Compass Therapeutics Q2 2025 Earnings Call Transcript

Quartr
Provided by Quartr
August 11, 2025

Key Takeaways

  • Positive Sentiment: Lead program Tevesimig shows fewer deaths than projected in the ongoing Phase II biliary tract cancer trial, suggesting a potential overall survival benefit.
  • Neutral Sentiment: Progression-free and overall survival analyses for Tevesimig are now expected in 2026 after lower-than-anticipated event rates delayed the readout.
  • Positive Sentiment: PD-1/PD-L1 bispecific CTX-8371 delivered two deep partial responses at low dose levels in NSCLC and TNBC, triggering planned cohort expansions later this year.
  • Positive Sentiment: Proprietary PD-1/VEGF bispecific CTX-10726 outperformed ivenesumab and matched pembrolizumab in preclinical head-to-head models, with an IND filing on track for Q4.
  • Positive Sentiment: Compass ended Q2 with $101 million in cash, providing runway into 2027 to support multiple upcoming clinical and regulatory milestones.
AI Generated. May Contain Errors.
Earnings Conference Call
Compass Therapeutics Q2 2025
00:00 / 00:00

There are 12 speakers on the call.

Operator

Greetings and welcome to Compass Therapeutics Second Quarter twenty twenty five Earnings and Business Update Call. At this time, participants are in a listen only mode. A question and answer session will follow the formal presentation. As a reminder, this conference is being recorded. It's now my pleasure to introduce Anna Gifford, Chief of Staff.

Operator

Thank you. You may begin.

Speaker 1

Good morning and thank you for joining us. My name is Anna Gifford. I am Chief of Staff at Compass Therapeutics. With me today is Doctor. Thomas Schutz, CEO and Vice Chair of the Compass Board.

Speaker 1

Our CFO, Barry Shin, will also join us for a short Q and A following Tom's comments. Earlier this morning, we released our financial results and a business update for the second quarter. The slide presentation accompanying this webcast and a copy of the press release are available on our website. Please note, we'll be making forward looking statements on today's webcast. These forward looking statements are described in our press release issued today in the company's SEC filings.

Speaker 1

With that, I'd like to turn this call over to Tom Stroetz. Tom?

Speaker 2

Thank you. We are incredibly excited today to be hosting this call with you this morning. As Anna just mentioned, earlier today, we released our quarterly financials for Q2 twenty twenty five. In addition to the financials, we also provided very important updates for three of our development programs. These updates are summarized on the next slide, and I'll then provide additional details for each of these program updates.

Speaker 2

Most importantly today for our lead program, Tevesimig, the DLL4 VEGF A bispecific antibody in the ongoing randomized trial in patients with advanced biliary tract cancer, there are currently fewer total deaths in the study than we have projected. While this disclosure is a simple fact, it is very important to say this sentence differently. More patients are alive today than we have projected. I understand clearly that this is an investor call, but it's so important to reflect on what this could mean for the patients enrolled in this study. I'll update the timing of the survival analyses in one minute.

Speaker 2

Next, for CTX-eight thousand three and seventy one, our PD-onePD L1 bispecific antibody, very unexpectedly, we have two deep partial responses in the early dose escalation cohorts in the ongoing phase one study. One partial response is in a patient with non small cell lung cancer, and one partial response is in a patient with triple negative breast cancer. Later this year, we'll be initiating cohort expansions in patients with non small cell lung cancer and triple negative breast cancer. I will describe CT scans for each of these two patients in a few minutes. We hope to present these data at a scientific conference later this year.

Speaker 2

We're also disclosing results from preclinical head to head studies of CTX-ten thousand seven hundred twenty six, our proprietary PD-one VEGF bispecific antibody, compared to the leading drug candidate in the class of ivenesumab. We will be presenting these data at a scientific conference later this year. So let's begin with Tivesemig. This slide summarizes the design of the ongoing randomized study in The United States in patients with advanced biliary tract cancer. This study is a two to one randomization of Tivesemig plus paclitaxel versus paclitaxel alone.

Speaker 2

The primary endpoint of the study is overall response rate. We announced those results about four months ago. The secondary endpoints in this order are PFS, OS, and duration of response. We're using, of course, the hierarchical testing methodology to control for alpha statistical spending in the study. The next slide summarizes the current status of the study that we call COMPANYON-two.

Speaker 2

On the top right, as I mentioned, we achieved the primary endpoint, so the study is positive by definition. We had a seventeen point one percent overall response rate, about tripling what was seen in the control arm with a p value of 0.031. On the top left box, I'll come back to this point in one minute. The trial was fully enrolled in August 2024, enrolled one hundred and sixty eight patients with advanced biliary tract cancer treated in the second line setting. As of today, we are currently at greater than seventeen months median follow-up in the study.

Speaker 2

So let's talk about the secondary endpoints of progression free survival and overall survival. It's hard to say this, but the secondary endpoints are triggered by a total number of deaths in the study. So that's how these time to event analyses are commonly done. We need eighty percent OS events to trigger the analyses of progression free survival and overall survival. And today we have fewer total deaths in the study than we had originally projected.

Speaker 2

When we projected that we would be presenting analyses of these endpoints in Q4, we made that projection in April. And since that time, the number of deaths in the study has continued to decline. Clearly, the eighty percent OS event threshold has not been met. So the analyses of PFS and OS are now projected to occur in 2026. I think the bottom of this slide is very important.

Speaker 2

Recall the study that was titled ABC06. That study was published in 2021 in Lancet Oncology by LaMarca et al. That was a randomized study of the three drug combination FOLFOX, 5FU, leucovorin and oxaliplatin in patients with biliary tract cancer treated in the second line setting. So the exact same population that we're treating in COMPANYON-two. If you look at the Kaplan Meier curves for that study, at 18, the overall survival was less than ten percent in that study, with a median overall survival in the FOLFOX arm of six point two months.

Speaker 2

Where we are today, and again it's important to point out these are this is a pooled survival number. We are greater than 20 overall survival with greater than seventeen months median follow-up. And we probably, although it's hard to predict, of course, we probably will not be at eighty percent mortality until we have something like greater than twenty months median follow-up. So very interesting data today, Obviously extremely important. And as we mentioned in our press release, obviously we don't know this, but it appears that Tivesamig could be affecting overall survival in this patient population.

Speaker 2

Okay, let's now move to CTX-eight thousand three and seventy one, our PD-onePD L1 bispecific antibody. Just a reminder of the differentiated mechanism of action here. Recall that this drug emerged from a screen using a proprietary technique at COMPASS in which we can screen bispecific drug candidates for synergy. That screen identified PD L1 as a synergistic partner for PD-one blockade. As I've discussed many times before, that was a rather unexpected scientific discovery.

Speaker 2

And because of that, we spent a long time investigating the mechanism of action. We published all that data, the PubMed ID for that paper is at the bottom of this slide. We have always envisioned 08/1971 to be on the leading edge of defining next generation checkpoint inhibition. This mechanism of action on the right hand side of this slide, with the bispecific being unequivocally a cell engager, and quite fascinatingly, the bispecific actually converts PD-one positive T cells into PD-one negative T cells by removing PD-one from the surface of those cells. So it is a very differentiated mechanism of action.

Speaker 2

And again, we believe that this drug could be on the cutting edge of defining next generation checkpoint inhibition. We're currently running a phase one study. This study is a standard three plus three dose escalation study. Importantly, we of course, as all phase one studies do, we started with a minimal dose of zero point one milligrams per kilogram. And we have finished enrolling the first four dosing cohorts zero point one, zero point three, one and three milligrams per kilogram.

Speaker 2

We have not seen any dose limiting toxicities in those 12 patients. So again, a three plus three design, three patients times four dose levels, 12 patients. We're currently enrolling the fifth dose level, which will be the ten milligram per kilogram dose level. The patient population in this study, importantly, is all post checkpoint inhibitor. So patients with melanoma, non small cell lung cancer, head and neck cancer, Hodgkin lymphoma, and triple negative breast cancer are being enrolled in this study.

Speaker 2

As I mentioned earlier, we now have two deep partial responses in the first patients enrolled in this study. And again, I will emphasize to you that the first dosing cohort was really a de minimis dose. These are CT scans on slide 10 from a patient in the study with non small cell lung cancer. For reference, these scan images across the top, the patient is lying on their back. Dark color is air, so that's the lungs.

Speaker 2

Lighter color is tissue and the bright white color is bone. Inside of the blue circle at baseline, you can see a 45 millimeter metastatic tumor in this patient, which over time completely disappears. In fact, this patient had 59 millimeters, 5.9 centimeters, more than two inches total of metastatic tumor, which actually all disappeared. Really interestingly in this patient, this patient actually had initial pseudo progression at a lymph node, which has been described with checkpoint inhibitors like Keytruda and Opdivo. And it's interesting to speculate on what that might mean.

Speaker 2

Subsequently, all of these patients target lesions disappeared. We also have two patients with non small cell lung cancer among five patients treated so far with prolonged stable disease for a clinical benefit rate of approximately sixty percent. So on the next slide, I'm going to spend a little bit more time on this slide because this slide is incredibly important. So this is a patient with metastatic triple negative breast cancer who had three metastatic target lesions at baseline. I'm showing two of these three lesions on this slide.

Speaker 2

The third lesion was a lymph node. Across the top, same thing as the previous slide, patient lying on her back. Black color is air. So inside the blue circle, you can see a metastatic tumor in the lung, which completely disappears by eight weeks. On the bottom, this is a sagittal view.

Speaker 2

So this is a reconstruction where you're looking at the patient from the side. Inside the blue circle on the bottom left is a metastasis to the pericardium, the lining of the heart. That metastasis is 52 millimeters in size, 5.2 centimeters, more than two inches. Both of these tumors completely disappeared. The other target lesion went from 15 millimeters to seven millimeters.

Speaker 2

So the total tumor decline in this patient from 87 millimeters to seven millimeters is greater than a ninety percent reduction in this patient treated in the fourth line setting who had previously received pembrolizumab. This patient is one out of three patients treated in the study with triple negative breast cancer. So moving to CTX10.726, our proprietary PD-one VEGF bispecific antibody. So this is a drug candidate that we worked on internally at COMPASS for about eighteen months. We nominated it as a development candidate earlier this year.

Speaker 2

We have disclosed previously that we have more potent PD-one blockade in vitro than has been reported for other drugs in the class. Over the past six months or so since we disclosed this as a development candidate, we've locked down our CMC process. I think one of the things that we have not talked much about at Compass is we've developed a fair amount of proprietary know how around bispecific manufacturing and our manufacturing process has commercial level yields for this drug already before we're in Phase one. We're on track to file our IND in The US in Q4 of this year. Today, we're announcing some really interesting preclinical head to head comparisons of CTX-ten thousand seven hundred twenty six with ivonesumab.

Speaker 2

These next three slides are, of course, complicated preclinical experiments, and I'm going to go through these in some detail. In this study, we're using a transgenic mouse model that expresses PD-one and PD L1 as human. So the extracellular domains of PD-one and PD L1 are knocked in as human, so you can directly test human targeted checkpoint inhibitors in this experiment. Importantly, though, there's no human VEGF in this experiment. I'll come back to that point in a minute.

Speaker 2

Here we're directly comparing the PD-one blocking arms of ten thousand seven hundred twenty six with ivanesumab. And you can see that in terms of tumor control in this mouse model, in a head to head study ten thousand seven hundred twenty six is superior to ivenesumab. For those of you who are looking at these graphs very carefully, you can see that the control and ivenesumab arms end at week twenty eight, because those animals had to be sacrificed due to uncontrolled tumor growth. On the next slide, in the same model, we compare 10,726 directly with pembrolizumab. So again, this experiment is simply testing the PD-one blocking arm of ten thousand seven hundred twenty six and comparing that head to head with pembrolizumab and ten thousand seven hundred twenty six is equivalent to pembrolizumab in this study.

Speaker 2

The next slide is a little bit more complicated experiment. So this is a xenograft experiment in which a human tumor, a non small cell lung cancer model called HCC eight twenty two is injected into mice. That tumor secretes human VEGF A. So this experiment tests both PD-one blockade and VEGF A targeting. These experiments, of course, are done in immunocompromised mice.

Speaker 2

So a human immune system is added back to the mice. PBMC is peripheral blood mononuclear cell. So on the bottom left, you can see the control in black, bevacizumab and ivaneseumab are about the same in this experiment, and the best drug in this head to head experiment is CTX-ten thousand seven hundred twenty six. As I mentioned earlier, we will be presenting these data at a scientific meeting later this year and filing our IND, which is on track for Q4. So on my last slide, we have some updated milestones here.

Speaker 2

And I think over the next six quarters, we have an incredibly rich milestone list here. So let's start with Tavessimig. In Q1 of the coming year, we'll read out our important progression free survival and overall survival from our randomized study. I would imagine that that readout would be followed by a very robust interaction with the FDA, which would put us into a position to potentially file a license application in the 2026. Of course, we have fast track status, fast track designation.

Speaker 2

So I would anticipate that we would get a priority review. We will be initiating our planned basket study for Tavessimig following that analysis in patients with DLL4 positive tumors, including potentially gastric cancer, ovarian cancer, hepatocellular cancer, etc. Still working on that design, but that study should be ready to go in the coming months. For CTX-four seventy one, we're planning to initiate our NCAM positive basket study later this year. That biomarker was discovered in the phase one study of CTX-four seventy one and we presented scientific data after that drug twice last year.

Speaker 2

And then finally for 08/1971, very important update on that program today. Next step is initiating the cohort expansions in patients with non small cell lung cancer and triple negative breast cancer. Those cohort expansions will begin later this year with clinical data from that those cohort expansions next year. Hopefully presenting the dose escalation data at a scientific meeting later this year. Finally for 10/1926, the preclinical update that we've provided today, We're going to present that data at a scientific conference later this year, IND filing in Q4, which should put us in a position to read out clinical data next year.

Speaker 2

And lastly, we also as part of our disclosure today, we ended Q2 with $101,000,000 in cash, which is cash runway here at Compass into 2027, executing on all these programs and delivering the milestones that you see here. So with that, thank you again for joining the call today. I'm happy to take questions.

Operator

Thank Our first question is from Andrew Barron with Leerink Partners. Please proceed.

Speaker 2

Hi.

Speaker 3

Just two questions from me. You're allowing crossover on the PAC arm to divasimig. So is there any chance that decreased deaths you're seeing reflects performance tosesimig from the drug crossover? Can you give us any idea how many patients are crossing over on progressing from the control arm? And then you mentioned interacting with the FDA, any comments on potential breakthrough designation?

Speaker 3

And then I have one on the DLL4 biomarker testing after that.

Speaker 2

Okay, two important questions. Thanks Andrew. So on your first question I just went back to the study schema. So yes, we allow progression. Mean, we allow crossover in the control arm following centrally confirmed progression.

Speaker 2

I'm gonna answer your second question next. Ballpark about half the patients crossed over in the control arm. So the statistical methodology that we're using, it's called the rank preserving structural failure time was the same methodology used in the IDH one inhibitor analysis in biliary tract cancer. That statistical analysis adjusts the overall survival analysis for crossover. Is the defined primary method of analysis of the overall survival endpoint.

Speaker 2

In terms of the general first question, I think potentially the answer to your question is yes. Potentially, even in patients treated in the third line setting, Tavessimid could be extending overall survival. Wouldn't that be fantastic? Because if you look at the presentation of the CLARITY data, the rank preserving structural failure time, that analysis was a little bit better than the intent to treat analysis, which indicates that the drug was active even after crossover. Now, in our presentation of the overall response data, and that data are currently in our corporate deck on our website.

Speaker 2

The rate of progressive disease at week eight was substantially different in the control arm than in the combination arm. Forty two point one percent progression at week eight versus sixteen point two percent progression. So it doesn't seem like paclitaxel alone is particularly effective. So happy to take your additional question, Andrew.

Speaker 3

Yep. And then just on BTD, any thoughts about doing that or would it not be if you're you're waiting for the OS analysis, would there not be any real benefit to applying for that at this

Speaker 2

point? Probably. Yeah. I know. I think we'll that's sort of a work in progress, but it's obviously something we would, you know, we're thinking very, very, very seriously about.

Speaker 3

Okay. And then just wondering, the DLL4 biomarker testing, how has that changed from that which was employed in some of the Korean trials?

Speaker 2

It's the same. We tech transferred that analysis into The US and we're using we used that And we're continuing to use that in the evaluation of biopsy specimens from some of the studies that we've done.

Speaker 3

Okay. Thank you.

Speaker 2

Thanks.

Operator

Our next question is from Maury Raycroft with Jefferies. Please proceed.

Speaker 4

Hi. This is Amin on for Maury. Thank you for taking our questions. Couple of questions from us. You mentioned the PFS always analysis happening in 1Q twenty six.

Speaker 4

Can you clarify whether enough events might come in during Q4 to allow for analysis in early q one? Or are you expecting that 80% of event threshold to actually be reached in q one itself? And I have a follow-up.

Speaker 2

Sure. Thanks for the question. I that's a very hard question. You know, what we had originally projected is that we would 80 we would hit the 80% event threshold by the end of q three. What we know today is that's not gonna happen.

Speaker 2

So beyond that, it's almost impossible to project accurately. And what we have simply said is we believe that the analysis will read out in q one.

Speaker 4

Alright. Sounds good. And when it comes to the readout, should we should we be thinking about a full dataset release, or will some of the data be held back for medical meeting presentation?

Speaker 2

Yeah, I think we're planning to present a priority data set at that time, which would be PFS, OS, demographic data and top line safety data with the rest of the data to be presented at a medical meeting.

Speaker 4

Okay, very helpful. Thanks.

Operator

Our next question is from Michael Schmidt with Guggenheim. Please proceed.

Speaker 5

Hey. Good morning. Thanks for taking my questions. I had just a logistical question, so if the companion two study in fact succeeds on PFS and OS, I guess what else needs to be done to support a possible BLA submission around CMC, for example? How far along are you with some of the other sections that are required for BLA submission?

Speaker 5

Sure.

Speaker 6

And then

Speaker 5

I had a separate question on AB three seventy one.

Speaker 2

Okay. Thanks, Michael. Yeah, great question. Our so called PPQ batches process performance qualification, the batches that are required for a BLA submission are all underway. So our CMC process should be very much locked down.

Speaker 2

That should not be limiting.

Speaker 5

Okay, great. And then, yeah, on 08/1971, interesting new data here today. Yeah, could you just provide some additional commentary on the dose level where these responses were seen? And yeah, have you seen any other patients with tumor size reduction? Or in fact, I think you mentioned two other patients with long term stable disease.

Speaker 5

Did you see tumor shrinkage in those as well?

Speaker 2

So a couple questions there. The non small cell lung cancer response was at the zero point three milligram per kilogram dose level and the triple negative breast cancer response was at the three point zero milligram per kilogram dose level. We're not releasing any other clinical data at this time. Again, to present all of that data at a scientific meeting later this year, including the patients from the ten mgkg cohort.

Speaker 5

Okay, anything else you can share on the treatment history of the two case studies? Obviously they did have a PD-one inhibitor before but anything else you could share there?

Speaker 2

Yeah, most of these patients, sort of a typical phase one population, lines of therapy. This patient with triple negative breast cancer had three lines of therapy in the metastatic setting, including previously some neoadjuvant and adjuvant therapy. So typical phase one population heavily pretreated all the patients in the study having received prior therapy with a checkpoint inhibitor.

Speaker 5

Great, thank you.

Operator

Our next question is from Birun Amin with Piper Sandler. Please proceed.

Speaker 7

Hey, yeah, hi guys. Thanks for taking my questions. Maybe just to start Tivesamag. Your projections for the OS analysis and timelines for Q1, is that based on the current event rate that you're seeing? You mentioned that the event rate had slowed since your projection earlier this year.

Speaker 7

Or is the projection based on a lower event rate from what one would anticipate? I guess I'm trying to assess confidence on the Q1 analysis.

Speaker 2

Yep, great question. So I think the short answer to your question, Biren, is yes. Our projection is based on the current mortality rate that we're seeing. And I think over the last approximately four or five months, we've clearly seen a decrease. So we're basing the q one projection on, the current rate.

Speaker 7

Got it. Okay. And then as far as the phase one IST, any update on that in terms of when we can expect first data from the quadruplet combination?

Speaker 2

No, I don't have an update on that study at this time. That study is enrolling patients at MD Anderson, but I don't have an update today.

Speaker 7

Okay. And then I do have several questions on 8,371. Congrats on the data in the dose escalation cohort. So I just wanted to maybe ask for the non small cell lung cancer patient, the patient had zero centimeters of tumor. Why is that patient not considered a complete response?

Speaker 2

Yeah, that is a great question. And actually that question applies to the triple negative breast cancer patient as well. Because so with this patient, this patient had some non target lesions that did not qualify the patient as a CR. For the triple negative breast cancer patient, the target lesion three is actually a lymph node and a lymph node less than ten millimeters in the short axis, and this is seven. By resist one point one is not pathological.

Speaker 2

So this patient's target lesion response was actually read as a CR. This patient also had non target lesions that did not disappear. So because of that, this patient is a resist PR.

Speaker 7

Got it. And then maybe just a few more on A371. You mentioned that the triple negative patient had prior pembro. What about the non small cell lung cancer patient? Did they have prior PD-one?

Speaker 7

And what was the therapy? Then also, can you talk about what their PD L1 status was when they received 8003 and '71?

Speaker 2

Oh, what a great question. So the answer to that question is I don't know. We did not read biopsy patients before the phase one study. I do know that the non small cell lung cancer patient at their diagnosis, so take that for what it's worth, had a very low PD L1 expression. But we did not re biopsy patients for the phase one study.

Speaker 7

Great. Thank you.

Operator

Our next question is from Steven Willey with Stifel. Please proceed.

Speaker 8

Hey, good morning guys. This is Tully on for Steve. Congrats on the progress. I just have two questions, one on toposimic, one on CTX-ten thousand seven hundred twenty six. Just to start with the Tombosemic, Tom, like, I know that you will present patient demographics later when, you know, both PFS and OS analysis are ready.

Speaker 8

But, like, the fact that you haven't accrued enough, like any death events, how confident are you that these patients are actually reflective of historical clinical trials and just read the real world data. So, that's the first question. Second question on the PTX10-seven 26. By the way, very nice, impressive preclinical data in terms of tumor shrinkage. What can you say about the safety data?

Speaker 8

And are you guys planning to present any preclinical data like prior to or soon after IND submission? Thank you.

Speaker 2

Thanks, Thule. A complex first question about demographics in this study. I'll simply say, you know, it's hard to know without the final data set, you know, and, you know, cross trial comparisons to demographics. I think I probably can't act can't really answer that. I think I'll simply say that the randomization in this study was stratified by three important prognostic variables.

Speaker 2

Performance status zero versus one, metastatic disease outside the liver. Yes or no. The vast majority of these patients had metastatic disease outside the liver, something like eighty percent. And it was finally, it was stratified by anatomic subtype intrahepatic cholangiocarcinoma or other. So, because the randomization is stratified, I think the demographics in the two treatment arms will be very well balanced.

Speaker 2

So, you know, I think that's very important. Yeah, thanks. Thanks for your comment on 10/1926. Yes, we will be presenting scientific data for 10/1926 at a scientific conference later this year.

Operator

Our next question is from Aden Hosunov with Ladenburg Thalmann. Please proceed.

Speaker 6

Hi, good morning. Congrats on the progress this quarter. A couple of questions from us. So first on tovezumab, the question is about the duration of response in the tovezumab arm of the trial. Could you provide any comments on the duration of response and are these patients who initially responded still on the trial?

Speaker 2

Thanks, Aidan. So I went back to the study schema here. So we don't have any analysis of duration of response at this time, because in the statistical methodology, the first two secondary endpoints to be analyzed are PFS and then OS. So duration will be the last secondary endpoint analyzed. So I don't have any information on that.

Speaker 2

Don't most of the patients are in survival follow-up. I have a number today on how many patients are still on the study. I'm sorry about that, Aiden.

Speaker 6

Okay. That's okay. Another question is on VEGF PD-one bispecific. So I'm just trying to understand how the future is going to look like for these assets. In the future, how do you see the regulatory path for your VEGF PD-one?

Speaker 6

And is it going to be as a single arm path or like a head to head to pembro or nevo? Just curious about your thoughts on this.

Speaker 2

Sure. You know, I think great question, obviously. So I think the way we've been thinking about this is I think the regulatory path depends on very thoughtful indication selection. And where our thinking is with this drug is where we want to explore indications where both VEGF targeting and PD-one targeting as mono therapies have been demonstrated to be effective. So what are some of those?

Speaker 2

So renal cell, nivolumab and VEGF kinase inhibitors, gastric cancer where the VEGF receptor blocking antibody, Simraza is approved, as well as PD-one targeted agents. Obviously, hepatocellular cancer, bevacizumab and atezolizumab are frontline standard of care. Maybe something like endometrial cancer, where VEGF kinase inhibitors have also been shown to be effective. And I think for some of these indications, say, the post PD-one VEGF patient with renal cell cancer, I think those could be single arm pathways to approval. I think the non small cell lung cancer indication is going to be obviously, as you know, incredibly competitive, and we would probably not go there first.

Speaker 6

Okay. Thank you. Very helpful.

Operator

Our next question is from Robert Driscoll with Wedbush Securities. Please proceed.

Speaker 9

Thanks. Good morning, Tom. Thanks for taking the question. Maybe just a follow-up on Biren's question. For the 8,371 expansion cohorts, do you expect to select patients based on PD L1 expression at this stage?

Speaker 2

So we don't. We expect to leave the selection criteria the same as for the dose escalation portion of the study.

Speaker 9

Okay and then anything you can say with regards to immune related adverse events here kind of acknowledging we're still in dose escalation.

Speaker 2

Sure. Yeah, you know, it's interesting. We believe that the way this drug might work, although we have some data to support this preclinically, ultimately, we're going to need a lot more data to support what I'm about to say. So just that caution. We believe that this drug could be anchored in the tumor microenvironment by PD L1 where it can provide very high concentration PD-one blockade in the tumor microenvironment.

Speaker 2

So I'll simply say that in the first four dosing cohorts, we've not seen any dose limiting toxicities. And look, as a next generation checkpoint inhibitor, there's no reason to believe that the safety profile might not be better.

Speaker 9

Got it. Looking forward to the update here. Thanks, Tom.

Speaker 2

Thanks, Robert.

Operator

Our next question is from Sean McLetchon with Raymond James. Please proceed.

Speaker 10

Hey, guys. Thanks for the question. Just a couple from me. How are you thinking about the necessary magnitude of benefit over paclitaxel on PFS, given that paclitaxel not a commonly used chemo in second line biliary tract cancer? And what gives you confidence that you've cleared the PFS bar for clinical adoption over FOLFOX?

Speaker 10

And then separately, could you give us some context on kind of how you're thinking around OS and how FDA may be approaching OS? What you need to see as a trend on an ITT basis versus a crossover adjusted basis? Thanks.

Speaker 2

Thanks Sean. So for the first question, I have sort of a two part answer perhaps. So the first part, I'll simply summarize what the statistical power calculations are for the PFS analysis. So, the PFS analysis is 80% powered for a hazard ratio of approximately So a hazard ratio of 0.6 or lower would I think obviously be spectacular.

Speaker 2

You know, I take your point about paclitaxel and I think our overall response rate data where we had forty two point one percent radiographic progression in the paclitaxel arm at week eight suggests that the median PFS in the paclitaxel arm is going to be in the two to two point five month range, about the same as has been seen with FOLFOX, for example, in the FOLFOX versus FOLFORY randomized trial. We recently completed some market research that was done by sort of a very well known leading market research firm. And I think we were very pleasantly surprised at the KOL feedback on PFS from that market research, which frankly, suggests that a hazard ratio of point six would be off the charts. So, you know, KOLs, you know, be happier, just given what they know about full fox, you know, you know, with, you know, even less benefit. But a hazard ratio of point six would be, incredible.

Speaker 2

The second question, I don't have any information on your second question. Never got any specific feedback from FDA about the difference between the ITT analysis and the RPSFT analysis of overall survival.

Speaker 6

Understood. Thanks.

Operator

Our next question is from Joe Pantginis with H. C. Wainwright. Please proceed.

Speaker 11

Hey Tom, good morning. Thanks for all the details today. First on tovecimig, first a logistical question. Can you just remind us the level of meetings that you've already had with the FDA and what is planned and what role the potential for accelerated approval based on response rates have had in those discussions, number one. And then number two, obviously there's a lot of talk here about the control arm.

Speaker 11

There's a lot of variables that are in this study. You've obviously talked about, it doesn't seem like paclitaxel and the control arm is contributing to anything with regard to the data you're seeing. So with that, I wanna ask about what are your thoughts on the perceived risk of any better than expected impact from the control arm, specifically from the fact that obviously these patients are receiving excellent clinical care? Mean, I sounds like a rhetorical question, but I just wanted to get your views on the procedure.

Speaker 2

Yeah, sure. Thanks, Joe. Maybe I'll take the second one first. So, again, in terms of the control arm, again, I'm going to go back to the rate of progressive disease in the control arm at week eight. Forty two point one percent radiographic progression at week eight.

Speaker 2

So we already have substantial progressive disease at week eight. And PFS, of course, is defined in the standard way, either radiographic progression or death. We, of course, have not done any analysis of PFS, in the study, you know, we're, you know, trying to be very rigorous statistically. But just based on the rate of progression at week eight, it doesn't seem like we're seeing something outlandish in the control arm. In terms of a formal interaction with the FDA, we had a formal interaction with the FDA regarding the design of this study.

Speaker 2

So that was, of course, some time ago. So we would, plan to have a much more robust and formal interaction with the FDA after we get the PFS and OS readouts from the study in the '26.

Speaker 11

I appreciate that. And then just quickly on 08/1971, can you take any broad strokes right now about the design and or numbers expected within the dose expansion cohorts for the two indications stated?

Speaker 2

Sure. Yes. So what we're currently planning, you know, in patients with triple negative breast cancer and non small cell lung cancer, a randomized study to two doses, you know, small randomized study, something like 50 patients ballpark, you know, in order, you know, to start to explore a couple of doses. Have not picked the doses yet, because we want to get all the data from the ten mg per kg dose level. We should have most of that data by the end of this quarter, which would put us in a position to initiate those cohort expansions in Q4.

Speaker 11

Got it. Thank you, Tom.

Speaker 2

Thanks, Joe.

Operator

There are no further questions at this time. I would like to turn the floor back over to Tom for closing remarks.

Speaker 2

Great. Thank you so much. And I'm just going to go to the last slide here again. Thank everyone for joining today and just highlight what the next twelve to eighteen months could look like for us. Read out from our randomized trial in patients with biliary tract cancer, followed by a robust interaction with FDA, and then potentially a license application, which would obviously be incredibly exciting.

Speaker 2

Couple more clinical trials with Tavasimig and four seventy one. And I think really exciting today, our cohort expansion for 08/1971. And as I mentioned earlier, we have always positioned eight thousand three hundred and seventy one to be on the cutting edge of defining next generation checkpoint inhibition. And the data that we've reported today really puts us on track to achieving that goal. And then lastly, our P1 VEGF A bispecific antibody 10,726.

Speaker 2

We have preclinical differentiation, from ivanesimab, Really looking forward to getting that drug into patients in 2026 and reporting, phase one clinical data. Thanks again, everybody. Happy to follow-up, with any questions, that any, of you folks, might have.

Operator

Thank you. This will conclude today's conference. You may disconnect your lines at this time, and thank you for your participation.

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