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spk11: Good afternoon, everyone. Thank you for standing by. Welcome to the Cytomics Therapeutics First Quarter 2022 Financial Results Call. Please be advised that today's call is being recorded. I would like to hand the call over to your host for today, Mr. Chao Cheng, Cytomics Vice President, Investor Relations and Corporate Communications. Please go ahead.
spk01: Thank you, Cindy. Good afternoon, and thank you for joining us. With me today are Dr. Sean McCarthy, Cytomics' Chief Executive Officer and Chairman, Dr. Amy Peterson, President and Chief Operating Officer, and Carlos Campoy, Chief Financial Officer. Earlier today, we issued a press release that includes a summary of our first quarter 2022 financial results and highlights the progress we made during the quarter. We encourage everyone to read today's press release and the associated materials. which have been filed with the SEC. Additionally, the press release and the recording of this call can be found under the Investors and News section of our website. Please note that during today's call, we will be making forward-looking statements. Because forward-looking statements relate to the future, they are subject to inherent uncertainties and risks, including the uncertainties surrounding the COVID-19 pandemic that are difficult to predict and many of which are outside of our control. Important risks and uncertainties are set forth in our most recent public filings with the SEC at sec.gov, including our Form 10Q that was filed today. We undertake no obligation to update any forward-looking statements, whether as a result of new information, future developments, or otherwise. With that, I'll now turn the call over to Sean.
spk05: Thank you, Chao, and welcome back, Carlos. Good afternoon, everyone, and thanks for joining us for an update on recent progress at Cytomix. Let me begin today's call by reaffirming our commitment as an organization to making the biggest difference we can for people with cancer. Our dedication to destroying cancer differently is embodied in our robust therapeutic pipeline that represents the potential for conditionally activated biologics to lead to new and differentiated anticancer therapies. Conditional activation holds great promise, and we remain highly focused on delivering new therapies based on our world-class research and development capabilities. Leveraging our ProBody therapeutic platform, we now have six experimental therapeutics in development. During Q1, we make great progress executing towards important data readouts from our lead programs. Now, I want to stress up front that we understand that in the current protracted bear market for small and mid-cap biotech, judicious financial stewardship has never been more important. At Cytomics, a central tenet of our integrated financial strategy has been the formation of foundational partnerships with global biopharma companies, including AbbVie, Amgen, Astellas, and Bristol-Myers Squibb. These alliances have not only broadened the impact of our technology platforms, by increasing the number of pro-body therapeutic candidates being advanced into clinical studies, but they've also added considerable financial resources in the form of non-dilutive capital, enabling us to consistently maintain balance sheet strength. We ended this past quarter with $263 million in cash and liquid assets, providing sufficient resources to advance our pipeline. We also continue to be active with our business development efforts relating to our platform and to our product pipelines. I'd like to make a few specific comments on our pipeline programs before handing over to Amy for additional perspective. Our most advanced wholly owned drug candidate, the conditionally activated ADC, Pralizatumab Ravtanzine, is one of two clinical stage ADC programs designed to open a therapeutic window for novel cancer targets that have proven inaccessible by conventional approaches due to their widespread presence on healthy tissues. Indeed, Pralizatamab is the first ADC targeting CD166, a transmembrane glycoprotein that has been reported to play a role in multiple aspects of tumor biology, including angiogenesis and invasiveness. CD166 is highly expressed on the cell surface of many cancer types and, as such, has attractive molecular properties as an ADC target. However, developing a conventional ADC against CD166 is precluded by its widespread presence on healthy tissues. Based on our published Phase I clinical data, we see monotherapy pralizatumab as having potential in the evolving treatment paradigm for hormone receptor-positive and triple-negative breast cancers. Patient enrollment in our Phase II study of pralizatumab in breast cancer has continued to progress well, and we remain on track to report initial data for both ARMS A and B of this study in the second half of this year. Furthermore, we continue to evaluate the combination of pralizatumab with our anti-PD-L1 probody, pacmelamab, in triple negative breast cancer. Our second lead conditionally activated ADC is CX2029, which is partnered with AbbVie. This potential first-in-class ADC targets CD71, the transferrin receptor. Presented at high levels on many cancers, CD71 has been seen for decades as a target with great potential, but it presents a high bar for the development of anti-cancer therapeutics because of its widespread expression in healthy tissues. We previously reported encouraging initial data on CX2029's activity in a phase two expansion study in patients with squamous non-small cell lung cancer, all of whom had received prior treatment with checkpoint inhibitors. Given the widespread use of checkpoint inhibition in squamous lung cancer and the lack of therapeutic options in the post-checkpoint inhibitor setting, We believe these initial Phase II results bring into focus a potentially significant commercial opportunity for CX2029. Our ongoing Phase II expansion study continues to enroll, and we remain on track to provide a data update in the second half of 2022. In addition to our ADC programs, our multi-modality platform has enabled us to enter the emerging field of T-cell engaging by specific antibodies. Specifically, we're excited to have advanced our first conditionally activated T-cell bispecific, CX904, into clinical study startup activities. CX904, partnered with Amgen, is directed toward the validated cancer target, EGFR, which is highly expressed on many solid tumors and presents a broad opportunity for this therapeutic candidate to make a difference for people with cancer. As we have previously reported, we are further broadening and exploring our probody platform's full potential by applying our conditional activation technology to the field of cytokines, starting with interferon alpha. Interferon therapy, if harnessed effectively, has the potential to redirect to the immune system to destroy tumor cells. Interferons have also demonstrated combination activity with immunotherapy to potentially expand the benefit to patients with IO unresponsive tumors. Despite its potential, however, the toxicity of interferon-alpha has limited its clinical use. We're therefore thrilled to have created a novel, masked version of interferon-alpha 2B designed to harness the powerful activity of this immune modulator to target and preferentially kill cancer cells more safely and effectively. The promising preclinical profile of this conditionally activated cytokine was the subject of our recent presentation at AACR, and we aim to rapidly advance this program towards clinical evaluation. We're excited about our execution and progress across our entire pipeline, and I'll now hand the call over to Amy to provide you with a more in-depth update on our clinical development activities.
spk04: Thank you, Sean. As mentioned, we continue to focus on execution of our Phase II studies and, to that end, have achieved important milestones. Beginning with Praladzatamab-Raptanzine, I'm pleased to share that Arm A of our three-arm Phase II study has completed enrollment towards our goal of 40 efficacy-evaluable patients with hormone receptor-positive HER2 non-amplified breast cancer. With this study milestone achieved, we are reaffirming our plans to report data from this monotherapy cohort in the second half of this year. As a reminder, the primary endpoint of this study is overall response rate. However, the focus to better assess for clinical benefit is on key secondary endpoints of clinical benefit rate at 24 weeks, or CBR24, and progression-free survival, the latter being a critical endpoint for a registrational study in this setting. Study conduct in RMB, designed to evaluate prelazacumab as monotherapy in patients with CD166 expressing triple negative breast cancer, And ARM-C, designed to examine the combination of Pralizacumab plus Pacmelamab, our anti-PD-L1 probody therapeutic in patients with PD-L1 positive and CD166 positive TNBC, is ongoing. And we remain on track for initial data from ARM-B in the second half of 2022. I would now like to move to CX2029, our CD71-directed conditionally activated MMAE conjugated ADC which is being developed in partnership with AbbVie. In December 2021, we reported an encouraging preliminary response rate of 18.8% and a disease control rate of 87.5% in 16 efficacy-evaluable patients with platinum and checkpoint inhibitor refractory squamous lung cancer. I'm delighted to share that we have completed enrollment towards our goal of 25 efficacy-evaluable patients and continue to track to a data update in the second half of 2022. Let's now turn our attention to the third treatment modality to which our ProBody platform has been applied, namely, solid tumor-directed T-cell bispecifics. We continue advancing our first conditionally activated T-cell engaging bispecific, CX904, which is partnered with Amgen. CX904 is designed to bind to both the epidermal growth factor receptor, or EGFR, on cancer cells and to the CD3 receptor on T cells. We believe that applying our ProBody technology to solid tumor-engaging TCBs will serve to localize T cell activation against EGFR within the tumor microenvironment. minimizing the potential for systemic T cell activation and the ensuing toxicities that have been associated with unmasked solid tumor-directed TCBs. As we previously reported, our IND for CX904 was cleared by the FDA, and we have subsequently initiated clinical study startup activities. The first in-human Phase I study of CX904 in patients with advanced solid tumors is on track to begin enrolling in the coming months. Finally, Bristol-Myers Squibb continues to develop BMS 986249 and BMS 986288, the pro-body versions of the anti-CTLA-4 antibodies ipilimumab and the non-feucosylated ipilimumab, respectively. BMS 986249 is in Phase II in combination with nivolumab in a randomized study versus ipilimumab plus nivolumab in patients with untreated advanced melanoma. The novel combination is also being evaluated in advanced hepatocellular carcinoma, castration-resistant prostate cancer, and triple negative breast cancer. BMS 986288 continues in phase one dose escalation, both as monotherapy and also in combination with nivolumab in patients with advanced solid tumors. To summarize, Cytomix has developed six experimental treatments that are currently in clinical development Over 500 patients have been enrolled in studies evaluating our pro-body therapeutic candidates. Our platform has now been applied to four different therapeutic modalities, antibodies, antibody drug conjugates, T cell bispecifics, and cytokines. Phase two studies of our product candidates are being conducted in nine different cancer types. We're on track to provide data updates from our two lead programs, Pralizacumab and CX2029, in the second half of this year. And with that, I'm very happy to turn the call over to Carlos for a financial overview.
spk09: Thank you, Amy. Citomics continues to have a strong balance sheet. As of March 31st, 2022, we had $263 million in cash, cash equivalents and investments, which we project will be sufficient to support operations well into 2023. For the first quarter of 2022, revenue was $17 million compared to $16 million for the corresponding period in 2021. The increase was largely related to the CD71 collaboration with AbbVie. R&D expenses increased $8 million to $31 million during the three months ended March 31st, 2022 compared to Q1 2021. The increase was driven by contract and service expenses in manufacturing and development in support of our preclinical and clinical portfolio. G&A expenses were $10.5 million during the first quarter of 2022, an increase of $1.3 million compared to the same period in 2021. The increase was mainly in personnel and professional expenses. As Sean previously mentioned, we exercise judicious financial stewardship with our capital and will continue to manage our cash resources strategically. I may now turn the call over to Sean.
spk05: Thanks, Carlos and Amy. In closing, I would like to again emphasize the terrific execution by the Cytomix team so far this year. We remain on track for important data readouts in the second half from our Phase II ADCs, and we've also continued to advance several earlier stage programs to maintain a broad and deep pipeline. Our versatile and multimodality platform supported by our ever-growing understanding of the tumor microenvironment, continues to provide us with optionality, both within our own programs and in our ongoing work with our biopharma partners. We remain as passionate as ever in our quest to destroy cancer differently. Before we open the call-up for Q&A, let me express my sincere gratitude to our retiring board members, Fred Gluck and Dr. John Scarlett. Both gentlemen have been with Cytomics for many years, and their contributions have been instrumental and invaluable to our growth, and I wish them all the very best for the future. So with that, operator, please open up the call for Q&A.
spk11: Thank you. As a reminder, if you would like to ask a question, you may press star 1 on your telephone keypad. And your first question from Kaveri Polman. Your line is now open.
spk10: Hi, good afternoon. Thanks for the update. My first question is regarding 2009. How different is the safety profile of this ADC from immunogen's ADC, especially in terms of ocular events? Because this is a higher dose that you're evaluating.
spk05: Yes, thank you, Mary. Thanks for the question. Let me kick that one off. So, first of all, the payload for 2009 Pranizatomab is, as you know, DM4. This is the metanzine, the same payload that Immunogen is indeed using on Mervituximab. And as we've reported previously, our phase one experience, the principal toxicity that we encountered as expected was ocular toxicity. We are taking measures to manage that with mandatory prophylaxis in the phase two setting. We've described the various elements of that prophylactic regimen previously, but in general terms, our experience in phase one with 2009 was pretty consistent with what Immunogen has seen in their programs, and we'll be reporting, of course, initial phase two data on both the activity and the safety side second half of this year.
spk10: Got it. And for HR positive, HER2 negative, breast cancer. How feasible is it to get an ORR? Is it that a lot of these patients have bone disease, which makes the durability more reliable readout, like CRPC? Just wanted to get some insight there.
spk05: Yeah, it's another great question. And, you know, the etiology of the disease, you're quite right to point out that these patients, particularly in the late-line setting as they come onto our study, are quite challenging to achieve objective responses in. That said, the primary endpoint for our study is ORR, but the more meaningful endpoint, we believe, and our investigators and advisors would agree with us, is CBR24, of course, as a clinical benefit rate for 24 weeks. which, of course, is a surrogate ultimately for PFS, which would be the most important registrational endpoint as this program moves forward. So it is a significant consideration within the context of hormone receptor positive disease, as you quite rightly point out.
spk10: That makes sense. And maybe a last one on the cytokine program. What's your rationale for selecting IFN-alpha as the lead asset? And how different it is from IL-12, which also kind of drives IF and alpha release?
spk05: Yeah, well, we have a broad cytokine program. There are multiple programs that we're working on. We haven't disclosed any of the additional cytokines beyond IL-12. interferon yet, but we do see a terrific opportunity for our conditional activation masking technology to have an impact broadly in this field where there's huge potential. Interferon is the first. We like interferon given its validation. It was indeed the first immunotherapy to be approved going back several decades. There is a fairly broad clinical experience with interferon both in terms of what it's known to be able to do as a single agent and in combination, but perhaps most importantly, what's known about its limitations from a safety standpoint and therefore the room for improvement using our technology. So it's interferon alpha-2B, again, a well-validated mechanism in immuno-oncology that we believe we can add significant value to, but as I said, also the leading edge of a broad-based program at the company.
spk10: All right, thanks for taking my question.
spk05: My pleasure.
spk11: Your next question from Gov and Scott. Airline is now open.
spk12: All right, thanks for taking my question. Just on probably the ZAPDEM and patient selection criteria for cohort C, I don't think you've disclosed the respective PD-L1-CD166 cutoffs, but what does the epidemiology data suggest on the prevalence of this population And can you maybe provide some color on the accrual rate for cohort C? Thank you.
spk05: Thanks, Gavin, for the question. Let me just clarify the question because you weren't coming across super clear to us, and then I'll ask Amy to comment. So I think the question is about really the size of the population in RMC of the Pralizatumab Phase II study, which is, of course, studying the combination of of Praluzetamab with our PD-L1 ProBody Pacmelamab. That was the question, right?
spk12: Yeah, that was the second part. The first part was just on the patient selection criteria and cutoffs. I don't think you've disclosed that in the past, but just any color there as well.
spk05: No, that's right. I'll take the first part. So you're correct, we haven't disclosed that. But regarding the patient selection, the epidemiology, if you like, of PD-L1 plus CD166. Let me ask Amy to comment on that briefly.
spk04: Sure. So PD-L1 expression, the prevalence is pretty well known. There are a couple of different diagnostic tests that can be used to establish PD-L1 expression. And so we allow patients who are PD-L1 positive by any one of those tests. With regard to overlap between CD166 and PD-L1 expression, there really is no reason to believe that they would either be convergent or divergent. The amount of overlap is a function of the expression of CD166 and the expression of PD-L1. and triple negative breast cancer. So we are continuing to look at CD166 expression levels, and PD-L1 is a requirement. And I think what we've said before is that PD-L1 population, the PD-L1 positivity rate is about 35% of triple negative breast cancer.
spk12: Okay, thanks. And just to follow up, when you present data, will you stratify it by any varying expression levels?
spk05: Yeah, so let me just briefly comment on that. In triple negative breast cancer, our experience in phase one, which we presented and published, was consistent with the heterogeneity of the disease in that CD166 expression is rather variable across the patients that we enrolled in phase one. It was a fairly small number of patients. It was 10 or 11, as I recall. We saw about half of the patients who had high CD166, high meaning IHC score of two or above. So we are, of course, very interested in understanding the relationship between CD166 expression and clinical activity, particularly in triple negative, given that the target expression is heterogeneous. It may lead to patient selection strategies in the future. We'll have a lot more to say about this, of course, with the Phase II data that we present in the second half of the year.
spk12: Great. Thank you for the answers.
spk05: You're welcome.
spk11: And your next question from Peter Lawson. Your line is now open.
spk06: Great. Thanks for taking the questions. Congrats on the enrollment of Arm A. Do you think we'll see a timing difference between Data from arm A and data from arm B. And then just if you could kind of walk through your expectations of the number of patients we should see and bar essentially for the arm A data. Thank you.
spk05: Yeah, hi Peter. So right now, we're working towards giving an update on both arms A and B at the same time, sometime in the second half. That's our goal. As Amy mentioned in her comments, Arm A, hormone receptor positive, is fully enrolled. The goal there has been to get to 40 efficacy-available patients, and so that will be the data set that we will share later in the year. Triple negative, Arm B, enrollments moving along well will have what we would refer to as a meaningful number of patients in RMB at that same time. That's what we're working towards. Triple negative enrollment has been a little slower, of course, given the different patient population. In terms of the bar, let me hand over to Amy just to comment briefly on, and I think the question was specifically with regard to RMA. what we're looking for there. And I think we've discussed this previously, but maybe we can just reiterate that.
spk04: Sure, happy to do so. And this comes to us from collaboration with our steering committee and speaking with people like Dr. Saratolani. And our expectation or our desire is that we're there for desire for something that would be interesting would be really a CBR24 rate that's around 30% or higher, and a progression-free survival rate that is really three to four months.
spk06: Gotcha. Thank you. And then, Sean, just kind of, I guess, on a more strategic and board-level question, just with the retiring board members, any changes you anticipate? What kind of ads you will make there or who will be added there in a sense. And then just thoughts about partnerships, adding additional partnerships. We've heard a lot from Pharma about increased likelihood of partnerships happening. Just your thoughts would be great.
spk05: Thank you. Yeah, great. Thanks, Peter, for the questions. Regarding the board, once again, I want to thank Fred and Chip for their service. over many years and nothing really to add at this point on any additional board evolution. Very happy with where we are from a governance standpoint and again we wish Fred and Chip all the very best. Regarding partnerships, as I mentioned on the call, business development has been an integral part of our business plan really since we got the company going. And we always realized that the breadth of our technology would both benefit from partnering in terms of the application of the technology across multiple modalities and programs, and also, of course, serve to a fairly significant extent as a financing mechanism for the company which has allowed us to really do a lot over the last few years. And Amy mentioned the 500 patients that we've been able to treat. We have an incredible depth of experience with conditional activation given the funds we've been able to raise both on the equity and the non-dilutive side. Our partnerships continue to be strong. We're absolutely thrilled with the progress we continue to make with all four of our partners. And we continue to have discussions about potential new alliances. And as I've always said, we will do the right deals at the right time. Great.
spk06: Thank you so much.
spk11: Your next question from Raul Yersong. Your line is now open.
spk07: Great. Thank you for taking our question. So, a couple from us. The first one is just curious about the next steps for the 2009, and particularly for the TMDC part, given you have monotherapy and the combo, would you weigh the combo data before you would make a decision for the monotherapy moving forward?
spk05: Yeah. Hi, Roger. So, you know, I think it's too early to comment at this stage. I think we're highly focused, as you could hopefully tell from the comments on the call right now on executing to these important data sets. We will specifically with regards to triple negative breast cancer of course we do expect to have the data for monotherapy in advance of the combination partly because of the need to screen RMC for both for patients with both PD-L1 and CD-166 we previously guided and continue to guide that RMC will come in in 2023 so It's really too early to comment on any potential next steps.
spk07: OK, that's understood. Maybe just a quick one, last one from us. In terms of the other cohorts for 2029, any comments around the enrollment and the timeline for the data readout?
spk05: No comment on timing. We continue to enroll across the multi-cohort study. We've reported today the significant progress that the team has been able to make in lung. We're very interested to see that full 25 patient cohort data given the encouraging 18.8% response rate that we shared in December of last year. And enrollment continues in the other cohorts. No updates on timing at this point.
spk07: Got it. Okay. Thank you for taking the question.
spk05: You're very welcome.
spk11: Your next question from Boris Becker. Your line is now open.
spk03: Great. Thank you. So my first question is on your Epilimumab ProBody, the one partnered with BMS. Could you comment on any kind of timing updates and what should we be expecting some data there?
spk05: Yeah, hi, Boris. So the IPI probody, otherwise known as BMS 986249, continues to make progress in the randomized phase two frontline melanoma study. It also is being studied by BMS in three other tumor types, and also not to lose sight of the probody version of the non-pucosalated version of IPI that is also in the clinic in phase one. We do not have any updates at this point on timing as to when that data will be available or shared.
spk03: Great. And maybe on 2029, can you comment on the CD71 receptor? What is the biologic function of this receptor? Is that known?
spk05: Yeah, it's actually very well characterized. CD71 is the transferrin receptor. Its biological function is to bind to transferrin in the blood and allow transferrin complex with iron to enter cells where the iron is delivered to the cellular metabolic machinery. The thing that's most interesting about the target is that it's actually one of the first proteins that was used to describe the biochemical process of receptor-mediated endocytosis. It cycles off of the cell surface very, very quickly. and for that reason has been thought of for a long time as a potentially ideal target for an antibody drug conjugate to deliver payload into cells. The problem is the target's present on all normal tissues because, of course, all normal tissues require iron for their metabolism. So it's been a very difficult target to drug until we've deployed the probody technology, and that's the basis of our program, CX2029.
spk03: And can you look at iron as a biomarker for some kind of engagement or activity then in this case?
spk05: You know, we haven't really looked at that in depth. I don't know that that would ultimately be fruitful. You know, in the clinic, what we've observed, and we've now done a lot of work in the clinic, as you know, we haven't seen any obvious correlations or issues with iron metabolism or even the metabolic state of iron metabolism in patients coming on to study. So, you know, it's something that we continue to think about, but not really a significant work stream for us at the moment. Great. Thank you for taking my questions. My pleasure. Thank you.
spk11: And your last question from Mitchell Kapoor. Your line is now open.
spk08: Hey there. Thanks for taking the questions. The first one, just for the second half data for ARMS A and B for Pralazadamab, thinking about the holistic profile, could you kind of describe what would be meaningful and then what would be considered beyond meaningful, kind of a great profile out of the datasets?
spk05: Thanks, Mitch, for the question. I think we'll stick with the meaningful, if you don't mind, and I'll ask Amy to comment.
spk04: Sure, sure. Meaningful. So, again, going back to hormone receptor positive HER2 non-amplified, that's the patient cohort that we enrolled in Arm A. That enrollment is complete, and the goal was to get 40 efficacy data from 40 efficacy evaluable patients. And here we're focusing on the endpoints that are really more extrapolatable and important to registrational studies, those being progression-free survival and clinical benefit rate at 24 weeks. Here we're looking for something that would be CBR consistent with 30 percent and PFS that is three months or better. I think anything north of that is going to be in your the best case scenario. So that's what we're looking for in arm A. In arm B, this is monotherapy in patients with CD166 expressing triple negative breast cancer there. The bar is a little bit different. Response rates can be meaningful, and certainly durability of response can be meaningful, and response rates can form the basis of accelerated approval studies, facetuzumab being the most recent example of this in triple negative breast cancer. Here, we're looking for response rates that are really upwards of 20%. According to our KOLs and our steering committee, we're looking for PFS that exceeds one scan, so that is greater than two months. Why are we saying that? Well, the ASCENT trial that was the phase three study of sasituzumab versus chemotherapy had response rates of 5% in the chemotherapy arm and median progression-free survival of 1.7 months. And sasituzumab got full approval on the basis of that study. It went from accelerated to full. And so we are in very likely the post-sasituzumab setting where there really isn't a whole lot of treatment options. So Really, 20% to 30% response rate and a PFS that is greater than two months would be something that we would be happy with.
spk08: Great. Thank you. And then on the recent AACR data, if you could just talk about, you know, the implications for the activated, conditionally activated cytokine profile for your pipelines and just kind of, you know, what that data signifies for you all.
spk05: Yeah, absolutely. So the work as presented at AACR extended from the in vitro characterization of the masking strategy for interferon alpha through to the in vitro and in vitro evaluation of the anti-cancer activity of the molecule both in masked form and in unmasked, protease-activated form. And then we also have extended our work into some preliminary assessment of tolerability in cinnamologous monkeys. And the data taken together show very clearly that we've broadened the therapeutic window for interferon-alpha-2b very significantly through localizing the activity into tumor tissue, localizing, if you like, the immunobiology that is stimulated by interferon alpha-2b into the tumor microenvironment, and we think this offers huge potential for the opening of a therapeutic window for interferon in cancer patients as a monotherapy, but I think even more importantly, in the combination setting. And the goal overall of this program is to, over time, will be, of course, to make a difference in patients where they are either unresponsive or have become refractory to immunotherapies. So we see a lot of potential for this program, both ourselves and with our advisors. We're very excited about moving it forward. And as I also mentioned, it's just one of a broad-based program that we now have at the company evaluating our masking technology to improve the therapeutic window of a wide range of different cytokines.
spk08: Great. Thank you very much. You're welcome.
spk11: Mara Goldstein, your line is now open.
spk02: Hi, this is for Mara Goldstein. I have a question on CX-209. I'm sorry, this has already been asked. I'll just jump onto the line. So in terms of the esophageal cancer and GJ, you know, cancers and the LBCL, Have you guided or what's your expectations in terms of the response rate in terms of the go or no-go decision? Thank you.
spk05: Yeah, thanks for the question. We haven't really discussed that yet. I think the question was asked a little earlier on regarding the timing and timing You know, the current status of the 2029 program is that we continue to enroll across the expansion cohorts where, as Amy mentioned in her comments, we've been highly focused on getting the lung cancer cohort fully enrolled to really further flesh out that signal that we reported at the end of last year in squamous lung. And we'll be providing additional updates on timing for the other cohorts as the year goes on. But nothing else really we can say today.
spk02: Got it, and on the lung cancer, I think you may have guided previously on the ORR rate of 20%. Is that still the threshold for that indication?
spk04: This is Amy. I'll take that question. Let me just step back a little bit and remind people what is the context of what happens in these patients in this setting. There's not a lot of information that we have with regard to response rate in squamous lung cancer patients who are refractory to both a platinum and a checkpoint inhibitor. With that said, When we look at the information that is available to us, for example, the randomized studies with dozotaxel, and you look at how dozotaxel performs in the second line following a platinum, not a checkpoint inhibitor as well, but just a platinum, the response rates there are 8%, 10%. They're very, very low. And so we think 20% is actually pretty encouraging given it's not just platinum refractory. It's platinum plus checkpoint inhibitor refractory squamous lung.
spk02: Got it. Got it. Thank you.
spk11: At this time, I would like to hand the call back over to Chao Cheng for his closing remarks.
spk01: Yes, on behalf of the executive team, I'd like to thank you all very much for joining us this afternoon. We look forward to updating you in the future on our ongoing progress.
spk11: And this does conclude today's conference call. Thank you all for participating. You may now disconnect and have a great day.
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