be enthusiastic about filling all three as fast as possible if, for whatever reason, one of the arms filled up more quickly, and there was, you know, promising and exciting data in that arm. You know, it goes to one of the earlier questions; it wouldn't preclude, you know, a potential regulatory path in, you know, one population while the other one continues to enroll, but I don't think we would intentionally slow down any of the arms. All three would be open, and we would work just as hard to get patients into all three arms.
You know one population while the other one continues to enroll but I don't think we would intentionally slow down any of the arms.
All three will be open and we you know would work just as hard to get patients in two or three arms.
Okay. Thanks, and then just with regard to the recent raising the strategic flexibility to provide you you had some other programs within tennis that <unk> would there be a consideration at this point of of.
Reconsideration of further in tennis that data or or prosecution of the activity there assuming success and 20 ones will and or how aggressive or you're being it with regard to additional licensing I know you've had six material success there, but it does this.
Briggs Morrison: Okay, thanks. And then just with regard to the recent increase in strategic flexibility that I provided you, you had some of the programs with antennastat. Would there be a consideration at this point of reconsideration of further antennastat data or prosecution of the activity there, assuming success in 2112, and or how aggressive are you being with regard to additional licensing?
Additional.
A string of the coffers help you with that.
[noise]. So first we have to interest that question you know we have intentionally decided to wait until we see the results of 21 12, we we as you know we had we thought some pretty promising data in combination with <unk>, both in lung cancer hinder melanoma, we consciously.
Decided to put that on hold and focused their attention of the company on what we thought were our best opportunities, including the breast cancer trial into men in program.
And then gvhd, it's so we've been focused on that.
You're 21 told US positive I think there there's two buckets of things we would think about in terms of further investment in that molecule. One would be additional life's not command has been opportunities in breast cancer of course. So you already have one positive 53. The question is are there other trials in different population.
Briggs Morrison: So, first we have to address that question. You know, we have intentionally decided to wait until we see the results of 2112. We, as you know, had, what we thought, some pretty promising data in combination with pembrolizumab, both in lung cancer and in melanoma. We consciously decided to put that on hold and focus the attention of the company on what we thought were our best opportunities, including the breast cancer trial and the Mennon Program. And then GVHD hit, so we've been focused on that. If 2112 is positive, I think there are two buckets of things we would think about in terms of further investment in that molecule. One would be additional life cycle management opportunities in breast cancer, of course. So, you already have one positive phase three.
Breast cancer patients, where we could tested drug and then we would also have the question of whether there are other do we do we.
Go back and re look at the data we had had in both lung cancer melanoma and see whether those are worth investing in in that we'd have to trade off you know which are the best uses of of our Capitol. So.
That's the way we think about that if 21 12 is positive I think of 21 12 is negative you know we'll have to do a lot of you know <unk> steep analysis to decide whether we would want to do anything more within tennis that having not had a positive pastry trial and having these wonderful opportunities with both men and and 63 52.
Briggs Morrison: The question is, are there other trials in different populations of breast cancer patients where we could test the drug? And then we would also have the question of, are there other, do we go back and relook at the data we have had in both lung cancer and melanoma and see whether those are worth investing in, and then we would have to trade off, you know, which are the best uses of our capital. That's the way we think about that if 2112 is positive. I think if 2112 is negative, we'll have to do a lot of, you know, deep analysis to decide whether we would want to do anything more within Dentistat, having not had a positive phase 3 trial and having these wonderful opportunities with both Mennon and 6352. So that's something we'd have to look at, you know, should it turn out that 2112 is not positive.
So that's something we'd have to look at you know should be should it turned out there 21 comes not positive.
Thank you.
Once again, if you do have a question for a store than and number one on your touch tone telephone keypad.
I'm sure no further questions at this time I would know what they're trying to conference over two words Morrison.
Briggs Morrison: Okay, thank you. Once again, if you do have a question, press star then the number one on your touchtone telephone. Keep going. I'm showing no further questions at this time. I would now like to turn the conference over to Briggs Morrison, CEO.
Yeah.
[noise], thanks, very much shopper and again, thank you everybody who's joined us on the call. It in the web cast today.
As I as I said, I thought 2020 would be and exciting a transformative year for our company and and we're on that path. So thank you offer your interest and.
Perhaps the next time, we talk to you will have results from 21 12.
Ladies.
Briggs Morrison: Thanks very much, Operator. And again, thank you, everybody who's joined us on the call and the webcast today. As I said, I think 2020 will be an exciting and transformative year for our company, and we're on that path. So, thank you all for your interest. And perhaps the next time we talk to you, we'll have results from 2112. Ladies and gentlemen, this concludes today's conference call. Thank you for participating. You may now disconnect.
This includes this conference call. Thank you for participating you may know disconnect.
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