Forma Therapeutics Holdings, Inc.
Q3 2021 Earnings Call Transcript

Published: 12 Nov 2021

[Operator:]

Good morning. Welcome to the Forma Therapeutics Third Quarter 2021 Financial Results and Business Update Conference Call. All participants are currently in a listen-only mode. Following management’s prepared remarks, we will hold a Q&A session. 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.

[Mario Corso:]

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; Pat Kelly, our Chief Medical Officer; Dave Cook, our Chief Scientific Officer; and Todd Shegog, our Chief Financial Officer. Before we begin, I’d like to caution listeners the comments made and financial information provided during this conference call, includes certain statements that are estimates, belief, 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, therapeutics, potential and clinical benefits and safety of our product candidates, planned regulatory submissions, our financial conditions and capital requirements, our business operations, 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 performance. 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 would 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 will also be holding an investor briefing on December 13, to discuss clinical trials results being presented at the ASH Annual Meeting. Further information on these events will be made available on our website www.FormaTherapeutics.com. With that I will now turn the call over to Frank, our President and Chief Executive Officer.

[Frank Lee:]

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 for a wealth of long term success. Along with the progress in advancing our science, I’m pleased with the progress we’re making and establishing Forma as a trusted partner in the sickle cell community. In October, we collaborate 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 third quarter. First with etavopivat 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 by its multimodal mechanism of action. We’ve completed enrollment in our open label extension the Phase 1 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 2/3 Hibiscus study and as a reminder, this study includes two co-primary endpoints, hemoglobin and VOC’s 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 etavopivat. 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 etavopivat has a 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 CPB/p300 inhibitor FT-7051, we reached an important milestone in October with the triple meeting presentation of the first inhuman results from our ongoing phase 1 trial in metastatic castration resistant prostate cancer. We are encouraged by the early data and the potential for FT-7051 to target the novel pathway of CPB/p300 inhibition. With respect to our third development compound, the IDH inhibitor Olutasidenib for relapsed refractory AML we plan to present new data from the azacitidine combination cohort at ASH. These data further support the potential for Olutasidenib 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 etavopivat and Olutasidenib. In addition by year end, we plan to start the phase 2 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 FT-7051 Phase 1 courage study in prostate cancer. And later in 22 we plan to have etavopivat Hibiscus study interim analysis one. 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. And I’ll turn over the call to Pat.

[Pat Kelly:]

Thank you, Frank. And good morning everyone. I will provide a brief overview of our development programs for etavopivat and Olutasidenib and then an outline of our presentation scheduled for the ASH meeting in December. Etavopivat 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 from formed by deoxygenated hemoglobin-S. The increase in ATP allows the cell to repair membrane damage incurred through the multiple cycles of cells sickling. Together the effects of decreased to 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 etavopivat 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 etavopivat has the potential to reduce the analysis and anemia 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 etavopivat may significantly reduced the debilitating vaso occlusive events that characterize sickle cell disease. We have also sought to elucidate the effects of etavopivat on the sickle RBC as measured by numerous markers of red blood cell health. We have designed a rigorous and comprehensive phase 1 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 etavopivat two week dosing cohorts and patients who have completed the etavopivat 12 week dosing cohort. We have previously demonstrated that two weeks of etavopivat daily can increase hemoglobin levels in 73% of patients with sickle cell disease. In open label treatment cohort, this hemoglobin response has been sustained with at 83% or five out of six patients completing 12 weeks of etavopivat dosing maintaining a greater than one gram per deciliter hemoglobin improvement. We have shown the two weeks of etavopivat dosing also significantly improves the sickle RBCs oxygen affinity with a delay in the point of sickling to lower oxygen levels and this improves the deformability of the RBC 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 and patients receiving etavopivat are healthier and living longer, leading to an improved hemoglobin response. These improvements are seen as early as two weeks of etavopivat dosing and are sustained in patients receiving 12 weeks of daily etavopivat dosing. In addition to the improved hemoglobin and reduction in hemolysis, we have reported our initial observations that etavopivat treatment can reduce systemic markers of inflammation and coagulation in patients receiving up to 12 weeks of etavopivat daily. This is encouraging data that supports our hypothesis, that by improving the health of the sickle RBC with chronic daily dosing of etavopivat we may produce the debilitating vaso occlusive events that characterize sickle cell disease. Finally, as previously reported, etavopivat daily is well tolerated that doses up to 600 milligrams daily which is 150% of the maximum dose being evaluated in the higher dose study with a safety profile that is consistent with the underlying sickle cell disease. As noted at our EHA presentation, the safety profile of the etavopivat 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 etavopivat 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’ dose for up to 12 weeks, evaluating the effects of 400 milligrams etavopivat on hemoglobin markers of hemolysis including reticulocytes, bilirubin and LDH, markers of systemic inflammation and coagulation. With approximately three patient years of etavopivat 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 Olutasidenib, our mutant ID H1 inhibitor being evaluated in patients with relapsed refractory acute myeloid leukemia or AML. Earlier this year, results were presented from the positive registration of phase to inner analysis in the relapsed refractory AML patients receiving 150 milligrams of Olutasidenib twice daily. At the upcoming ASH meeting in Atlanta, we will provide an analysis of the molecular characteristics of response to Olutasidenib in these patients. In addition at the ASH meeting results from cohorts receiving Olutasidenib in combination with azacitidine will also be presented, showing benefits of the combination in various sub population, including treatment naive AML patients. With that, I’m going to now turn the call over to Dave, who will provide an update on FT-7051 for prostate cancer.

[Dave Cook:]

Thanks, Pat. I’m going to spend the next few minutes discussing our clinical stage CPB/p300 inhibitor FT-7051. FT-7051 targets the antigen 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 FT-7051 is applicable to a broad range of resistance mechanisms, because CPB/p300 modulates AR via the N-terminal domain. This means the tumors expressing the AR-v7 splice variant for example, which lacks the C-terminal AR hormone binding domain, and for which there are no approved treatments, or potential therapeutic targets for 7051. In addition, the tolerability profile of FT-7051 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 1 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. And these results presented at the triple meeting in October showed an encouraging safety profile as well as biologic effects consistent with inhibition of the CPB/p300 pathway. Data as of September 1 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 CPB/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 experience a treatment emerged in 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% of 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 valuable patients in this 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.

[Todd Shegog:]

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 30, 2021 was $43.3 million, which compared to a net loss of $27.6 million for the quarter ending September 30, 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 30, 2021, compared to $24.8 million for the quarter ended September 30, 2020. This increase was primarily attributable to R&D staffing, equity based compensation and costs for 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.

[Operator:]

Thank you. Now first question coming from the line of Mark Breidenbach with Oppenheimer. Your line is open.

[Mark Breidenbach:]

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 the 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 enzalutamide before starting 7051. Maybe some thoughts around that observation would be appreciated. Thanks so much.

[Frank Lee:]

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 or plan 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 pass are viable. And we plan on providing some additional information on hemoglobin as a surrogate endpoint for clinical benefit, which is very specific to etavopivat’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.

[Pat Kelly:]

Yes. Thanks Frank. Yes I think just echo what Frank has just said, the broad potential differentiating profile of etavopivat we’ve always considered a number of opportunities to explore clinically meaningful endpoints that as part of our life cycle efforts and these studies could include looking at sickle cell disease related complications and cardiopulmonary, CNS, renal disease and others. And many of these are already in progress. We’re initiating the transfusion dependent sickle cell study with etavopivat as well as our pediatric trials. So 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 etavopivat experience and its unique mechanism of that action. But you can also imagine that there’s a lot of data or epidemiological information that help support the potential benefits of 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 in the community. I’ll turn it over to Dave.

[Dave Cook:]

Yes good morning Mark. Hi. Thanks for your question on 7051. And just to clarify for everyone else on the line there’s a phenomenon known it’s based on androgen deprivation in which patients can have a transient spontaneous response upon withdrawal of androgen happens in a very small number about 1% of patients. And we looked 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 FT-7051. 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 market change in the rate of PSA decline. In fact, it was a sort of level PSAs followed by a very sharp decline upon establishment of treatment of 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 FT-7051, that rate of growth stabilized. So we think that based on those multiple lines of evidence and of course in with a lot of discussion, that this is clearly a response to 7051 and not some other phenomenon.

[Operator:]

And our next question coming from the line of Maury Raycroft with Jefferies. Your line is now open.

[Maury Raycroft:]

Hi, everyone. Good morning, and thanks for taking my questions. I’m just clarifying and following up on a prior question for the additional information that you would be showing to FDA for etavo is there a precedent for this or is this novel potential endpoint based on a etavo specifically?

[Frank Lee:]

Well broadly this is based on our recent discussions with the FDA and as Pat mentioned, this could certainly include mechanistic or epidemiologic and also clinical data on etavopivat and certainly we have a number of clinical trials as Pat articulated to collect those kinds of information. So that that’s kind of background and context Pat, I don’t know if you have additional thoughts here.

[Pat Kelly:]

Yes, 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 broad base some new or evolved end points will be part of that discussion with the FDA and as part of the ongoing discussions with the FDA.

[Maury Raycroft:]

And then, even though there’s no plan to just the design, is it possible to maybe informally collect VOC data earlier than planned and include that to support an accelerated approval path?

[Frank Lee:]

I don’t think. Go ahead Pat yes.

[Pat Kelly:]

I was just going to say I don’t think we’re in a position to 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.

[Frank Lee:]

And 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 cells study into this year, early next year, as well as the FAO and the two different patient populations. So the totality of data will be will be important in the discussions overall. In addition, as Pat mentioned, at the ASH presentation, we’ll have an analysis among other things, patient’s baseline history of VOC versus what we’ve observed on treatment as well.

[Operator:]

Our next question coming from the line of Alethia Young with Cantor Fitzgerald. Your line is open.

[Alethia Young:]

Hey, guys, thanks for taking my question, a couple. One, I just wanted to talk a little bit about do you haven’t really seen the VOCs with the dosing or the taper like some other people have in the similar class? So I wanted to get your perspective on why that might be the case. And then, as we get on 7051, just went off a little bit about kind of the path forward, and is there possibility for maybe faster pathway based on the Pacific mutational profile? Thank you.

[Frank Lee:]

So Pat, you want to maybe take the first question?

[Pat Kelly:]

Yes, I think as we highlighted in our presentation in June it’s a very well tolerated molecule. Patients on treatment had very low rates of any sickle cell related pain events. In the washout period, which is an extended we follow them for four weeks, we did have vaso occlusive events there that we’re taught by the investigator to be related to the disease under trot 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 what our position has been that in the setting of taking away a medication that makes patients feel better and has more energy, that part of part of that discontinuation the caution should be with the patient and the investigator to make sure that the patient doesn’t over exert themselves because their capacity to function may be reduced, because now they they’re no longer protected. And so that’s lovely been seeing and we’ll provide a further update on that at the ASH meeting as well.

[Frank Lee:]

Dave?

[Dave Cook:]

Sure. Hi Alethia, 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 genetic analysis, as well as analysis of AR splicing for every patient in the study. And that may lead to identification and particularly sub susceptible patient groups. I’ll note that I think our responder had a mutation in the C terminal 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 yet to pay attention and to see it but 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 insulin resistance or potentially Type 2 diabetes, and truly was not emergent on treatment. However, it hadn’t, since it hadn’t been seen previously, is 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.

[Operator:]

Our next question coming from the line of Robin Garner with Craig-Hallum. Your line is open.

[Robin Garner:]

Thank you. I wanted to ask about the upcoming studies in transfusion dependent sickle cell patients in female, is there any? Are there any changes to the design of those studies and what else might you hope to show from this please?

[Frank Lee:]

So Pat, perhaps you can provide a quick overview there.

[Pat Kelly:]

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 have been no changes to that design. It’s a pilot to understand the biology of etavopivat in 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 transit blood transfusions. So it’s a study to ask that question, can we affect the need for iron, infusion, blood transfusions a patient population while controlling their hemoglobin-S levels.

[Frank Lee:]

And I’ll just add, approximately 20% of sickle cell patients are transfusion dependent. So it’s a significant need.

[Robin Garner:]

And for the patient, who was the responder in the 7051 study, do you have any update on that patient that might passed the data that’s already been presented, for example, helping us to understand the durability of that response to today?

[Pat Kelly:]

Yes. We don’t have any update. And in fact, we guided to not expect regular updates. We don’t want to be as friend of ours said salami slicing. We’re going to try to provide come back with robust data sets as opposed to individual patient vignettes. So that’s where kind of where we will be in the future.

[Frank Lee:]

And, as we discussed before, we’re broadly getting to mid next year, to provide a more substantial update on 7051. So we look forward to that.

[Robin Garner:]

And my last question is just what steps in addition need to occur before you could submit that NDA for Olutasidenib?

[Frank Lee:]

We have been working on the NDA package, and we made very-very good progress. So I’ll say that. So I think that we’ve always said that we are pursuing a partnering strategy with Olutasidenib 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 we’ve made very good progress overall Olutasidenib and our strategy is still part of strategy. So stay tuned.

[Operator:]

I’m showing no further questions at this time. I will now like to turn the call back over to Mr. Frank Lee for any closing remarks.

[Frank Lee:]

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.

[Operator:]

Ladies and gentlemen that does conclude conference for today. Thank you for your participation. You may now disconnect.