All right. Good morning, everyone. I'm Stephen Willey, one of the senior biotech analysts here at Stifel. Glad to have with us from Compass Therapeutics, CEO Tom Schuetz. Tom, I know we got a lot to cover here. I'm just going to jump right into Q&A. Appreciate you taking the time to do this, as always. Sounds great. Thanks for the invitation. Yeah. Let's start with COMPANION-002. You disclosed the secondary endpoint data last month. Obviously, a very statistically significant and clinically meaningful improvement on PFS with tovecimig. We did see a numerical detriment to intent-to-treat overall survival, clearly impacted by this unexpectedly outsized benefit in patients who were crossing over from the control arm. Maybe you can just start by contextualizing these results relative to second line standard of care treatment options. I know you've had some more time to maybe process and think about the data. Do you have any additional hypotheses about why these crossover patients ended up with a median overall survival that more closely resembles what you would expect to see with first line standard of care therapy? Okay. Many questions embedded in there, but need to just take one thing head-on. We did not see a numerical detriment. That needs to be stated clearly and unequivocally from the beginning. The hazard ratio is not known to be above one, just period. I think that's very important. The P value was 0.78, right? If the hazard ratio were 0.95 with a P value of 0.78, and I said that there was a trend toward improved overall survival, that would be laughable. Right? The hazard ratio was driven by an incredible effect of the drug in the control arm. The problem with the intent-to-treat analysis is the so-called control arm is a mix of two very different sets of patients. One group of patients that got chemotherapy alone, and one group of patients that got chemotherapy plus the active drug. The nominal hazard ratio is simply a reflection of an effect of the drug in the patients who cross over to receive the drug. Frankly, we view it, I certainly view it as evidence of an effect of the drug on overall survival. You mentioned we've had a lot of time with the data. I've talked to investors. One investor recently said to me, he goes, "If the hazard ratio were 0.85, and you found by analyzing the control arm that the patients who crossed over to receive tovecimig did much worse, and that's what drove the hazard ratio to 0.85, that would not be good for you." I fundamentally agree with that. I think we believe strongly that the data suggests that we actually have an effect on OS, and you asked me to contextualize it, which I think is a very important part of your question. In this patient population, second-line BTC, 3-drug chemotherapy regimens in multiple different studies, ABC06, the CHOI randomized trial, have median OS of around six months, right? If you look at the median OS of patients in our study who received tovecimig plus paclitaxel, the median OS is 9.9 months. Clearly, we're seeing something different than with those other trials. Fascinatingly, if you look at the patients who received paclitaxel alone, their median OS was 6.1 months, straight in line with what you see with other chemotherapy regimens in this disease. Now I just want to comment on one other thing. You mentioned in the very first sentence of your question that we reported the secondary endpoint data. Let's keep in mind that we already hit the primary endpoint. Of overall response rate. The study by definition is positive, and as you know, the vast majority of drugs in oncology that are approved in the U.S., something like 78%, think about that number, by the way, are approved based on endpoints other than OS. We feel incredibly good about our planned FDA interaction this summer, and we're preparing and continuing to prepare for a Biologics License Application to the FDA in the second half of this year. Okay. As you prepare for those discussions, what do you think the primary discussion points with FDA will be about? What sort of additional analyses do you need or want to execute between now and those discussions happening to, I guess, bolster the value proposition of tovecimig in this treatment setting specifically? Sure. A topic of discussion will be full approval versus Accelerated Approval. Our regulatory consultants have advised us to seek full approval, based on the data we have. At the end of 2025, there was an extremely important meta-analysis published in the journal Hepatology, which was a meta-analysis of BTC studies, which showed a correlation of PFS with OS in this disease. Which is not surprising because, unlike many other solid tumors, these patients die of anatomic complications in the biliary tree. Biliary obstruction leads to, unfortunately, death in these patients. Preventing a tumor from getting larger is probably of great clinical benefit for these patients. We hit the primary endpoint, hit the key secondary endpoint of PFS, OS clearly affected by crossover. We have a solid argument for full approval. If the conversation is Accelerated Approval, this is exactly what the Accelerated Approval regs are designed for. Unmet needs with endpoints like ORR and PFS. I'd be happy to have that discussion with FDA. Okay. I know when we were trying to go back and look at some of the regulatory precedents around the way that FDA has handled intent to treat overall survival data. There appears to be a couple of different versions of the agency. Yeah Emerged, right? There's the version that kind of put a flag in the ground around, you cannot have an intent-to-treat hazard ratio of greater than one. That was PSMAfore, that was TIVO-3. You've got this other version of FDA that went ahead and approved data from the TROPION-Breast01 trial. Yep With a hazard ratio on overall survival, which was a co-primary endpoint. No crossover. No crossover of greater than one. Yep We've saw these decisions happen contemporaneously from FDA, right? Yeah. They were being stringent around PSMAfore, yet two months before, they had granted approval to Dato in, I think it was January 2025. What version of the Agency do you think? Yeah You're going to be dealing with when you meet with them this summer? Are there other analogs that you would point to as potential surrogates for this case for leniency? Yeah. Maybe other examples here, crizotinib or olaparib, sotorasib, COPIKTRA. There are many examples of this. You asked sort of a two-part question here. Believe me, I'm not living inside of a cave. I know that there have been lots of perspectives on FDA. I'll just give you my perspective. I've not seen any changes in FDA for us. Our medical reviewer for the IND is the same. We're in the same division. It's the same people that we've been dealing with for the last four or five years. I don't really see any difference for us. I would love to maybe challenge you on your use of the word leniency here. Again, if you're doing a straight-up randomized trial and you lose, you need leniency. If you do a randomized trial with crossover, and those crossover patients do incredibly well, you don't need leniency. It's a good point. I will strike leniency from my vocabulary. Okay As it pertains to FDA's consideration. All good. You talked about the prospect of a potential Accelerated Approval. What does a confirmatory study look like? Have you thought about that at all? How quickly could you get that trial off the ground? Sure. We spent a little time thinking about that. I think, maybe as some very preliminary thoughts here, I'll give you two examples of a confirmatory trial. One would be a second-line study, which would be tovecimig paclitaxel versus FOLFOX. That's a very simple design. That's a straight-up overall survival trial. Probably, let's make the math easy, six versus nine. Powered for a hazard ratio of something like that, right? That's probably a study that we would do ex U.S., because the one thing we would absolutely have to avoid in that study would be patients from the FOLFOX arm crossing over to receive commercial tovecimig pac, right? That's one example. Another example, which is probably a larger study and a longer study, would be a frontline study where we added tovecimig to a frontline regimen like Gem/Cis/Durva. That is the study that's ongoing at MD Anderson. Not a randomized trial, it's a single-arm trial. We're getting early safety and efficacy data from that study, and that would help inform our design of a frontline study. Those would be two examples. I think they both have some pluses and minuses, but those are our preliminary thoughts so far. Okay. Is there a chance that any of that frontline MD Anderson data gets submitted to FDA as a supportive piece of evidence in your conversation with them in terms of just substantiating the benefit of this drug? I know it's an open label trial. Yeah. I know it's investigator-sponsored. Yeah. I don't know the answer to that. We have, as part of our routine, required annual reporting to our IND, included safety data from that study in our annual reports to FDA. That's an interesting question. Maybe, but I'm not sure. Okay. Maybe you can talk a little bit about what the framework for communicating this FDA feedback to investors will look like. I'm guessing you'll probably disclose when the meeting is scheduled. Is that a fair assumption? I'll just give you a ballpark timing. Right now, May 20th, we're just finishing up our analyses of some of the data from the study. Ballpark meeting request by the end of this month, so just call it approximately June 1st. 30 days later, approximately July 1st, meeting package goes in. Meeting is probably scheduled for approximately the first week of August. I think we should have written feedback from the FDA, I would think certainly by Labor Day. I think I would like to be able to say exactly what I said to you earlier. I'd like to be able to say, FDA agreed that the data support the submission of a Biologics License Application, which we intend to initiate in the fourth quarter of 2026. That's what I'd like to be able to say. Okay. I think one thing that you asked me earlier that I think is important also is that we're currently doing some additional crossover adjusted statistical analyses. There are several other statistical analyses that can be used. to adjust for crossover, and we're doing some of those. I think as you know, the IDH1 inhibitor, TIBSOVO, the addition of the crossover adjustment was a post hoc addition to that study. We're doing those to see if anything is teased out by that. Okay. Yeah, I know there's certainly regulatory precedent for post hoc analyses. Yep. I believe AstraZeneca, in its post hoc analysis of the TROPION data, actually tried to argue that there was a proportion of patients who post-progression ended up receiving another topo containing ADC. When you backed out those 20% of patients, you had this demonstrable improvement in hazard ratio. I don't know to what extent FDA. Actually considered that. Interesting. Okay There is precedence for post hoc analyses. Yeah As you're fully aware of. Yeah, we're continuing to follow the patients for OS, and sometimes that changes as well. Maybe we can switch gears to the pipeline. I know you're going to be presenting CTX-8371 data for the first time at ASCO. You've qualitatively spoken about the deep and durable responses that you've seen in a few different tumor types. What else should we expect to be presented at the meeting? Should we expect a meaningful amount of dose expansion data? Any color you can provide around what that presentation might look like, and then if you can also just speak to what we should expect to see at ASCO in the presentation itself relative to what gets put in the abstract. Sure. Yeah, we're super excited about our PD-1/PD-L1 data. That's going to be presented at ASCO on Saturday the 30th, 10 days or so from now. What will be in the poster is full analysis of the dose escalation cohort, full safety data. Drug incredibly well-tolerated with no dose-limiting toxicities and a full update on the early efficacy signals. Something that we have not showed previously are the PET scans from the patient with Hodgkin's lymphoma, which look super cool in that patient at a very deep metabolic PR. We're also going to update the durability of the two responses at the highest dose levels, the Hodgkin's lymphoma patient and the triple-negative breast cancer patient. The triple-negative breast cancer patient has now been on drug for more than a year. With a durable and deep response that is continuing. We'll present that. The cohort expansion data that you mentioned. Based on the three responses that we saw, non-small cell lung, triple-negative breast, and Hodgkin's lymphoma, we initiated cohort expansions earlier this year in those three indications. That study's enrolling quite well. I think we've got more than 10 patients already enrolled in the cohort expansions, so we'll have some early safety data from that. Just based on scan timing, we're not going to have any efficacy updates for the cohort expansions, and we'll probably update the efficacy data from the cohort expansion patients later this year. Okay. Maybe you can just speak a little bit. I know that these were all heavily pre-treated PD-1 experience patients. Can you just speak a little bit to the mechanism with respect to why you believe you're able to resensitize a response in these patients with a PD-1, PD-L1 drug? Sure. Yeah, thanks. Boy, that's a very scientifically complex question for sure. I think when we initially discovered that drug, we did a screen for synergy with PD-1 blockade, and we used our StitchMabs technology to screen bispecific drug candidates. Quite fascinatingly, what emerged from that screen is that PD-L1 blockade is the best partner for PD-1 blockade. Because that was a little unexpected, we spent a long time investigating the mechanism of action, and we found a couple of very interesting things. First of all, in addition to both dual ligand and receptor blockade, that drug is unequivocally a cell engager. That's one very important part of it. The most interesting thing scientifically is that the bispecific exposes a metalloproteinase cleavage site on PD-1, leading to the cleavage of PD-1 off the surface of effector T cells. This drug actually converts PD-1 positive T cells into PD-1 negative T cells. We also block the cis inhibition of CD80 by PD-L1 with our unique PD-L1 binding component of the drug. This drug frees CD80 to agonize CD28 in the draining lymph node in the tumor microenvironment. It's a very unique mechanism of action. Other PD-1 or PD-L1 blocking drugs don't do any of those additional three things. Okay. Will there be any translational or biomarker data that you might be able to present to support this unique mechanism? Not at ASCO. Okay. We're working on that. We have monkey data that confirmed PD-1 cleavage that we're ultimately working on publishing that as well. We also will be doing some translational work in this study to help investigate those mechanisms of action in humans. I think Hodgkin's lymphoma is a very unique place to study that because I think Hodgkin's lymphoma is the malignant cell. The Reed-Sternberg cell has a locus amplification of PD-L1. It's a PD-L1-driven malignancy. If we can show responses in more patients with Hodgkin's lymphoma in the dose escalation, the response was one of one patient treated. If we can show more responses in patients with Hodgkin's lymphoma and really start to tease out the mechanism of action a little bit better, I think that would be super interesting work that we could do. Agreed. How are you just thinking about next steps for this program? I know you've intimated a desire to perhaps want to try to combine this with other assets in the pipeline. Do you need to have that single agent dose expansion data in hand before you initiate any of that combination work, or is that something that you can start in parallel? Two-part question. For the first part, next steps. The cohort expansion, those cohorts are reasonably robust. Triple-negative breast cancer, 28 patients, 14 each at the two top dose levels of three and 10 mg/kg. Non-small cell lung, the same, 28 patients, 14 at two doses. 12 patients with Hodgkin's lymphoma, six at each of those two doses. It's 68 more patients, and that will give us a really good data set to think about monotherapy paths to approval. Your second question is much more interesting to me. I'm going to give you a very hard no to your question. We are not going to wait to initiate some combination studies. What we're really interested in doing is combining CTX-471 with tovecimig. We've got some designs on the table right now. Next weekend at ASCO, we've got a series of meetings with investigators talking about those studies and how we think about combining CTX-471 with tovecimig, just to amplify, if you will, the original observation of Avastin plus TECENTRIQ in hepatocellular. That, in my mind, was the study that really suggested that combining checkpoint inhibition with angiogenesis disruption is a meaningful therapeutic combination. With tovecimig plus CTX-471, that's both plus. Double angiogenesis inhibition, double checkpoint inhibition, and that's a combination that we're really excited about. You're also mechanistically pursuing that biological combination or that biology through CTX-10726. Yes. This is a PD-1 VEGF-A. I think you've guided to having some dose escalation data in the back half of this year. Yep How are you just strategically thinking. Yeah About this program right now, how you resource it Yep Where you think you may have an opportunity for differentiation? We developed that drug internally, as you said, a PD-1 VEGF, a bispecific antibody. We'll see data from other drugs in that class at ASCO, of course, next weekend. We thought about when defining our phase I indications, we picked four indications where either checkpoint inhibitors or angiogenesis inhibitors have demonstrable efficacy signals. We picked hepatocellular, bevacizumab, gastric, ramucirumab and atezo, renal cell, cabo/nivo, and endometrial, lenvatinib plus nivo. Just thinking about those four indications, that's where we're going into in our phase I study. Look, honestly, I always admired what Regeneron did with LIBTAYO. When the PD-1 field was incredibly competitive, Regeneron found an indication, cutaneous squamous cell cancer of the skin, and they got LIBTAYO approved with a very thoughtful development program. I think every other drug in this class is going after non-small cell lung cancer. We're trying to think a little bit more creatively about clinical indications. Yep. Interestingly, LIBTAYO leveraged that foothold in melanoma into a label- Exactly turned into a big oncology. Yes. By the way, phase IV study is much easier. Yep. Maybe just last question here. Can you just speak to the current balance sheet and what that allows you to execute on here? Yep. $195 million at the end of Q1, which is runway into 2028. That's preparing for the tovecimig launch next year in the U.S. That is all of the cohort expansion study for A371, our NCAM-positive basket study for CTX-471, which we didn't talk about, and our full phase I program for CTX-10726. Feel very good about our cash runway, and it'll allow us to execute and hopefully deliver some transformational data for each of these four drugs that we have in the clinic. All right. Very good. Appreciate the time, Tom, and I'm sure our paths will be crossing at ASCO here in the next week or two. All right. That'd be awesome. Great. All right. Thanks so much again, Steve. All right. Take care. Take care. Thanks, everyone.