Traws Pharma Inc (TRAW) 2022 Q1 法說會逐字稿

Ladies and gentlemen, thank you for standing by. Welcome to the Onconova Therapeutics First Quarter 2022 Financial Results and Business Update Conference Call. (Operator Instructions) As a reminder, this call is being recorded today, May 11, 2022.

At this time, I would like to turn the call over to Avi Oler, Senior Vice President of Corporate Development and General Counsel.

Thank you, operator, and welcome, everyone, to Onconova's First Quarter 2022 Financial Results and Business Update Conference Call.

Earlier this afternoon, we issued a press release reporting our financial results and business progress. If you have not yet seen this press release, it is available in the Investors & Media section of our website at www.onconova.com.

Today's call will begin with our President and CEO, Dr. Steve Fruchtman, providing an overview of our recent progress and corporate strategy. Dr. Fruchtman will then ask our Chief Medical Officer, Dr. Mark Gelder, to review our clinical programs. Our CFO, Mark Guerin, will then report our first quarter financial results before we move on to a question-and-answer session.

Before turning the call over to Steve, I'd like to remind everyone that statements made by management during this conference call will include forward-looking statements under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995, which involve risks and uncertainties that can cause actual results to differ materially. Forward-looking statements speak only as of the date they are made as the underlying facts and circumstances may change. Except as required by law, Onconova disclaims any obligation to update these forward-looking statements to reflect future information, events or circumstances. For more information on forward-looking statements, please review the disclaimer in today's press release and the risk factors in the company's SEC filings.

With that, it is my pleasure to turn the call over to Steve.

Thank you, Avi, and good afternoon, everyone. Our clinical programs continue to make strong progress over the past months, as we efficiently executed on the corporate strategy we've spoken about on our past earnings calls. This strategy has us internally focused on our narazaciclib program, while leveraging relationships with thought leaders from industry and academia to continue the development of rigosertib through investigator-sponsored studies based on the mechanism of action of rigosertib to target cancer indications of interest.

As many listening may recall, narazaciclib is an orally available, multi-targeted kinase inhibitor. It has a low nanomolar affinity for CDK 4 and 6 and other kinases that play important roles in tumor cell proliferation, metastasis and survival. It can also stimulate anticancer immunity through the inhibition of the CSF1 receptor and disrupt several pathways linked to the described mechanisms of drug resistance for this class of drugs. We believe this inhibitory profile positions narazaciclib to be a highly differentiated and potentially a best-in-class therapy. And we look forward to the publication of an abstract at the upcoming ASCO 2022 Meeting that describes this topic further.

Currently, 2 ongoing Phase I trials are evaluating narazaciclib in patients with solid tumors. These trials are collectively designed to inform the development of later-stage studies and also seek to begin clinically demonstrating the advantages of narazaciclib's differentiated pharmacologic profile. Dr. Mark Gelder will be speaking about these studies in more depth.

So for now, I'll just remind everyone that they evaluate both a continuous dosing schedule and a 3-weeks on, 1-week off schedule. These dosing regimens mimic the drug administration schemes for those of the FDA-approved CDK 4 and 6 inhibitors. I'm pleased to say today that each of narazaciclib's Phase I trials remains on track, and that we expect to identify the optimal recommended Phase II dose in the second half of this year.

As these trials continue to progress the indications and treatment regimens, the plan to pursue in the later-stage studies are coming into focus. While it would be premature to talk about the specifics of these studies, before they are finalized, I will say now that indications such as hormone receptor positive, HER2-negative breast cancer, multiple myeloma and mantle cell lymphoma are among those in addition to others that are drawing our interest. This interest is based both on preclinical data and the fact that hormone receptor positive, HER2-negative breast cancer is the only indication in which CDK4/6 inhibitors are currently FDA approved. But with the knowledge of the unfortunate reality that resisted to the currently approved drugs are very commonly seen.

Shifting gears, I'll now briefly mention some high level updates on rigosertib, which targets the RAS and PLK1 pathways. Rigosertib also acts as an immune modulator due to its ability to generate novel antigens on cancer cell membranes, which promotes the infiltration of autologous T cells into the tumor microenvironment and thus, recognize the cancer cells as [SPARC] and they have the opportunity to thus control their proliferation.

There are currently 2 investigator-sponsored studies of rigosertib ongoing, with a third expected to begin by the end of June. Two of these studies seek to leverage rigosertib's immunomodulatory effects by examining it in combination with a PD1 checkpoint inhibitor. Last year, we reported preliminary data from the first of these studies, which is in KRAS-mutated non-small cell lung cancer.

These data were highly encouraging, as we observed responses with different KRAS mutations who had failed prior checkpoint inhibitor therapies. This finding differentiates rigosertib from other approved KRAS targeted agents, since responses are seen in different KRAS mutations and thus, demonstrates rigosertib's potential to be both KRAS mutation independent and to also overcome the mechanisms driving checkpoint inhibitor resistance in KRAS mutated non-small cell lung cancer. We look forward to the continued progress of this trial. And we expect to report additional data at a major medical meeting by the end of this year.

We expect the second trial of the rigosertib checkpoint inhibitor combination therapy to begin later this quarter. This study will enroll patients with metastatic melanoma, who are refractory to checkpoint blockade. I'm pleased to report today that the FDA recently approved this trial to proceed after reviewing its design, which Dr. Mark Gelder will speak about shortly. In addition to the ongoing and planned investigator-sponsored studies I just mentioned, rigosertib is also being evaluated as a monotherapy in an investigator-sponsored study in recessive dystrophic epidermolysis bullosa, also known as RDEB, complicated by squamous cell carcinoma of the skin.

Unlike the 2 combination studies I mentioned, this trial seeks to take advantage of rigosertib's ability to potently inhibit the PLK1 pathway. On our last earnings call, I discussed some very exciting initial data from the trial, which showed a durable complete response of over a year in an extensively pretreated patient with RDEB and metastatic refractory squamous cell carcinoma, who remains in complete remission today. Though single-patient data must always be viewed with caution, it's important to realize that RDEB-associated squamous cell carcinoma is an ultra-rare disease that tragically is invariably fatal.

Additionally, we think these initial data could have an important read through into several more prevalent squamous cell indications, which is a concept that Mark Gelder will discuss in a few moments. However, before Mark begins his contribution to today's call, I'd like to first extend my thanks to those responsible for the progress we will be discussing. This includes all of our shareholders, employees, partners and investigators. Of course, most importantly, this list also includes the brave patients who participated in our clinical trials, as well as their families. It's the unmet need of patients that inspire the Onconova team, as we work to develop our clinical programs based on expert science.

With that, I'll now turn the call over to Mark Gelder. Mark?

Thank you, Steve, and good afternoon, everyone. It is my pleasure to provide an update on our recent clinical progress and future plans, starting with a discussion of our lead narazaciclib program. As Steve mentioned, narazaciclib is currently being advanced in 2 complementary Phase I dose escalation studies in patients with solid tumors. One in the United States and one in China, where we are collaborating with HanX Biopharmaceuticals.

The U.S. trial is evaluating a continuous daily dosing schedule in patients with advanced solid tumors. Enrollment remains ongoing in this trial's fourth cohort, which is evaluating a 160-milligram dose of narazaciclib administered orally each day. The safety findings coming out of this study continue to be very promising, as we have not observed any dose-limiting toxicities or clinically meaningful cases of neutropenia, although we are beginning to see anticipated on-target effects.

If the final data from our U.S. study confirm narazaciclib's favorable safety profile with daily dosing, it will provide an important point of differentiation between narazaciclib and the approved CDK4/6 inhibitors, palbociclib and ribociclib. Due to their associated bone marrow toxicity that leads to neutropenia, these 2 drugs are administered with a 3-week on, 1-week off dosing schedule to allow time for bone marrow recovery. We believe that avoiding an interrupted dosing schedule with narazaciclib could potentially contribute to enhanced efficacy.

Alongside our progress in the US, we have also seen narazaciclib's Phase I trial in China proceeding as planned. The study continues to enroll patients into its fifth cohort, which is evaluating a 200-milligram oral dose of narazaciclib administered each day with a 3-week on, 1-week off dosing schedule. Given the favorable safety data seen in this trial to date, HanX is currently preparing a protocol amendment that will allow for continued dose escalation. Thanks to the progress we've made in both of narazaciclib's Phase I dose escalation programs, we remain on track to identify a recommended Phase II dose later this year.

Looking ahead, we expect to utilize this dose in future trials, including a Phase II basket study, enrolling patients with various cancers, such as CDK4/6 inhibitor refractory hormone receptor positive, HER2-negative metastatic breast cancer. Our planned future trials also include studies that will be designed to evaluate narazaciclib alone and in combination with other anticancer agents in indications where CDK4/6 inhibitors are not currently approved.

Before moving on from our discussion of narazaciclib, I'd like to briefly highlight the robust preclinical data set supporting our development plans. Some key aspects of this data set include results suggesting narazaciclib potently inhibits CDK2, which is essential to DNA replication and one of several reported drivers of resistance to the currently available CDK4/6 inhibitor therapies.

Additionally, narazaciclib has been shown to inhibit ARK5, also known as NUAK1, which is a kinase that promotes cancer cell survival in hypoxic microenvironments and serves an important role in cell adhesion and metastasis. As Steve mentioned, narazaciclib also has strong affinity for the CSF1 receptor, the inhibition of which leads to activation of an anticancer immune response.

Beyond data on narazaciclib's inhibitory activities, our preclinical data set also includes results indicating that it can suppress the growth of cancer cell lines that are resistant to palbociclib, which is currently the most widely prescribed CDK4/6 inhibitor. Additionally, we are also highly encouraged by more recently generated in vitro data, which shows narazaciclib killing breast cancer cells that lack the retinoblastoma gene.

This is a significant finding as the expression of retinoblastoma protein is critical to the anticancer activity of the current CDK4/6 inhibitors and mutation of the retinoblastoma gene is another resistant pathway. Therefore, we believe these results further position narazaciclib to be studied in areas beyond those where palbociclib and other anti-CDK4/6 therapies are currently approved, as well as in patients resistant to currently approved CDK4/6 inhibitors.

I also mentioned that narazaciclib was shown to cause less bone marrow toxicity than palbociclib in mirroring studies. As mentioned earlier, it's palbociclib's association with bone marrow toxicity that necessitates its 3-week on, 1-week dosing schedule. Collectively, these preclinical findings support our enthusiasm for narazaciclib's development following the identification of the recommended Phase II dose. Through the progression of our ongoing and planned trials, we aim to show how narazaciclib's differentiated pharmacologic profile may lead to improved patient outcomes. We look forward to the program's continued advancement and to providing more details on our future clinical plans once they have been finalized.

Moving on, I'd now like to speak about rigosertib's investigator-sponsored program, starting with the anti-PD-1 combination studies. Steve mentioned earlier, these include an ongoing Phase I/II trial evaluating rigosertib and nivolumab in combination in KRAS-mutated non-small cell lung cancer, and a planned study designed to evaluate rigosertib in combination with pembrolizumab in patients with refractory metastatic melanoma.

An important point to note about each of these trials is that the inclusion criteria limits the respective patient populations to those who have previously failed therapy with a checkpoint inhibitor. Rigosertib's potential to overcome checkpoint inhibitor resistance is supported by previously reported preclinical data, highlighting its immunomodulatory effects. These data show rigosertib reversing the cold immunosuppressive tumor micro environments that often underlies checkpoint inhibitor resistance by promoting the expression of novel antigens, such as CD40 on cancer cells. This recruits immune effector cells into the tumor, which can then be stimulated by checkpoint inhibitors to mediated cancer cell death.

We also have early clinical evidence of rigosertib's ability to overcome checkpoint inhibitor resistant, thanks to preliminary data from the non-small cell lung cancer trial I just mentioned. A preliminary update from the trial reported last September showed a 29% overall response rate and a 43% disease control rate. Given that all of the patients enrolled in this trial had previously failed treatment with the standard of care PD-1 checkpoint inhibitor, these data suggest that rigosertib may enhance the efficacy of anti-PD-1 therapy and strongly support the activity of the study doublet.

I should also emphasize a point made earlier, which is that responses were observed in patients with different KRAS mutations. This sets rigosertib apart for other approved KRAS agents, designed to only target patients with a particular KRAS mutation such as G12C. Since our last update, the trial's dose expansion phase has continued to enroll patients. While data from prior patients has been maturing, we expect to provide updated results from the trial later this year. An additional study that will evaluate the same rigosertib-nivolumab doublet, but with potentially higher doses of rigosertib is also been considered since we have yet to reach a maximum tolerated dose in the current trial.

Moving on. The second investigator-sponsored trial I'll speak about today is the upcoming study designed to evaluate rigosertib in combination with the anti-PD-1 antibody, pembrolizumab, in advanced metastatic melanoma. As mentioned earlier, this trial will also exclusively enroll patients who have failed prior checkpoint inhibitor therapy. There is a pressing unmet need in this population, as approximately half of metastatic melanoma patients lack effective treatment options after progressing on a checkpoint inhibitor. This is a quite frequent occurrence in the syndication, as 40% to 60% of metastatic melanoma patients will show acquired or primary resistance to PD-1 inhibition.

To attempt to address this need, we and the investigator sponsoring the trial will be collaborating on an open-label, 2-stage single-arm Phase II study. The primary endpoint of the trial will be overall response rate, while key secondary endpoints will include progression-free survival, overall survival and biomarker assessments intended to shed light on rigosertib's ability to remodel the tumor microenvironment.

If prespecified response criteria are met during the first stage of the trial, the study will proceed to Stage 2, where additional patients will be enrolled. The design of the study was recently approved by the FDA and is now awaiting IRB approval at the academic center where it will be conducted. We expect this to occur later this quarter, which will allow the trial to open for enrollment.

The last investigator-sponsored study I'll mention today is the ongoing trial evaluating rigosertib monotherapy in the RDEB-associated squamous cell carcinoma, which has shown a durable complete response in a heavily pretreated patient. Since we spoke about the background of this trial and its initial data on our last earnings call, today, I will focus on what we believe these data mean from a broader perspective.

Let me start by quickly recapping the scientific rationale behind this trial. RDEB is caused by a lack of Type 7 collagen protein, which leads to extreme skin fragility and chronic wound formation. Over time, many RDEB patients develop squamous cell carcinoma with the overexpression of the protein PLK1. This led the trial's investigator, who is one of the world's leading experts on RDEB to run a drug screen for inhibitors of PLK1. Of all of the agents tested in this extensive screen, rigosertib was found to be the most potent inhibitor of PLK1, suggesting it may have activity against cancer driven by PLK1 overexpression.

With the observed complete response in the ongoing investigator-sponsored trial, we now have clinical proof-of-concept supporting this hypothesis. Given the wide array of cancers with PLK1 overexpression, we believe these recent proof-of-concept data highlight rigosertib's potential to address unmet needs beyond just RDEB-associated squamous cell carcinoma. The recent data is now driving conversations with key opinion leaders interested in additional investigator-sponsored studies in more prevalent indications, such as other subtypes of squamous cell carcinoma. In parallel, the ongoing trial in RDEB patients continues to advance.

Lastly, I'd like to once again emphasize that rigosertib's clinical development will be pursued primarily through investigator-sponsored studies and that we plan to continue dedicating our internal resources primarily through [narazaciclib]

With that, I'll now let Mark begin his discussion of our recent financial results.

Thank you, Mark, and thanks to everyone who has joined today's call.

I am pleased to say that Onconova remains in a strong financial position. As of March 31, 2022, the company had cash and cash equivalents of $50.8 million compared to $55.1 million as of December 31, 2021. Based on our current projections, we believe our current cash position will be sufficient to fund our ongoing clinical trials and business operations, including the pursuit of corporate development opportunities for more than 18 months. This runway is expected to take us through the achievement of multiple important milestones.

Turning now to a review of our first quarter financial results. Research and development expenses for the first quarter of 2022 were $2 million compared to $1.9 million for the first quarter of 2021. General and administrative expenses for the first quarter of 2022 were $2.2 million, and this compares with $2.2 million for the first quarter of 2021. We reported a net loss for the first quarter of 2022 of $4.1 million, or $0.20 per share on 20.9 million weighted average shares outstanding. This compares with a net loss for the first quarter of 2021 of $4.7 million or $0.32 per share on 14.6 million weighted common shares outstanding.

This completes my financial review. I'll now turn the call back over to Steve to provide a summary of our anticipated milestones before we move on to Q&A.

As always, thank you, Mark. We expect to achieve several important clinical milestones over the upcoming months. Starting with narazaciclib, we remain on track to establish its recommended Phase II dose in the second half of this year. This will then enable the subsequent initiation of a Phase II basket trial in a number of important indications, including hormone receptor positive, HER2-negative refractory metastatic breast cancer.

Beyond narazaciclib, we expect the investigator-sponsored trial, evaluating rigosertib-pembrolizumab combination therapy in melanoma to open for enrollment later this quarter. We also expect the continued advancement of the ongoing Phase I/IIa trial of rigosertib plus nivolumab in advanced KRAS-mutated non-small cell lung cancer. Updated data from this study are expected with great anticipation by year's end.

Finally, we continue to assess opportunities to potentially expand our pipeline through strategic licensing and collaborations. With regards to these efforts, I will emphasize 2 points. First, any action here will be data driven, based on the science and market size underlying the opportunity. Second, we intend to take a highly selective approach in these efforts as we continue to have very strong conviction around the therapeutic and commercial potential of our current assets.

With that, we will now open the call for questions. Operator?

(Operator Instructions) Our first question comes from Charles Zhu with Guggenheim.

Regarding CDK4/6 inhibition, to what extent is neutropenia an on-target effect? And do you need to observe neutropenia in order to also see a therapeutic effect associated with your inhibitor?

Mark Gelder, would you like to take that?

Sure. And thank you for the question. So neutropenia is an "on target effect" of CDK4/6, particularly CDK6 inhibitors. If you look at the Phase I data from palbo, ribo and abemaciclib, you'll see that neutropenia was the dose-limiting toxicity or DLT associated with both palbociclib and ribociclib. And it was really the neutropenia that was responsible for the ultimate dose selected to move forward in their Phase II and III clinical trials, and it was also responsible for the necessity of a 3-week on, 1-week off schedule. Abemaciclib, also a very potent CDK4/6 inhibitor, also has some associated neutropenia. But if you look at the Phase I data with abemaciclib, diarrhea was their primary DLT. And because they had some neutropenia but it was not actually the dose-limiting toxicity, and the neutropenia that was observed did not necessitate a 3-week on, one-week off dose schedule, abemaciclib has a continuous daily dosing.

So do we anticipate seeing some neutropenia as we continue with our dose escalation? Absolutely, we do. We will not be surprised at all. We expected. Based on our preclinical data, do we think that the neutropenia associated with narazaciclib will be as severe or profound as that with palbociclib or ribociclib? No, we do not. And what do we anticipate will be the DLT associated with narazaciclib? We don't really know yet what our "DLT" will be. We have not seen a DLT in our study here in the US. But do we anticipate we will see some neutropenia? Yes, we do. Am I hopeful? Are we all hopeful that the neutropenia will not necessitate a 3-week on, 1-week off schedule? But the jury is still out.

Our next question comes from Ahu Demir with Ladenburg.

My question will be on narazaciclib as well. I'm curious to hear what is the extent of preclinical models we are expecting to see at ASCO? Any additional color would be much appreciated.

I'll ask Dr. Gelder again to take that. Mark?

So we submitted an abstract to ASCO, describing the kinase inhibitory profile associated with narazaciclib. We did not submit an abstract that describes any of its activity in terms of preclinical models such as PDX or xenograft data.

That's helpful. My follow-up question will be again on narazaciclib. How many active site is currently open? And do you plan to open additional sites? Curious on the enrollment status. I'm sorry, I joined late. I hope I'm not asking something you already covered.

Mark?

Yes. So again, thank you for the question. In our Phase I study here in the US, we have 3 active Phase I sites, who have all been enrolling very well. And do we anticipate opening additional sites for the dose escalation, the Phase I dose escalation study? No, we do not. As we open additional studies part of the basket trial, once we achieve the recommended Phase II dose, will we open additional sites for the basket studies? Absolutely, we will. Yes.

That's helpful. My last question will be, are there any rational combinational strategies you could use to pair it with narazaciclib? Are you considering any of those, given the safety profile has to match, of course? But just curious if there are any rational matches with narazaciclib.

Mark?

Yes. So again, thank you for the question. Great question. And I think that if you look at where the currently approved CDK4/6, where their approval is, i.e., hormone receptor positive, HER2-negative metastatic breast cancer and you look at the combination therapies employed with the 3 approved agents, i.e., either aromatase inhibitors, SERDs, et cetera, we will be doing combination studies with one or more aromatase inhibitors. We'll be doing combination studies with one or more SERDs. We will -- we are also planning some additional combination studies that we think make a very good mechanistic sense and we will be outlining those in the future. But yes, we are planning combination studies with at least 2 other, if not more, anticancer agents.

And, Ahu, just to give Mark Gelder a break, as you know, mantle cell based on the mechanism of action of narazaciclib and as we mentioned, it's of great interest to us. And based on the anticipated profile and perhaps some preclinical studies planned. drugs like ibrutinib in mantle cell are the standard of care. So we could anticipate looking at combinations with the typical anti-mantle cell drugs used such as ibrutinib as well.

Our next question comes from Joe Pantginis with H.C. Wainwright.

So sticking with naraz a little bit. Obviously, everything we are discussing today is the completely classical route to identify the RP2D in the second half. So I wanted to ask my question this way. With all the initiatives at FDA, how are you going to look to reconcile if that's the right word, the initiatives with the FDA to identify the minimal effective dose?

Well, I tried to give Mark a break, but I can't. Dr. Gelder, would you like to handle that?

Sure. So what I can tell you is that we have recently completed and finalized a protocol amendment for the ongoing Phase I dose escalation study, where we are going to incorporate a PD, pharmacodynamic marker, so that we will not only be looking at the safety profile with each dose escalation, but we will also be looking with the PD marker. And this will allow us not only to identify the "MTD" or maximally tolerated dose, but also a dose where we achieve maximal biologic effect based on the PD marker.

Got it.

So that protocol amendment has been finalized, has been signed, and the amendment has been sent to the 3 sites for submissions to the IRB, has been submitted to the FDA as well.

Yes. Okay. And then so talking about markers, that's a good segue for my next question. I guess earlier in your prepared comments when you talked about on-target effects that you're seeing already and, of course, you already had the discussion about neutropenia, any other details about what other on-target effects you are seeing and how you're measuring them?

Go ahead, Mark, please?

So the other on-target effects that we're seeing are again primarily related to bone marrow and bone marrow precursors. And so looking at hematocrit, hemoglobin levels, looking at platelet counts, again, looking at white blood cell counts, et cetera. So we are -- this is primarily through looking at different laboratory values and the CBC is the most sensitive indicator of CDK6 inhibition.

Got it. And then my last question. Just switching gears. When you look at the potential for a Phase II in RDEB, obviously, there's no standard of care really. And I was just wondering at this point, could you take any broad strokes as to the design or size of this study? One would guess that it wouldn't be that big.

Well, I'll take that. I think actually, Joe, it could be tiny. This is such an ultra-rare disease. 100 patients, new patients reported per year in the US. Most of them die unfortunately of wounds and infections before they develop squamous cell carcinoma. But the fact that we have one complete remission rate-limiting step in my view is to get more patients because of the ultra-rare nature of the disease. I don't think we would have to do a controlled Phase II trial.

I think if we have a few more patients, we have the dose, we know the dose. There are few more patients on the current trial. If responses are seen, the plan would be to go directly to the FDA to ask for an approval in this rare indication based on the response rate observed and how durable the response has been to date. So that would be our plan, get a few more patients, hope for a robust response that we've seen to date and then go to the FDA with our data and have a discussion with the FDA about an approval or what next steps would it take to get such an approval.

Our next question comes from Robert LeBoyer with NOBLE Capital Markets.

I'm opposed to giving Dr. Gelder a break. So I'd like to ask the question about the rigosertib trial that's coming up. Based on the discussion earlier, it sounds as if we are going to do a (inaudible) trial with rigosertib with KEYTRUDA in metastatic melanoma. And this is going to start with a phase using a single-arm in a single center and then go to a second stage with additional patients. Could you elaborate as much as you could on the number of patients, treatment time and time for data or starting the second phase?

Sure. Steve, do you want me to handle that? Or do you want to go (inaudible)? No, no. Please, Rob has good taste and he sounds like he prefers you. So go ahead, Mark, please.

So the study is going to be conducted. It's a Phase II study -- a Phase I/II study. It's going to be conducted at a single academic center that has a very high-volume melanoma patient population. It will -- the inclusion criteria are such that all patients will have been required to have failed a prior checkpoint inhibitor therapy. And by failed, I mean, progress on prior therapy. It's not going to include patients who are intolerant, because this is a combination of rigosertib and pembrolizumab. And in Stage 1, there will be 10 patients enrolled. If a certain response rate is met as defined in the protocol, it will then progress on to Stage 2. Currently, Stage 2 will take place at the same institution.

They feel confident that they have a very adequate patient population to enroll this trial quickly. The Stage 2 will enroll an additional, approximately 20 patients. And if all goes well and as planned and looking at the volumes that they do have, we do believe that they can meet the enrollment targets. But if all goes well, we should have data from the first stage by the first part of next year.

We believe that we will have Stage 1 fully enrolled by the end of the year and that we should have some response data the first part of next year. Remember, the primary endpoint is response rate per RECIST. And so it's going to take a minimum of 2 cycles. Some patients may have responses early, i.e., after 1 or 2 cycles. But maybe that we don't see responses in other patients until 3 or 4 cycles. So we don't anticipate having results of the first stage until the first part of next year. But this is going to be conducted at an academic center with a very high volume of melanoma. Yes.

I'm showing no further questions in the queue. At this time, I'd like to turn the call back to the speakers for any closing remarks.

Thank you, operator. I would like to once again thank all of those participating today and for your very insightful questions. We are excited about our recent progress and look forward to the continued execution of our corporate and clinical plans as outlined today. Please stay safe, and have a nice evening and take care.

Ladies and gentlemen, thank you for your participation in today's conference call. This concludes the event. You may now disconnect.