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11/12/2021
Good morning. Welcome to the Formal Therapeutics 3rd Quarter 2021 Financial Results and Business Update Conference Call. All participants are currently in a listen-only mode. Following management-prepared remarks, we will hold a Q&A session. To ask a question at that time, please press the star key followed by 1 on your touch on telephone. If anyone has difficulty hearing the conference, please press star 0 for any operator assistance. As a reminder, this call is being recorded today, November 12, 2021. I would now like to turn the conference over to Mario Corso. Please go ahead, sir.
Thank you, operator. This is Mario Corso, Senior Director of Investor Relations at Forma. Good morning to our listeners and welcome to today's call to review third quarter 2021 financial results and business update. On this call, I'm joined by Frank Lee, our President and Chief Executive Officer, Patrick Kelly, our Chief Medical Officer, Dave Cook, our Chief Scientific Officer, and Todd Chigog, our Chief Financial Officer. Before we begin, I'd like to caution listeners that comments made and financial information provided during this conference call include certain statements that are estimates, beliefs, forward-looking, and are subject to various risks and uncertainties. Any statements made during this call that are not statements of historical or current facts are intended to be forward-looking statements pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. We want to emphasize that such forward-looking statements reflect our current expectations and assumptions regarding timing, enrollment, success and data announcements of our current and ongoing clinical trials, therapeutic potential and clinical benefits and safety of our product candidates, planned regulatory submissions, our financial condition and capital requirements, our business operation, development plans, the potential impact of COVID-19 on our business and clinical development, and relationships with third parties and collaborators, and are neither predictions nor guarantees of future events or performances. Actual results could differ materially from those stated or implied by these forward-looking statements due to risks and uncertainties associated with our business, including those under the heading entitled Risk Factors in our quarterly report on Form 10-Q for the quarter ended September 30, 2021, that will be filed with the SEC today, and in subsequent reports, including our current reports on Form 8-K. The company disclaims any obligation to update or revise any forward-looking statements, except as required by applicable law. Before turning the call over to Frank, I'd like to mention two upcoming activities as outlined in today's release. We will be participating virtually in the Jefferies London conference next week, and we'll also be holding an investor briefing on December 13 to discuss clinical trial results being presented at the ASH annual meeting. Further information on these events will be made available on our website, formatherapeutics.com. With that, I will now turn the call over to Frank, our President and Chief Executive Officer.
Thank you, Mario. Good morning, everyone. FORMA continues to make good progress on our purpose to transform the lives of patients with rare hematologic disorders and cancers. Our portfolio includes potentially transformative molecules for patients with sickle cell disease and other hemolytic anemias, prostate cancer, and acute myeloid leukemia. Our clinical programs have important upcoming catalysts for growth and positions FORMA well for long-term success. Along with the progress in advancing our science, I'm pleased with the progress we're making in establishing FORMA as a trusted partner in the sickle cell community. In October, we collaborated with the Sickle Cell Disease Association of America to launch the Sickle Cell Clinical Trial Finder. It can be daunting and complex for sickle cell patients to learn more about clinical trials enrolling in a specific geographic area, and this resource allows users to easily find information about all the sickle cell clinical trials and about the clinical trials process itself. We're honored to be a part of this important effort that benefits the entire sickle cell community. Now I'd like to turn to the quarter, third quarter. First, let's have a PVAT, our once daily PKR activator with the potential to be a foundational therapy for sickle cell disease by not only addressing the anemia but improving red blood cell health via its multimodal mechanism of action. We've completed enrollment in our open-label extension of the Phase I sickle cell disease trial and plan to present the updated results along with the completed MAD data at ASH in December. We continue to open sites and enroll patients in our Phase II-III hibiscus study. And as a reminder, this study includes two co-primary endpoints, hemoglobin and VOCs, that support the traditional approval pathway. In addition, the study design also provides for the potential to pursue accelerated approval. And based on recent discussions with the FDA, we plan to provide additional information on hemoglobin as a surrogate endpoint by the time of accelerated approval submission, given the unique mechanism of action of atapivac. We've had productive discussions and plan to closely collaborate with the FDA moving forward in support of our overall development program, which is designed to ensure timely approval and to provide clinically meaningful and a differentiated data package. Based on the emerging data, we believe Atava PVET has the potential to be a pipeline and a product and have made progress in planning for a comprehensive development program, which includes the Hibiscus study, which includes patients, sickle cell patients age 12 and above, sickle cell pediatrics down to age six months, Sickle cell patients that are transfusion-dependent, thalassemia, both transfusion-dependent and non-transfusion-dependent. In addition, planning for additional studies is underway. Turning to our CBPP300 inhibitor, FT7051, we reached an important milestone in October with the triple-meeting presentation of the first inhuman results. from our ongoing phase one trial in metastatic castration-resistant prostate cancer. We're encouraged by the early data and the potential for FT7051 to target the novel pathway of CBP P300 inhibition. With respect to our third development compound, the IDH inhibitor elutisidinib for relapsed refractory AML, we plan to present new data from the azacitin combination cohort at ASH. These data further support the potential for ludicidinib to offer a differentiated profile, particularly given the impressive duration of response. We also continue to make good progress in preparation for a new drug application submission. Looking forward, I'm pleased to share some key events over the coming months. In December, at ASH, we plan to present four presentations on atavapivat and alucidinib. In addition, by year-end, we plan to start the Phase II study, which includes transfusion-dependent sickle cell patients and thalassemia patients, both transfusion-dependent and independent. Going into the first half of next year, we plan to start the sickle cell pediatric study and to host our first R&D day. Mid-2022, we plan to have additional data from our FT7051 Phase 1 Courage Study in prostate cancer. And late in 2022, we plan to have a TAVA-PVAT Hibiscus Study Interim Analysis 1. We're now guiding to the latter part of 2022. As we discussed before, the COVID-19 pandemic has created substantial challenges for both the clinical trial sites and for sickle cell patients, many of whom reside in areas disproportionately impacted by the pandemic. We're observing conditions improving over time and are working very closely with the clinical sites and the sickle cell community. With that, I'd like to acknowledge those who have helped navigate the ongoing challenges posed by the COVID-19 pandemic, including patients, investigators, healthcare workers, and our employees, as we pursue our purpose to transform the lives of patients living with rare hematologic disorders and cancers. I'll now turn over the call to Pat.
Thank you, Frank, and good morning, everyone. I will provide a brief overview of our development programs for Etavo PVET and elutacitinib, and then an outline of our presentation scheduled for the ASH meeting in December. Etavo PVET is a once-daily selective PKR activator with a distinct multimodal mechanism of action. This multimodal mechanism is important in that it decreases 2,3-DPG, improving oxygen binding to hemoglobin S, which decreases polymerization, thereby reducing the sickling and hemolysis of RBCs caused by the rigid structures formed by deoxygenated hemoglobin S. The increase in ATP allows the cell to repair membrane damage incurred through the multiple cycles of cell sickling. Together, the effects of decreased 2,3-DPG and increased ATP, we believe, will improve the RBC health and lifespan, thus modifying the course of sickle cell disease. The goal of the Etavo-PIVAC clinical program has been to generate data that would support an improvement in both the anemia and the vaso-occlusive events that characterize sickle cell disease. We believe Etavo-PVET has the potential to reduce the hemolysis and anemia of sickle cell disease by improving RBC health and lifespan. These direct effects on the sickle RBC may reduce the inflammation and hypercoagulability risk associated with sickle cell disease, and then ultimately, through chronic dosing daily, Etavo-PVET may significantly reduce the debilitating vaso-occlusive events that characterize sickle cell disease. We have also sought to elucidate the effects of atavopevit on the sickle RBC as measured by numerous markers of red blood cell health. We have designed a rigorous and comprehensive phase one program, and we were pleased with the clinical data presented at the EHA meeting in June, and recently in the updated data in our abstracts accepted for oral presentations at the ASH meeting in Atlanta next month. The following key clinical data have been observed in patients who have completed the Atavo PVAT two-week dosing cohorts and patients who have completed the Atavo PVAT 12-week dosing cohort. We have previously demonstrated that two weeks of Atavo PVAT daily can increase hemoglobin levels in 73% of patients with sickle cell disease. In the open-label treatment cohort, this hemoglobin response has been sustained with 83% or five out of six patients completing 12 weeks of atopopivet dosing maintaining a greater than one gram per deciliter hemoglobin improvement. We have shown that two weeks of atopopivet dosing also significantly improves the sickle RBC's oxygen affinity with a delay in the point of sickling to lower oxygen levels. And this improves the deformability of the RBCs compared to pretreatment levels. This reduction in RBC sickling, along with the improved RBC deformability, has translated into a significant reduction in markers of hemolysis and a significant reduction in the absolute reticulocyte counts, indicating that the sickle RBCs in patients receiving atavopivet are healthier and living longer, leading to an improved hemoglobin response. These improvements are seen as early as two weeks of atavopivet dosing and are sustained in patients receiving 12 weeks of daily Etavo PVET dosing. In addition to the improved hemoglobin and a reduction in hemolysis, we have reported our initial observations that Etavo PVET treatment can reduce systemic markers of inflammation and coagulation in patients receiving up to 12 weeks of Etavo PVET daily. This is encouraging data that supports our hypothesis. that by improving the health of the sickle RBC with chronic daily dosing of Etavo-PVET, we may reduce the debilitating vaso-occlusive events that characterize sickle cell disease. Finally, as previously reported, Etavo-PVET daily is well tolerated at doses up to 600 milligrams daily, which is 150% of the maximum dose being evaluated in the hibiscus study. with a safety profile that is consistent with the underlying sickle cell disease. As noted at our EHA presentation, the safety profile of Atavo PVET in the 12-week dosing cohort has been notable for a low rate of vaso-occlusive adverse events of any grade with no hospitalizations for VOC observed in patients while on Atavo PVET treatment. Looking forward, next month, updated open-label extension results will be presented at the ASH annual meeting. This will include the results from 15 patients dosed for up to 12 weeks, evaluating the effects of 400 milligrams Etavo PVAT on hemoglobin, markers of hemolysis, including reticulocytes, bilirubin, and LDH, markers of systemic inflammation, and coagulation. With approximately three patient years of Atavo PVAT exposure in the 15 patients treated for up to 12 weeks, we will provide an analysis on the patient's sickle cell-related adverse event profile relative to their prior VOC history requiring hospitalization. Now turning to alutacidinib, our mutant IDH1 inhibitor being evaluated in patients with relapsed refractory acute myeloid leukemia, or AML. Earlier this year, results were presented from the positive registrational Phase II interim analysis in the relapsed refractory AML patients receiving 150 milligrams of elutisidinib twice daily. At the upcoming ASH meeting in Atlanta, we will provide an analysis of the molecular characteristics of response to elutisidinib in these patients. In addition, at the ASH meeting, Results from cohorts receiving elutacitinib in combination with azacitidine will also be presented, showing benefits of the combination in various subpopulations, including treatment-naive AML patients. With that, I'm going to now turn the call over to Dave, who will provide an update on FT7051 for prostate cancer.
Thanks, Pat. I'm going to spend the next few minutes discussing our clinical stage CBP P300 inhibitor, FT7051. FT7051 targets the androgen receptor pathway by a novel mechanism that has the potential to address many of the resistance mechanisms seen for standard of care AR signaling inhibitors. We believe the mechanism of action of FT7051 is applicable to a broad range of resistance mechanisms because CBP P300 modulates AR via the N-terminal domain. This means the tumors expressing the ARV7 splice variant, for example, which lacks the C-terminal AR hormone binding domain and for which there are no approved treatments are a potential therapeutic target for 7051. In addition, the tolerability profile of FT7051 may support its potential for use in earlier lines of prostate cancer therapy and in combination with standard of care. We began enrolling a phase one in the first quarter of this year. The study is designed to enroll up to 45 men with metastatic castrate-resistant prostate cancer. These men have failed at least one line of therapy and are typically heavily pretreated, receiving one or both of abiraterone and enzalutamide, and in many instances, also chemotherapy prior to entering our study. The trial utilizes an open adaptive design, starting with a dose of 25 milligrams with titration to as many as seven higher doses on a three-week on, one-week off cycle based upon predefined safety and tolerability criteria. Initial results presented at the triple meeting in October showed an encouraging safety profile as well as biologic effects consistent with inhibition of the CBP P300 pathway. Data as of September 1st were presented in the initial eight men enrolled in the trial, the pharmacodynamic measures looked encouraging for 7051. The 150 milligram dose achieved drug concentrations that approached the predicted efficacious dose based on modeling of preclinical data. In addition, skin biopsies demonstrated a reduction in histone acetylation, a key marker of innovation of the CBP P300 pathway. All but one of the treatment emergent adverse events were grade two or lower, with no events leading to treatment discontinuation. One patient experienced a treatment emergent grade three hyperglycemia, which was medically managed. Following a dose reduction, this patient remained on treatment and experienced a PSA decline of greater than 50% at 12 weeks and greater than 80% at 16 weeks. His nodal tumor, which was progressing prior to enrollment, was classified as stable disease and confirmed by radiography. Notably, this response represents the first of valuable patient in the trial. We plan to share more comprehensive results at a scientific conference toward the middle of next year. I'll now turn the call over to our Chief Financial Officer, Todd.
Thank you, Dave, and thank you to everyone for joining us on today's call. I will first spend a few minutes discussing our financial results for the third quarter of 2021. and then discuss our cash position and outlook. Our net loss for the quarter ended September 30th, 2021 was 43.3 million, which compares to a net loss of 27.6 million for the quarter ending September 30th, 2020. The increased net loss was driven by increased spending in support of our preclinical and clinical development programs as well as employee hiring to support our operations. Research and development expenses were $30.7 million for the quarter ended September 30th, 2021, compared to $24.8 million for the quarter ended September 30th, 2020. This increase was primarily attributable to R&D staffing, equity-based compensation, and costs for our clinical and preclinical development programs. General and administrative expenses were $12.7 million for the quarter ended September 30, 2021, compared to $7.5 million for the quarter ended September 30, 2020. The increase was primarily attributable to equity-based compensation, staffing costs, and professional fees. Our cash, cash equivalents, and marketable securities balance as of September 30, 2021, was $531.8 million compared to $645.6 million at year-end 2020. Cash use in the quarter reflects operating expenses and working capital requirements to support operations. Overall, we continue to be in a strong financial position with funding through the third quarter of 2024. Operator, we can now take questions.
Thank you. Ladies and gentlemen, if you need to ask a question at this time, please press the start and the one key on your touch-tone telephone. To withdraw your question, press the pound key. Please stand by while we compile the Q&A roster. And our first question coming from the line of Mark Reidenbach with Oppenheimer. Your line is open.
Hey, good morning, and thanks so much for taking the questions. Just a couple from me. I guess I have to ask with regard to the additional information that the FDA would want to see before making a decision on allowing accelerated approval based on hemoglobin response. Can you give us an indication of what type of information? This would be a little bit more color on that, would definitely be appreciated. And the second question is on the prostate cancer program and the early data that was presented at the TRIPLE meeting. I was hoping Dave maybe could comment on the observation that the PSA responding patient, we actually saw the PSA level spontaneously start to decline after discontinuing entelutamide, but before starting 7051. Maybe some thoughts around that observation would be appreciated. Thanks so much.
Thanks for the question, Mark. It's Frank Lee here. Let me address the first part of the first question and then hand it over to Pat to provide additional color. First, as we talked about before, our strategy is to pursue the most differentiated label possible to help as many patients as possible and get there as quickly as possible for patients. And so with that said, I want to make a few things clear. First, we have no changes are planned for the hibiscus study at this current time. And as I mentioned, a quick reminder, the current study design includes two co-primary endpoints, hemoglobin and VOC, that support the traditional approval path. In addition now, as we've talked about before, it provides also the potential to pursue an accelerated approval, which is going to be dependent on the data that we're able to generate on hemoglobin as a surrogate endpoint. And so, as I mentioned in my opening remarks, based on recent discussions with the FDA, we believe both the traditional and accelerated approval paths are viable. And we plan on providing some additional information on hemoglobin as a surrogate endpoint for clinical benefit, which is very specific to TavoPVAT's unique mechanism of action. And we also believe that a similar approach will be required for other molecules with unique mechanism of action pursuing the accelerated path. And again, that said, I think it's worthwhile to speed drug development for patients and try and get there as quickly as possible. So that said, let me turn it over to Pat to provide some additional color on the type of data that we could potentially provide. So Pat.
Yeah, thanks, Frank. Yeah, you know, I think just to echo what Frank has just said, You know, the broad potential differentiating profile of TAVO-PVET, you know, we've always considered a number of opportunities to explore clinically meaningful endpoints as part of our lifecycle efforts. And, you know, these studies could include looking at sickle cell disease-related complications in cardiopulmonary, CNS, renal disease, and others. And many of these are already in progress, right? We're initiating the transfusion-dependent circle cell study with etabopivac as well as our pediatric trial. So, you know, through our broad efforts from the hibiscus trial as well as these additional studies, we feel we'll be able to have a very complete package from the etabopivac experience and its unique mechanism of that action. But you can also imagine that there's a lot of data or epidemiological information that helps support the potential benefits of a hemoglobin response in sickle cell disease. And so it'll be a package that includes, we believe, a very broad set of information derived from our own studies as well as information out in the community. I'll turn it over to Dave for the...
Yeah, good morning, Mark. Hi. Thanks for your question on 7051. And just to clarify for everyone else on the line, there is a phenomenon known that's based on androgen deprivation in which patients can have a transient spontaneous response upon withdrawal of androgen. It happens in a very small number, about 1% of patients. And we look carefully at this with our investigators to establish whether or not that was the case here. And there were multiple reasons why that was excluded. The first really has to do with the time duration. The last patient was withdrawn from androgen signaling inhibitors, enzalutamide, about three and a half months prior to being treated with FT7051. And that duration is kind of, you would have seen an androgen deprivation response before coming on to study. The second, it's very clear there was a marked change in the rate of PSA decline. In fact, it was a sort of a level PSA, followed by a very sharp decline upon establishment of treatment with 7051. And the third and perhaps most important thing is during that interval between stopping enzalutamide and starting 7051, the patient's nodal tumor was evaluated radiographically and was shown to be increasing in size. It was only upon treatment with FT7051 that that that rate of growth stabilized. So we think that based on those multiple lines of evidence and, of course, with a lot of discussion, that this is clearly a response to 7051 and not some other phenomenon.
All right, perfect. Thanks so much. Thanks, Mark.
Our next question coming from the line of Mario Raycroft with Jefferies, the Atlanta Southland.
Hi, everyone. Good morning, and thanks for taking my questions. Just clarifying and following up on a prior question, for the additional information that you would be showing to FDA for Atavo, is there precedent for this or is this a novel potential endpoint based on Atavo specifically?
You know, broadly, this is based on our discussion, recent discussions with the FDA. And as Pat mentioned, this could certainly include mechanistic or epidemiologic and also clinical data on tab of PBAT. And certainly we have a number of clinical trials, as Pat articulated, to collect those kinds of information. So that's kind of, you know, background and context. You know, Pat, I don't know if you have additional thoughts here.
Yeah, I think with any new mechanism, there's always opportunities to push the field forward, and we feel that this is an opportunity with this remarkable, I guess I should be careful, what we believe is a very important mechanism that's going to benefit sickle cell patients, a broad base that You know, some new or evolved endpoints will be part of that discussion with the FDA, and it's part of the ongoing discussions with the FDA.
Got it. Okay. That's helpful. And then even though there's no plan to adjust the design, is it possible to maybe informally collect VOC data earlier than planned and include that to support an accelerated approval path?
I don't think we can. Go ahead, Pat. Go ahead. Yeah, I was just going to say, I don't think we're in a position to, you know, have that level of detail. I think, as Frank said, the current design of the Hibiscus study is intended to support these efforts, and that'll be part of our discussion with the FDA.
And I'll add the totality of the data. Certainly, as we mentioned, we're going to be starting the pediatric study early next year. We'll also start the transfusion-dependent sickle cell study into this year, early next year, as well as the THAL and the two different patient populations. So the totality of data will be important in the discussions overall. In addition, as Pat mentioned, at the ASH presentation, we'll have an analysis of the, among other things, patient's baseline history of VOC versus what we've observed on treatment as well. Got it. Okay, thank you for taking my questions.
Thanks, Mari.
Our next question coming from the line of Alethea Young with Cancer. You want to start, Ben?
Hey, guys. Thanks for taking my questions. A couple. One, I just wanted to talk a little bit about you haven't really seen, you know, the VOCs with the dosing or the taper like some other people have in a similar class. So I wanted to get your perspective on why that might be the case. And then on 7051, I just wanted to talk a little bit about kind of the path forward and is there a possibility for maybe a faster pathway based on a specific mutational profile? Thank you.
So, Pat, you want to maybe take the first question?
Yeah, I think, you know, as we highlighted in our presentation in June, you know, it's a very well-tolerated pathway. Molecule patients on treatment had very low rates of any sickle cell related pain events. In the washout period, which is an extended, you know, we follow them for four weeks, we did have vaso-occlusive events there that, you know, were felt by the investigator to be related to the disease under study. I think when you take away a disease-modifying therapy, you will see recurrence of that disease. The role of a taper has many different connotations to it. I think our position has been that in the setting of taking away a medication that makes patients feel better and have and has more energy, that part of that discontinuation, you know, the caution should be with the patient and the investigator to make sure the patient doesn't overexert themselves because their capacity to function may be reduced because now they're no longer protected. And so that's, you know, what we've been seeing. And we'll provide a further update on that at the ASH meeting as well.
David. Sure. Hi, Alethea. Regarding 7051, obviously we're always looking for ways to accelerate development. And so one of the things we've got in the phase one is a full genetics analysis as well as an analysis of AR splicing for every patient in the study. And that may lead to identification of particularly susceptible patient groups I'll note that I think our one responder had a mutation in the C-terminal, a point mutation in the C-terminal domain that was associated with enzalutamide resistance. That being said, I think the other thing to note about the drug thus far, and it's still very early, of course, is its safety and tolerability profile, because the largest opportunity is to move upstream, particularly in combination with standard of care. And the last thing I'll point out, and this was pointed out at the triple meeting, but maybe isn't fully, you have to pay attention in order to see it. But, you know, the one patient who had a grade three hyperglycemia, that was identified. And we then did a hemoglobin A1C analysis. And the A1C was high. A1C, of course, is an integrated measure over the previous 90 days or 100 days. So it's pretty clear to us that this was a patient who had undiagnosed either hemoglobin insulin resistance or potentially type 2 diabetes and truly was not emergent on treatment. However, since it hadn't been seen previously, it was classified as a treatment emergent AE. So we're really happy with the safety profile, and that may lead to an expanded opportunity set for 7051. Great. Thank you.
And as a reminder, to ask a question, please press star 1. Our next question coming from the lineup, Robin Garner with Craig Hallam. Your line is open.
Thank you. I wanted to ask about the upcoming studies in transseason-dependent sickle cell patients and thalassemia. Are there any changes to the design of those studies, and what else might you hope to show from those studies?
So, Pat, perhaps you can provide a quick overview there.
Sure. It's a phase two with three cohorts, including, and just very quickly, the thalassemia patient population, non-transfusion dependent and transfusion dependent, as well as sickle cell patients who are on chronic transfusions for either primary or secondary stroke prevention. There's been no changes to that design. It's a pilot to understand the biology of etabopivac and the setting of a patient's on, and specifically for the sickle cell disease patient population, the effect on maintaining a hemoglobin level and reducing the frequency or the need for chronic blood transfusions. So it's a study to ask that question. Can we affect the need for, you know, iron infusion, blood transfusions in the patient population while controlling their hemoglobin S levels.
And I'll just add, you know, by our estimates, you know, approximately 20% of sickle cell patients are transfusion dependent, so it's a significant need.
Okay, thank you. Okay. And for the patient who was the responder in the 7051 study, do you have any update on that patient that might pass the data that's already been presented, for example, helping us to understand the durability of that response to today?
Yeah, we don't have any update. And, in fact, we've guided to not expect regular updates. We don't want to be, as a friend of ours has said, salami slicing patients. we're going to try to come back with robust data sets as opposed to individual patient vignettes. So that's kind of where we will be in the future.
And as we've discussed before, we're broadly guiding to mid-next year to provide a more substantial update on 7051. So we look forward to that.
Okay, thank you. And my last question is just what steps, in addition, need to occur before you could submit that NDA for elutacitinib?
You know, we've been working on the NDA package, and we've made very, very good progress, so I'll say that. So, you know, I think that, you know, we've always said that we are pursuing a partnering strategy with elutisodinib, and certainly to make sure that – we have line of sight to the partner and we can collaboratively file the NDA would be very important because obviously the partner will be carrying forward the NDA and eventually marketing the product. And so, you know, we've made very good progress overall on the Lewis side nib and our strategy is still a partner strategy. So stay tuned.
Great. Thank you so much.
I am showing no further questions at this time. I would now like to send a call back over to Mr. Franklin for any closing remarks.
Well, we thank everyone for taking the time to participate in today's call. We made good progress during the third quarter of 2021 on three compounds focused on rare hematologic diseases and cancers and certainly look forward to sharing more progress on our development programs and This concludes today's call, and have a great day. Thank you all.
Ladies and gentlemen, that's the conference for today. Thank you for your participation. You may now disconnect.