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spk14: Good afternoon and thank you for standing by. Welcome to CENCOR's third quarter 2023 conference call. Please be advised that this call is going to be recorded at the company's request. Now, I would like to turn the call over to your speaker today, Charles Lyles, Head of Corporate Communications and Investor Relations. Go ahead, Charles.
spk04: Thank you and good afternoon. Earlier today, we issued a press release which outlines the topics we plan to discuss today. It's available on www.cencor.com. Providing comments on the call is Basil Dahyad, President and Chief Executive Officer, and Nancy Valenti, Chief Development Officer. Afterwards, we will open up the call for your questions, and we'll be joined by John Desjarlais, Chief Scientific Officer, and John Cush, Chief Financial Officer. Before we begin, I would like to remind you that during the course of this conference call, Zencore Management may make forward-looking statements, including statements regarding the company's future financial and operating results, future market conditions, plans and objectives of management, future operations, the company's partnering efforts, capital requirements, future product offerings, and research and development programs. These forward-looking statements are not historical facts, but rather are based on our current expectations and beliefs and are based on information currently available to us. The outcome of the events described in these forward-looking statements are subject to known and unknown risks, uncertainties, and other factors that could cause actual results to differ materially from the results anticipated by these forward-looking statements, including but not limited to those factors contained in the risk factors section of our most recently filed annual report on Form 10-K and quarterly report on Form 10-Q. With that, I'll pass the call over to Basil.
spk05: Thanks, Charles. At CENCOR, we're advancing a broad internal development portfolio of engineered antibody-based therapeutics in oncology and autoimmune disease that we've built with our array of modular, continually advancing exMAP protein engineering tools. We're taking multiple simultaneous shots on goal in the clinic, and we use emerging data from clinical studies to guide which programs we advance, which we terminate, and which we partner. A stringent review of this data and the status for competitors allows us to prudently focus our resources and cash on programs with the greatest potential. We're now focusing on the tremendous opportunity for our targeted T-cell engager bispecifics in solid tumors. The class of CD3 T-cell engagers has recently shown great potential for bringing tumor-targeted T-cell therapy to bear against solid tumors, a long-standing challenge for both antibody and cell therapy modalities. At the recent ESMO conference, our partner Amgen presented highly encouraging interim results for a phase one study of xyloridamig in patients with advanced prostate cancer. Valoratomic is an XMAB 2 plus 1 CD3 T-cell engager targeting steep 1. We created a 2 plus 1 bispecific to address a challenging target with limited extracellular exposure. Amgen reported that during dose expansion and optimization, a 41% resist response rate has been seen in high-dose cohorts, and that preliminary durability, while early, is encouraging. We look forward to further updates and progress with Amgen's plans for additional studies and earlier lines of treatments. Enhanced customization afforded by the 2 plus 1 format enables antibodies to bind more avidly to and selectively kill those tumor cells with higher antigen density, potentially sparing normal cells. As a consequence, opens the door to a wider range of solid tumor targets than were previously accessible to T cell engagers. And leading our own internal pipeline for this modality in phase 1 is XMAB819, targeting EMPP3 and renal cell carcinoma. followed by eczema 541 targeting cloud and 6 and ovarian cancer and other tumors. Our second set of tumor-targeted T-cell engagers are co-stimulatory bispecifics that engage CD28 on T-cells for targeted immune activation. CD28 co-stimulation is some promise for enhancing anti-tumor immune activity, and Zencore's CD28 platform has been engineered to expand the therapeutic window of co-stem activation by using reduced-potency CD28 bindings. Our CD28 bispecific, XMAB808, which targets the broadly expressed tumor random B7H3, is in a phase one study in advanced solid tumors. In addition, this quarter, our partner Janssen, now J&J Innovative Medicine, has advanced both of our CD28 collaborative programs, submitting an IND for the prostate cancer candidate and a CTA in Europe for the B-cell malignancy one. We anticipate further expanding our pipeline of T-cell engaging bispecifics in the future. As part of our efforts to provide sufficient resources to advance these programs, today we're announcing that we have added $215 million in cash to our balance sheet from selling a portion of our royalty interests in Ultimaris and Mangevy to OMERS, a Canadian pension fund. These two products were created with Zencore's modular XMAB FC domains and technologies, which are the foundation that enables our diversified approach to building value. Our platform has been fundamental to the creation of three XMAB-based medicines marketed by partners, which have generated royalty income that further drives innovations in our protein engineering and supports the advancement of our internal pipeline. We believe that the strengthened financial position from this deal offers us additional flexibility to execute on our internal clinical development programs, the greatest potential for success. And the deal's structure lets us retain potential economic upside from the sales performance of Ultramarys and NonGD. We've also made changes to our pipeline. We're terminating development of our Phase I PD-1 by ICOS program, XMAB-104, and are closing the gynecologic tumor cohorts in our ongoing Vudalamab Phase II monotherapy study. For XMAB-104, efficacy data in expansion cohorts in MSS colorectal cancer did not meet pre-specified criteria. And for Vudalamab and GYN tumors, we see a rapidly changed competitive environment. We will keep supporting patients currently enrolled in the studies, including by continuing to provide study drugs. Now, on to F. balbur-pendicin alpha, formerly XMAB306. That's our co-development program with Genentech, where we have decided to opt out of our cost-sharing arrangement and P&L split, because as the clinical trial reach and cost of the program continues to expand, we've had to prioritize it against other highly promising programs. We're still very supportive of the program and Genentech's development plans. We elected, per the contract, to shift to a milestone royalty structure. We'll provide additional detail when the specifics are finalized, but we would anticipate terms commensurate with a license of an asset at this stage of development. As a result of the royalty deal, along with these program reductions and a continuing focus on reducing costs, we are guiding that we have cash runaway into 2027. Now for a review on our wholly owned clinical portfolio, I'll turn it over to Nancy Valenti, our Chief Development Officer.
spk01: Thanks, Basil. First, Fudalimab, our T-cell selective checkpoint inhibitor targeting PD-1 and CTLA-4. As Basil mentioned, in our Phase II monotherapy study, we have closed the cohorts enrolling patients with gynecologic tumors based on data from small cohorts in ovarian, cervical, and endometrial, where we did not see data that would support moving forward in the rapidly changing competitive landscape. We will now focus our attention on prostate cancer. both in this monotherapy study and in the study in combination with standard of care therapies. And we're on track to initiate our first line non-small cell lung cancer study by year end. In this study, we have a design that gives us an early look at safety and efficacy from two dose level cohorts in combination with chemotherapy. And this is prior to the second part of the study that randomizes against standard of care pembrolizumab and chemo. Next, with our other dual checkpoint inhibitor targeting ICOS and PD-1, XMAB104, those signs of activity in microsatellite-stable colorectal cancer were observed early on. Expansion cohorts did not meet the pre-specified activity threshold, and we are stopping program development. Before moving to earlier stage programs, one note on Pomodamab. which we licensed to J&J Innovative Medicine in 2021. We are wrapping up our internal clinical work, and we would anticipate further development activities will be done by Janssen. Now, among our internally developed cytokines, our Treg-biased IL-2FC being developed in autoimmune disease, XMAB564, continues to enroll patients with either atopic dermatitis or psoriasis in multiple dose escalation. And our potency-modulated IL-12 FC in advanced solid tumors began dosing patients in a phase one dose escalation study in the third quarter. Finally, our clinical XMAB 2 plus 1 bispecifics, which Basel introduced. Both XMAB 819 and XMAB 808 which respectively are ENPP3 times CD3 and B7H3 times CD28 antibodies, continuing dose escalation. We and the investigators remain enthusiastic about the potential of these programs. We are also on track later this year to submit an IMD for a third internal 2 plus 1 bispecific, XMAB541, a CLAWDIN6-targeted CD3 engager, to be developed in ovarian cancer and other solid tumor types. Since the CLAUDINs are so similar in structure, selecting specifically for CLAUDIN 6, especially over CLAUDIN 9, 3, and 4 is critical. The 2 plus 1 format and our protein engineering really provides for CLAUDIN 6 selectivity. And in our preclinical work, we see beautiful selectivity for CLAUDIN 6, avoiding CLAUDIN 9 and 3 and 4. especially compared to other Clawdon 6 times CD3. We're really excited about getting this molecule into the clinic, continued progress with 819 and ExMav 808, and expanding more into solid tumors with more T-cell engagers. With that, we also have one more item before moving on to Q&A.
spk05: Thanks, Nancy. First, I'll say please refer to our press release for financial results. On a related note, For 23 years, all financial functions at Zencore have been led by one person, John Cush, who has also, at some point through the years, come to oversee investor relations, facilities, IT, and CMC operations. It is impossible to encapsulate so briefly how much we have relied on John for over two decades, pulling us out of some truly dire situations over those years. As we announced last month, John plans to retire early next year in March, and we thank him for his critical role in pursuit of creating and advancing new medicines for patients. Now, with that, we'll open up the call for questions. Operator?
spk14: Thank you. At this time, we will conduct the question and answer session. As a reminder, to ask a question, you will need to press star 1 1 on your telephone and wait for your name to be announced. To withdraw your question, please press star 1 1 again. One moment, please, while we compile the Q&A roster. Our first question comes from the line of Edward Tenthoff from Piper Sandler. Your line is now open.
spk11: Great, thanks. Can you hear me okay?
spk05: You're a little staticky, but we'll try.
spk11: Okay. If I have to, I'll try to pick up the receiver. So, you know, first, John, wishing you all the best in retirement. I'm sure you're going to miss all the craziness with Baz, so it's been a ton of fun working with you. I appreciate all the color and congrats on the OMERS deal. I wanted to kind of get a little bit more of a sense with respect to PLAMO in terms of your comments about stopping internal development. Does this change, you know, the ongoing studies at all? Does this change your ownership at all? I just want to get a little bit more color what that means. Thank you.
spk05: Oh, sure, Ted. Sorry if that came off a little bit confusing. No, this is a no change whatsoever from the plan we've had with Janssen for the last two years. The plan was always that we would finish the ongoing phase one study when we completed the work with our subcutaneous formulation, and then they would just pick up all clinical development activities themselves. The deal structure hasn't changed. It's just whose hands are doing the work. That was more of an update on We've essentially finished the sub-Q phase one. We're wrapping that up. And Jensen's picking up therapy. So there's no change. Sorry for the confusion. No worries at all.
spk11: And can you just remind us what studies are ongoing for that one?
spk05: That's the phase one where we're wrapping up the subcutaneous dose escalation and expansion. And then we anticipate that the molecule would be studied in combination with the lead B cell malignancy CD28 program. that they just filed a CTA for where they're planning on studying that with multiple agents, both internal to J&J Innovation and us. So that's always been the game plan, and we're anticipating that next step soon, we hope. Awesome. Thanks so much.
spk14: Thank you. One moment for our next question. Our next question comes from the line of Dane Leone from RJF. Your line is now open.
spk02: Thank you for taking the questions and congrats on the progress. And John, wish you the best in retirement. It's been a pleasure working with you over the years. Maybe we could expand a little bit on the design of the frontline non-small cell lung cancer study with the DellaMab. It sounds pretty interesting. I think probably... Two questions for us on the study design. Firstly, how much of the dose finding do you already have an idea about given the ongoing prostate and other solid tumor studies that could be informative? Two, what would be the actual patient population with regards to mutational burden, PD-1 status, cut points, et cetera, that you would envision. And presumably this would be an ex-US study primarily. Thank you.
spk05: I'll let Nancy, you know, pick up the ball on that one.
spk01: Yeah. So the study design is a phase 1D2. We're going to study two different cohorts of two different doses of Udalimab in two cohorts. and then make a determination of those dose or even a dose between that to take into combination with standard care chemotherapy for non-small cell, non-squamous. We do have a lot of information about the dose from our prior phase one dose escalation from, as you said, our studies in gynecologic malignancies, prostate cancer, and so we use that to pick these doses to look at. The other part of the question was?
spk05: The patient population, like PD-L1 status.
spk01: Oh, yeah. PD-L1 status is zero to 49, and yeah. And it's, you know, so it's zero to 49, first line, standard of care treatment, We're opening the study in the United States and also XUS as well. So, we do plan to enroll patients in the United States.
spk02: Do you have a general timeline at this point of when you would have initial outcomes based results that would be informative of potential next steps or just even the correct dose?
spk01: Yeah, so we're in the process of initiating the study right now. It's really hard to tell right now, you know, when we'd have the part one and the part two. Part one obviously would come first. We'd be able to look at that data, share that data externally. It's very hard to predict when that would happen. And then once we see that, we'll move on to the randomized phase two portion against PEMBRO and chemo.
spk08: Great. Thank you.
spk14: Thank you.
spk13: One moment for our next question.
spk14: Our next question comes from the line of Etzer Darut from BMO Capital Markets. Your line is now open.
spk18: Great. Thanks for taking the questions. This may be the first one, just maybe for modeling purposes, if you can. sort of maybe help us understand to the extent that you can sort of the residual royalties and or milestones that you would receive for unjubile, altomerous, just as how we should think about how to model any residual sort of upside here from the deal. And then secondly, just, you know, curious on sort of the focus on the two plus one, We saw some, you know, encouraging data from AMG 509 and ESBO. Just wondering if you're seeing any other kind of interesting clinical signals so far from your other 2 plus 1 molecules in the clinic. I know they're early, but just wondering if maybe you're starting to see, you know, sort of an evolution here of a profile that you really like, that you're sort of doubling down, if you will, on sort of solid tumors. Thank you.
spk05: Hey, thanks, Ed. So I'll answer the second question first before I turn it over to John Cush on the royalty deal. So, you know, we're not disclosing any data around any of our ongoing programs, or for that matter, some of our partners still have ongoing 2 plus 1 programs, like Astellas is moving forward with their Cloud 18.2. So we'll give data later. I will say that we and our investigators remain enthused, and there's a really great unmet need for certainly any renal cell carcinoma treatment highly cytotoxic antibody. And so we're pedal to the metal, but we're not going to share any details about the trial just yet. On the royalty deal and some of the residuals, John, you want to go to that?
spk03: Yeah, sure. It's two separate transactions. One is the Altamiris deal, which there's caps from 26 to 28. The first 35 million Omeris gets, we get the excess over that. Beginning 29, the first 12 million goes to Omeris and we get the excess There's also a potential milestone of $12 million for sales, which we could earn for Altamira sales from July 1, 2023 to June 30, 2024. The second transaction is the Monjuvi, which we received $22.5 million up front. Omeris gets 130% of that up front payment, or $29.5 million. And in any excess, we receive the residuals.
spk06: Got it. Great. Thank you.
spk13: Thank you. One moment for our next question.
spk14: Our next question comes from the line of Charles Xu from Guggenheim Security. Your line is now open.
spk12: Hey guys, this is Rosie on for Charles. Thanks for taking our questions and congrats on all the progress. I have two questions regarding budalimab. So in the frontline non-small cell lung cancer setting, could you maybe comment on how budalimab is differentiated from the competitor by specific? And then for the monotherapy setting, you provided guidance to data for the prostate cohort in early 2024. Could you maybe talk a little bit regarding how you're setting expectations for that data readout?
spk05: So I'll take the second one first, and then Nancy, you want to take the one on the frontline lung? Yes. You know, we're going to have a greater N that we're going to report. So we've reported relatively small numbers of patients out of the trial so far, and we haven't reported any out of the monotherapy trial. So we're just going to really, it's about increasing the numbers so we can zero people in on where we think their strongest potential is, you know, of the various cohorts in our combo study as well as in the monotherapy. And in terms of setting expectations, I think the landscape's, you know, shifting a lot in prostate cancer. I think we're certainly very aware of the xyloritmic data from Amgen in a similar line of therapy, you know, showing the 41% OR, obviously very excited because we made the thing, but also, you know, mindful of that. And so I think we're looking at a bar that might be shifting a little bit. And it's just, this is about us determining where we fall relative to that bar with a higher number of patients. So I don't think we can, offer too much more than that.
spk01: And I think you asked about differentiating from our competitors. Yeah, and so, you know, John can also, I guess, chime in here, but Fidelimab was designed specifically and optimized to have reduced potency in some ways to be very effective, but also to be very tolerable. as far as toxicity goes. The idea is that it would bind to, you know, dually bind to T cells that have both expressed, and these are in the tumor itself versus the circulation. The data so far, you know, when we compared our data to some of the competitors, it's a little bit hard, but when we look at When we try to look at phase one or dose escalation compared to dose escalation, what we saw was we have very heavily pre-treated patients that are checkpoint failed or experienced, and our competitors often have checkpoint-naive patients, so it's very hard to do that apples-to-apples comparison. But even with that, by doing so, when we looked at the efficacy across products and the safety, we thought we had something that was probably similar, and likely to be less toxic as we moved it into earlier settings. So that's how I would summarize the differentiation.
spk12: Great. Thank you. And maybe just a follow-up on XMAV564. Can you provide any color on how enrollment has progressed for the multiple ascending dose study?
spk05: Oh, the enrollment's really not It's a relatively small study. The number of patients relatively small enrollment is not really the driver of the timeline at all. It's the escalation safety windows that you have to wait through to go to the next dose level in the next cohort in the multiple ascending dose.
spk12: Thank you.
spk14: Thank you. One moment for our next question. Our next question comes from the line of Gregory Renza from RBC Capital Markets. Your line is now open.
spk17: Hi. Thank you so much for taking our question to support on for Greg. I have a question on the T-cell engager. I'm just curious if you can talk about the learning from cellular data, particularly on the adverse events. I'm just curious if you think the adverse event is within the acceptable and expected level for the class, and if that's that's something that you can do to mitigate that, you know, for your study. Thank you.
spk05: Yeah, I'll take that. I think it's the adverse events they saw, I think, were deemed certainly by Amgen quite within the range of acceptable. They're aggressively expanding the program. I think one of the things they're going to have to work on, and I think they're well positioned, is educating a new community of oncologists about T-cell engagers and cytokine release syndrome. This is the prostate cancer community. They're not used to it. They're not used to IRAEs because they're not used to checkpoints, but I think they'll get there. I think we've seen these kinds of adoption of highly active agents work its way through the oncology community when we saw ADCs start to emerge about four or five years ago more broadly. So I think it's well within the range. And what we saw, the learnings we saw from them were really nothing new. It's you use priming doses and step-ups. You have to be thoughtful about optimizing them. And one of the things they did is they adopted a somewhat more aggressive premedication routine before the infusions while they're stepping up the doses, when they're jumping from a prior dose being lower to the next one higher. And that's just the usual premedication people have done with Rituxan for decades. You know, a Tylenol, a Benadryl, and then a corticosteroid. They just intensified that somewhat, and it had a big, big impact. So those are the kinds of things we're considering. And and being very aware of. Anything to add there, Nancy?
spk01: You know, I agree. I think it's this class of drugs does have cytokine release that's expected. And I think as people get more comfortable managing it, it won't be a deal breaker. The efficacy is really strong. And you have to remember, these were patients that were multiply pretreated. They had a median of four prior therapies. Yeah. So, you know, to see a response rate like they saw, 41%, it's pretty amazing for these kind of patients. And so, you know, it's great to see this and other CD3s moving forward and showing this kind of activity because it shows that T-cell engaging bispecifics are going to have a role in the treatment of solid tumors. which is very exciting for patients as well.
spk13: Thank you so much. Thank you. One moment for our next question.
spk14: Our next question comes from the line of Alex Stranahan from Bank of America. Your line is now open.
spk08: Hey, guys. Thanks for taking our questions. Just a couple from us. One more on AMG509. We've heard some differences in opinion on PSA50 reductions as a good surrogate for response, although it seems consistent in the five patients that's the maximally tolerated dose. So any thoughts on PSA50, how we should be thinking about that in terms of response, and then I've got to follow up.
spk05: I think PSA50 is definitely an indicator that something is happening to the patient that I'm not aware of comprehensive data sets to let you really look at that versus resist response. That's what I'm assuming your question was. I'm not aware of good data sets to let you look at concordance there because it hasn't been standard to look at resist in the clinical trials in that prostate community over the years. Now, I think that's changing, but, you know, we'll wait and see. I just want to emphasize that concordance with PSA50s or not And that program, Zolaritamib, saw really outstanding resist responses in people with measurable tumors. I do know that just from all of the prostate cancer doctors we've worked with and talked to, they view PSA50 as a good thing if it drops. Sorry, a good thing if you can achieve it. How it concords with the specifics of it in an individual patient, there is not enough data.
spk08: Okay, got it. That's helpful. And then just one more on the royalty sale. Is the decision to do this versus another financing option that you may have at your disposal just in terms of the pull forward of the expected economics? And how important was it to maintain the upside on the two assets? Just trying to get a sense of your conviction on the opportunity. Thanks.
spk05: I think it was very important to maintain the upside on the assets because there's a lot of momentum in certainly Altamira's sales, and I think there's a lot of data still coming for Mangevy as that landscape in lymphoma continues to evolve. And so it was absolutely critically important for us to have the caps for Mangevy, the sort of total overall cap, and then the annual caps for Altamira's. um you know we're we're excited by both molecules i think the why we did the deal i think it's because the equity cost of capital now in the markets is is very challenging and we've got a lot of programs we want to invest in particularly around these t-cell and gators so it made sense to do the royalty deal we've been monitoring the royalty markets now for gosh four years now since we've started and we've all we're always looking for when the timing is right from both the the deal side and our needs side, and this was when it all came together.
spk06: Great. Thank you.
spk13: Thank you. One moment for our next question.
spk14: Our next question comes from the line of Boris Beaker from TD Cowen. Your line is now open.
spk16: Great. Thanks. This is Nick on for Boris. Just a quick one for me. But for XMAP 808, I know it's targeting B7H3. There are a lot of companies who are now looking at B7H4. That's kind of become like an interesting space for people and for some docs. So I'm just wondering what you guys think about that and the difference between B7H3 versus B7H4 and how B7H3 could potentially outperform B7H4. Just general thoughts on that. Thanks.
spk07: Yeah, I mean, they're two really different targets. I mean, the reason they're called B7s is they're part of the B7 family, which includes CD80, CD86, PD-L1, so on and so forth. But when we look at them as targets for T cell engagers or ADCs, they have kind of some overlap, but lots of non-overlap in terms of which histologies they're overexpressed in. I think of B7H4 as like a cervical cancer, triple negative cancer marker, whereas I think of B7H3 as being broadly overexpressed across a much wider range of histologies.
spk16: That's helpful. Would you ever think about going into B7H4 then? Or is that like a later deadline?
spk07: Yeah, we've certainly thought about it. I mean, you know, there is a B7H4 marker CD3 T-cell engager in phase one, I believe. And we would prefer to work on targets that somebody else isn't already tackling. And we're making a lot of internal investments on finding novel targets for placing our T-cell engagers.
spk16: Understood. Thanks very much.
spk14: Thank you.
spk13: One moment for our next question. Our next question comes from the line of Peter Lawson from Barclays.
spk14: Your line is now open.
spk10: Hey, good afternoon. This is Alex on for Peter. Thank you for taking our questions. Just on the 819-UE and PP3 by specific program, have you started dosing patients with the sub-Q formulation, or are you still dose escalating with the IV formulation at this point?
spk05: We expect to have, you know, I honestly don't know if as of today the sub-Q started, but it's very imminent. We've opened it, and I just don't know. We'd have to text our medical lead on that one. So it's up and running, and if not today, very, very shortly on the sub-Q. We're planning on running them in parallel. We wanted to get the IV going at first just to get a little data, get the ball rolling, and then that way we could start the sub-Q with a little bit of knowledge. But, no, they're both going to go in parallel.
spk10: Okay, great. And so when you report phase one data, would you anticipate having a recommended phase two dose at that point?
spk06: I'm sorry, could you repeat? I was distracted for a second.
spk10: No worries. When you report phase one data, would you anticipate having a recommended phase two dose?
spk06: That's the idea, yes. Okay, great. Thank you.
spk13: Thank you.
spk14: One moment for our next question. Our next question comes from the line of Mara Goldstein from Mizuho. Your line is now open.
spk09: Hi, this is Jerry Gongong from Mara Goldstein. Thank you for taking our questions. First on XMAP 306, could you share when you might expect to be eligible to receive milestones? And for the second question, on the Dalimab, what are your thoughts on positioning that candidate in renal cells given competitor PD1 and CTL4 bispecific data indication? Thanks.
spk05: So, first I'll just touch on the 306. You know, we're finalizing the details of the contract conversion, and we do have development. We expect to have development. regulatory and commercial milestones, and a sort of a standard structure. I couldn't speculate on as to the timing yet, unfortunately. But we'll, of course, disclose a lot of details, commensurate with how we usually disclose for licensing contracts when that amendment is finalized. For Vudalamab, if I understood properly, you have – your question is about positioning in RCC?
spk01: Yeah, because of the recent –
spk05: Right, right. You want to take that one, Nancy?
spk01: Yeah, I mean, we're aware of, I can't say the 5752 product in renal. Some of these names are challenging. And it's very interesting with, you know, great high efficacy. Looks like the toxicity is manageable. And so we're pleased to see a product in the same class as Vudalamab showing activity like this. I mean, it helps us, it helps confirm that this is a product that's going to be important in different tumor types. We're not going into renal cancer ourselves. We've, you know, we made decisions a few years ago on, based on phase one data into which tumor types we'd go into. It was a span of tumor types, you know, and eventually we decided to go into some that were, you know, checkpoint sensitive and some that were checkpoint resistant. And that's kind of where we are right now. We're probably not going to add another tumor type after we added lung, you know, in the last year.
spk09: Got it. And if I may ask one more question, also wishing, you know, John, the best wishes. Um, when do you expect to target a new CFO in your search?
spk06: I'm sorry. What do you expect to talk when? Oh, yeah.
spk05: I mean, starting the search right now. We're starting to search right now. This is going to be a long, hard search to replace John. So we've got to start now if we're going to be ready by, by, uh, end of March.
spk09: Got it. Thanks for taking our questions.
spk06: Sure.
spk14: Thank you. One moment for our last question. Our last question comes from the line of Brian Chang from JPM. Your line is now open.
spk15: Hey, guys. Thanks for taking my question. John is also set to see you go. Looking forward to reconnecting in the future. Just on 564, I recall that we may be expecting some psoriasis data sometime in the early part of next year. So the first is, can you just talk about the timing of the data read? Have you been able to narrow the timing of your guidance? And also, as you think about psoriasis as a testing ground for 564 mechanistically, do you have a sense of what we should expect in terms of you know, using PASI score. What PASI scores are you aiming for so that you can have a strong conviction to move this specific program into other diseases where T-REX is as important? Thank you for taking my question, Zeng.
spk05: Hey, thanks, Brian. I'll take the second one first. So we've always intended psoriasis as a population where we could gather the critical biomarker data, which is the peripheral blood biomarker data on Treg counts, the opposing cell types that you don't want to have expand, because we have to, from regulatory reasons, do our multiple setting dose in patients, not in healthy volunteers. So psoriasis is a great way to do that, and you have easy access to biopsy samples if you want to go there to get additional information. So we've always been targeting in the psoriasis population Treg counts and numbers to select a dose and a dosing interval rather than looking at PASI scores as a driver. That's something I think we've guided since we started. We did add the atopic dermatitis based on intriguing very early and small numbers durability data we saw last year from a competitor program as a way to sort of glean potential there. And so that was sort of the rationale for AD. But in that case as well, it was to glean durability and long-term potential, sorry, long-term sort of disease-remitted potential generally for the class. We think both of those areas are difficult and challenging and very large indications. And we've, of course, been looking around at other smaller indications. As we've mentioned, we'd be ready to disclose as we go forward. get closer to the time to jump off onto the next set of trials once we're done with dose escalation. You know, as for timing, we're still guiding to 2024, and we'll fill you in when we get there.
spk13: Great. Thank you so much. Thank you.
spk14: This concludes the question and answer session. I would now like to turn it back to Basil Dahiat for closing remarks.
spk05: I would just like to say to everybody, thank you so much for joining us this afternoon, and have a wonderful evening.
spk14: Thank you for your participation in today's conference. This does conclude the program. You may now disconnect.
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