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spk10: Thank you, Victor. Good afternoon, and thank you for joining us. With me today are Dr. Sean McCarthy, Cytomix's President, Chief Executive Officer, and Chairman.
spk05: Dr. Amy Peterson, Chief Development Officer, and Carlos Campoy, Chief Financial Officer. Earlier today, we issued a press release that includes a summary of our fourth quarter and full year 2020 financial results and highlights the important progress we made during the year. 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 a recording of this call can be found under the Investors and News section of our website at citomix.com. 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 uncertainties surrounding the COVID-19 pandemic that are difficult to predict and many of which are outside our control. Important risks and uncertainties are set forth in our most recent public filings with the SEC at sec.gov, including our Form 10-K 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 would like to turn the call now over to Sean.
spk06: Thank you, Chow, and good afternoon, everyone. Thanks for joining us today. 2020 was a highly productive year for cytomics in spite of the COVID pandemic as we continue to execute our strategic plan to deliver on the promise of our technology platform for transforming the lives of people with cancer and building a sustainable oncology-focused commercial organization for the long term. To that end, we are well on our way as we continue to work diligently towards initial readouts in 2021 from ongoing phase two work on our lead conditionally activated antibody drug conjugates, CX2009, or Pralazetamab-Ravtanzine, and CX2029. Let me begin by reiterating that we are the leader in the emerging field of conditional activation of antibody therapeutics. Our approach, the ProBody platform, is designed to increase the exposure of therapeutic antibodies in cancerous tissue compared to normal tissue by leveraging the protease-rich tumor microenvironment. We believe that disease localization of therapeutic antibodies will be an important therapeutic concept for many years to come, and we're only at the beginning of what this approach will ultimately do. Cytomics is blazing the trail of conditional activation, and we believe this can lead to important advances in oncology, perhaps in other therapeutic areas. Cytomics has demonstrated versatility of conditional activation across multiple antibody modalities, including immune checkpoint inhibitors, antibody drug conjugates, and by specific antibodies. Our robust clinical pipeline now comprises five probody therapeutic candidates, four of which are in phase two evaluations across nine cancer types. We have purposefully applied our probody technology to two different but complementary therapeutic strategies that we believe offer an appropriate balance of risk. Firstly, we have advanced pro-body therapeutics directed against validated immuno-oncology targets, such as CTLA-4 and PD-L1, with the goal of developing best-in-class assets and expanding the reach of these foundational anti-cancer therapies. Secondly, and in contrast, we have challenged ourselves to drug the undruggable and, in doing so, create potentially first-in-class cancer therapies for which we all agree there remains enormous unmet medical need. This strategy has led us to exciting programs evaluating CX2009 and CX2029, antibody drug conjugates against novel tumor antigens, CD166 and CD71, respectively. Moreover, our two therapeutic strategies dovetail into novel combination approaches, such as our ongoing phase two study combining CX2009 with CX072, our proprietary anti-PD-L1 inhibitor in triple negative breast cancer. thus illustrating the potential of our platform to unlock novel and potentially powerful combination strategies. I'll now briefly summarize our pro-body therapeutic pipeline before handing over to Amy for some additional detail. CX2009 is a wholly owned conditional antibody drug conjugate targeting CD166, currently in a three-arm phase two study in HER2 non-amplified breast cancer, which we initiated in the fourth quarter of 2020. Given that breast cancer remains the second leading cause of cancer deaths in women, and about 80% of breast cancer is HER2 non-amplified, we believe the opportunity for CX2009 is significant. The target of CX2009, CD166, is a glycoprotein that, among other functions, plays an important role in the formation and maintenance of tissue architecture. While its biological roles are not fully understood, CD166 is an attractive target to us since it's expressed at high levels in many types of tumors, including breast cancer. However, CD166 is also broadly expressed in normal tissues, thereby compromising its potential role as a conventional ADC target. CX2009 has demonstrated single-agent clinical activity in several cancer types, including breast, ovarian, lung, and head and neck cancers. We anticipate the initial data from our ongoing Phase II breast cancer study towards the end of this year. Turning to CX2029, a conditional antibody drug conjugate that targets CD71, which is also now in phase two. CD71 is a transmembrane glycoprotein receptor ubiquitously expressed in most normal tissues that functions in cellular iron uptake through its interaction with transferrin. CD71 is overexpressed on many cancers to allow tumor cells to meet their increased iron requirement for growth. While the high expression on malignant cells and its ability to be readily internalized makes CD71 an intensively studied target for the delivery of drugs into malignant cells, it's remained an elusive and undruggable target to date due to its broad expression on normal cells. Using our ProBody platform, we believe we have created a therapeutic window for CD71. And in partnership with App-V, we are now exploring this asset in phase two expansions in four different tumor types, with initial data anticipated in the fourth quarter of this year. In addition to our progress with CX2009 and CX2029, we're also very pleased to report that our partner, Bristol Myers Squibb, continues enrollment in its ongoing randomized phase 1-2a study of the anti-CTLA-4 probody, BMS986249, in patients with previously untreated, unresectable stage 3-4 melanoma. And BMS has expanded the scope of the Part 2b evaluation to include three new cohorts. These new cohorts are enrolling patients with advanced hepatocellular carcinoma, castration-resistant prostate cancer, and triple negative breast cancer. BMS also continues enrollment into a phase one study of a second anti-CTLA-4 pro body, BMS 986288. In addition to this continued clinical progress in our alliance with BMS, we look forward to continuing collaborative discovery and development activities towards generation of additional pro-body therapeutics in oncology. Turning now to our preclinical pipeline, where we continue to explore and leverage our platform, and specifically to our third investigational antibody drug conjugate, CX2043, which targets EPCAM, also known as CROPE1. EPCAM has been regarded as a high potential oncology target for decades, but efforts to generate systemic anti-EPCAM therapeutics have to date not been successful. However, locally derived approaches have shown some success, and in fact, a recombinant fusion protein that targets EPCAM has recently been submitted to the FDA for approval in bladder cancer, but this agent has to be instilled directly into the bladder. This is because EPCAM, or epithelial cell adhesion molecule, as the name suggests, is present on the majority of normal epithelial tissues, and conventional anti-EPCAM biologics administered systemically have significant dose-limiting toxicities. In contrast, our anti-EPCAM conditional ADC, CX2043, designed to be delivered systemically, has shown in pre-physical studies potent anti-tumor activity across multiple cancer types and superior tolerability in animal models compared to the corresponding unmasked conventional ADC. CX2043 is currently in IND-enabling studies, and an IND application is anticipated for late 2021. Another preclinical candidate, which we continue to advance towards the clinic, is CX904, our T cell engaging bispecific probody that we're developing in partnership with Amgen. CX904 targets the CD3 receptor on T cells and the epidermal growth factor receptor, or EGFR, on tumor cells. Now, although both EGFR and CD3 are validated in their own rights, we see this combination as undruggable for conventional bispecific approaches due to the extraordinary potency of both mechanisms when combined. In collaboration with Amgen, we continue our work towards unlocking potential in this target combination with our ProBody platform with the goal of ID filing this year. Staying with the bispecific theme, we're also excited about our recently initiated drug discovery activities under our collaboration with Astellas, also aimed at broadening the therapeutic window of bispecific T-cell engagers. Now I'd like to hand the call over to Amy for a deeper dive into our lead programs and where we're taking them. Amy.
spk01: Thank you, Sean. Hi, everyone. I'm going to start with CX2009, or prelizatumab-raptanzine, and lay out our strategy for demonstrating the value we believe is inherent in this asset. CX2009 is a potentially first-in-class conditionally activated ADC with the potential to address two major subsets of breast cancer. At the 2020 San Antonio Breast Cancer Symposium, we provided clinical updates from our phase one work in patients with HER2 non-amplified breast cancer, as well as translational data. The clinical update reinforced data previously reported at ASCO. Two confirmed responses occurred in patients with hormone receptor positive disease, and compelling but unconfirmed responses were observed in three patients with triple negative breast cancer. including one patient who had progressed on taclitaxelpembrolizumab and subsequently progressed on sasituzumab dovetecam. Encouragingly, our data to date suggests that CX2009 does not appear to show cross-resistance to other approved breast cancer treatments in either hormone receptor positive or triple negative disease. The clinical benefit rate, or CBR, was 41% at 16 weeks and 28% at 24 weeks. These data indicate that responses can occur early on and can be durable. Furthermore, these data speak to the potential tolerability of this agent, and indeed there are a handful of patients that remained on treatment for nearly a year. CX2009 was generally well tolerated with manageable adverse event profile at the recommended phase 2 dose of 7 mg per kg every three weeks. and ocular toxicity was the most frequently observed adverse event. Also at San Antonio, we provided data from exploratory translational studies. In circulation, CX2009 was found to be predominantly intact. That is, it remained masked. Conversely, unmasked antibody drug conjugate was measurable to an appreciable percent in tumor specimens biopsied four days following the first infusion. Furthermore, the concentration of activated intratumoral CX2009 was found to be significantly correlated with CD166 expression. This further supports investigation as to whether CD166 selection could be used to enrich the patient population. We believe that collectively these data underscore the potential of targeting CD166 with CX2009 and support its initial Phase II investigation in breast cancer. Let me just provide a quick recap on the design of the Phase II study. CX2009 will be investigated in three parallel and rolling arms. Arm A will evaluate monotherapy CX2009 in patients with hormone receptor-positive HER2 non-amplified breast cancer. This is the largest subset of breast cancer, representing over two-thirds of all patients with breast cancer. Arm B will evaluate monotherapy CX2009 in patients with triple negative breast cancer. Arm C, also enrolling patients with TNBC, will evaluate CX2009 in combination with pacmilabab or CX072, our conditionally activated anti-PD-L1 antibody. Our previously reported preclinical work on CD166 in combination with PD inhibition and that of others provides clear rationale for combining ADCs with checkpoint inhibitors, and we're excited about this first clinical evaluation of a pro-body, pro-body combination. Each arm is expected to enroll approximately 40 evaluable patients, and ocular prophylaxis is mandatory. The primary endpoint of the study will be objective response rate based on central radiology review. Other endpoints include duration of response, CBR 16 and 24, and progression-free and overall survival. Analysis will be performed separately for each arm on efficacy-evaluable patients. CD166 is highly expressed by IHC in greater than 80% of hormone receptor-positive breast cancer patients. Thus, we will not select for CD166 expression in arm A. High CD166 expression has been observed in approximately 50% of triple negative breast cancer, so we will require that patient tumors express CD166 in order to be eligible for arms B or C. We started the study in December of last year and anticipate initial data to be available in the fourth quarter of this year. Moving on to CX2029, our anti-CD71 conditionally activated antibody drug conjugate employing the MMAE payload. At ASCO 2020, we provided the first data ever demonstrating successful targeting of this receptor with an ADC approach. We provided an additional update in the fourth quarter focusing on the 12 patients with squamous histology that enrolled into the study, including four patients with squamous non-small cell lung cancer and and eight patients with head and neck squamous cell carcinoma. That analysis highlighted that of the four patients enrolled with squamous lung, one achieved a best response of stable disease lasting approximately six months, and two had confirmed partial responses, one with a duration of response approaching six months. The fourth patient was enrolled at one mg per kg, a dose not expected to be clinically active, and progressed on steady. For head and neck squamous cell carcinoma, all eight patients received two or three mgs per kg. We observed a best response of stable disease or better in seven of the eight patients, including one patient with a confirmed partial response who remained on treatment for nine months and one patient with stable disease who remained on treatment for eight months. Of these 12 patients, none discontinued treatment due to an adverse event. In all patients, the most commonly occurring grade three or higher adverse event was anemia, which was predictable and manageable using one of four interventions, red blood cell transfusion, growth factor support, dose delay, or dose reduction. No patient discontinued CX2029 treatment for anemia. While anemia is an expected payload toxicity from MMAE, the rate and severity were higher than what has been reported with other MMAE ADCs, and we're continuing to work with experts in the field to investigate the mechanisms contributing to this toxicity, which could include CD71 biology in red blood cell production, as well as the effects of various interventions, so that we may better mitigate the side effect in the Phase 2 expansion study. Taken together, the exciting results from our Phase 1 dose escalation for CX2029 and have led us, in collaboration with our partner, AbbVie, to launch a Phase II multi-cohort study evaluating patients with squamous non-small cell lungs, head and neck squamous cell carcinoma, esophageal or GEJ cancer, or diffuse large B-cell lymphoma. As previously announced, we dosed the first patient in this trial in November of last year. And with sites actively recruiting patients, we anticipate initial data to be available in the fourth quarter of 2021. With that, I would like to turn the call over to Carlos to review our financials.
spk09: Thank you, Amy. We have continued to successfully finance ITOMX's operations. Just last month, we raised approximately $108 million in net proceeds from a follow-on public equity offering. which added to the $360 million in cash equivalents and short-term investments we had as of December 31st, 2020, puts us in a strong financial position. We believe our strength and balance sheet will allow us to continue to advance our clinical pipeline of conditionally activated antibodies to introduce new product candidates from our pro-body platform technology into human testing, and to meet projected operating requirements into 2023. Let me now highlight some of the financial results for the quarter and year ended December 31, 2020. Total revenues were $16 million and $100 million for the quarter and full year, respectively, compared to $8 million and $57 million for the corresponding periods in 2019. Research and development expenses were $22 million and $113 million for the quarter and full year, respectively, compared to $36 million and $132 million in 2019. General and administrative expenses were essentially flat for the quarter and full year compared to 2019, amounting to $9 million for the quarter and $36 million for the year. With that, I'll turn the call back to Shawn.
spk06: Great, thanks, Carlos. So 2020 was a highly productive year for Cytomics in which we saw our clinical stage pipeline advance to now encompass phase two evaluations of four probody therapeutics across nine cancer types, all while contending with the challenges posed by the COVID-19 pandemic. We have demonstrated that our probody technology has the potential to widen or create therapeutic window, first in class and validated oncology targets. But we continue to execute on our strategic plan to deliver on the promise of our technology for transforming the lives of people with cancer. Our leadership in the research, discovery, and development of conditionally activated antibody candidates positions us well for future growth as we now drive to important phase two data sets for CX2009 and CX2029, and also advance our pipeline broadly. We're pleased with the ongoing progress within our strategic partnerships, especially the recent commitments from BMS to expand their evaluation of BMS 986249 in three additional tumor types beyond melanoma. In addition to deepening, broadening, and advancing our unique pipeline of pro-body therapeutics throughout 2020, we continue to build strength throughout the company, including the appointments of Ms. Hallie Gilbert and Dr. Mani Mahindru to our board of directors. Their appointments exemplify our commitment to creating a stronger and more inclusive board and also underscore our strong corporate culture of diversity, equity, and inclusion across our entire organization and in the community at large. I'd like to take a brief moment here to sincerely thank Cytomics board member, Dr. Charles Fuchs, for his valuable guidance and friendship over the years. Effective April 1st, Charlie will step down from Cytomics board after taking a new role at Genentech, and we wish him the very best. In summary, 2020 was a year like no other, but I am proud to say Cytomics came out stronger in every dimension. I'd like to convey my gratitude and appreciation to our entire Cytomics team for their incredible efforts in 2020. Also to our partners and our investors for their continued support. We look forward to speaking with you all again soon as this exciting year progresses. We plan to host a virtual analyst and investor briefing in April with key opinion leaders and to provide you with background on our ProBody technology our conditional ADC strategies, and the outlook for the year ahead. With that, let's open the call up for Q&A. So back to the operator.
spk10: To ask a question, you need to press the one on your telephone. And to withdraw your question, press the pound key. Please stand by while we compile the Q&A roster. Our first question will come from the line of Terrence Flynn from Goldman Sachs. You may begin.
spk04: Hi. Good afternoon. Thanks for taking the question. Maybe two for me. I was just wondering if you can give us some perspective on the clinical trial environment right now and maybe kind of end of last year into this year. Are sites generally back open in enrolling patients? And then how does this factor into your enrollment timelines over the course of the year? And then the second question I have relates to 2009. Obviously, the treatment paradigm for triple negative breast has been evolving here. There's been a second entry of a PD-1 as well as Tredelvi, and just wondering how you expect 2009 to be positioned there if it's approved. Thank you.
spk06: Yeah. Hi, Terrence. Thanks for the questions. Let me make a couple of general comments on our experience at sites and enrollment that I'll hand over to Amy, who may want to add, and then Amy will address the 2009 question as well. So, you know, we certainly, as you all know, last year, in fact, gosh, almost a year ago, we were all wondering what was going to happen with COVID. We did, in fact, at that time with our 2009 phase one expansion, we did slow that down. We paused enrollment and we took advantage of that pause to rewrite the study as a formal phase two study, which is what we've launched at the end of last year. We have, I would say, seen, like others, that enrollment across the pipeline has come back over the course of the, towards the back end of 2020. Still not ideal in certain ways, mostly limited by one's ability to obviously get into sites. That said, we feel pretty good about our guidance on data for the 209 and 2029 programs by the end of this year. So with that, let me hand over to Amy to comment, particularly on your question on 2009 and triple negatives.
spk01: Yep, got it, thanks. So regarding the recent entrance of PD-1s, yes, we are aware of that in the front line. And what we actually are excited about is that CX072, when we looked at the data in the phase one study, we actually enrolled a cohort of triple negative breast cancer and saw some very compelling signs of activity in this disease specifically. So we know checkpoint inhibition works. We know our checkpoint inhibitor works. We know that right now the best partner with checkpoint inhibitor happens to be chemotherapy. ADCs are a sort of modified version of chemotherapy and we certainly have observed single agent activity with 2009. So we're looking forward to that combination in part C. Now how we position 2009, what we have shown in our corporate presentation is we do have a patient, and I mentioned her in the earnings call, we do have a patient with triple negative breast cancer who had very large volume disease alterating through the skin. She received Pembrolizumab with Paclitaxel as her frontline therapy, and her best response to that was disease progression. She then got Sacituzumab, and her best response to that was disease progression. On our study, she had an early and marked response. Unfortunately, she developed keratitis, needed to come off treatment to have that treated. By the time she resolved, her disease had to be remeasured. She progressed, and we couldn't reinitiate treatment per resist. But she still had a dramatic response, even at that time, after two cycles, really, I want to say 16 weeks on treatment. As we think about positioning 2009 in triple negative breast cancer, sasituzumab, we're well aware, has accelerated approval. We understand what accelerated approval looks like for them. We also are aware that as of this date, we have no reason to believe that there's cross-resistance to either checkpoint inhibitor or sasituzumab with monotherapy 2009, and that's exemplified in the response that we saw in the patient I just described. So for accelerated approval, we would have to go after approved therapies, which would be a checkpoint-based therapy in the frontline and sasituzumab potentially thereafter. And we'll be looking to see how we position it further as we get data. I hope that answers your question.
spk04: Great. Thanks so much.
spk10: And our next question will come from the line of Peter Lawson from Barclays. You may begin.
spk03: Hi, everyone. This is Mitchell on for Peter. Thank you for taking our questions. The first question I have is, what is the bar for efficacy for CD71 therapies, and what would be considered positive results from the Phase II expansion to support moving forward with the program? And then kind of along those lines, what is the scope of data we can expect from CX2029 and 4Q21 and how many patients of data about could we expect?
spk06: Yeah, thanks for the question, Mitchell. Let me give a couple general comments. Obviously, given the scope of the work that we're doing with CD71 in multiple indications and also the novelty of the target, we're not in a position to really comment on specific bars or expectations at this point. We're super excited about these studies. And in terms of scope of data, so just to recap, those four indications are squamous non-small cell lung, squamous head and neck, esophageal GEJ, and DLBCL. And we've guided in recent months that we're looking to data from the first couple cohorts by the end of this year, Our goal is to enroll up to 25 patients in each of these arms. So where will we be exactly by the end of the year? Not sure, but we're working towards, as I said, disclosure of data across those first two cohorts by the end of this year. Does that help?
spk03: Absolutely. Thank you very much.
spk10: Our next question will come from the line of Boris Peeker from Calend. You may begin.
spk07: Great. Thanks for taking my question. Maybe the first one, just a quick one. When you assess the CD166 level, curious, is that a fresh biopsy or using archival tissue, and how does that impact the measurement?
spk01: Yeah, go ahead, Amy, please. Okay, thanks. Yeah, it is a mix. Breast cancer patients tend to have archival tissue. Of course, we enrolled more than just breast cancer patients. So it's a mix of some fresh, but for the most part, it's archival. And what we are doing now is really trying to better understand the role that CD166 plays in the biology of cancer and how its expression may or may not change over time. I think it's important to remember it is an adhesion molecule. And so there may not be specific pressures to up-regulate or down-regulate as the tumor progresses. But at this point in time, we're beginning to investigate and trying to understand expression levels. And then therefore, what's the best timing of tissue acquisition for our study? But for the studies that we have ongoing, we will allow archival tissue. Gotcha. That's helpful.
spk07: Also, I'm curious, on BMS, you mentioned that they started enrollment of a second CTLA-4 pro body. Just curious, can you comment, what's the difference between the first one and the second one? Yes.
spk06: Let me chip in on that one. So, yes, that's been in the works for a while. The second one, what we call 288, is a pro body version of a non-fucosylated version of IPI And so the strategy there that BMS has been taking, and of course they can speak to it much more effectively than we can, the strategy is that the non-fucosylated version is intended to be a more potent version of IPI because it's a more effective depleter of intratumoral Tregs. And BMS presented data at AACR last year actually on both the IPI probody and the non-fucosylated probody showing how the probody approach can enhanced therapeutic window for both. So the goal of this second program is to even further broaden the reach of CTLA-4 therapy in the long run.
spk07: Great. Thank you very much for taking my questions.
spk06: You're very welcome.
spk10: Our next question will come from Mara Goldstein from Mizuho Securities. You may begin.
spk11: Hi, Tim. This is Gabriel on behalf of Merrill Goldstein, and thanks for taking our questions. Just a couple of questions here. How should we think about the data readout for 2029 in fourth quarter? Was there a particular reason as to why two of the tumor types are prioritized, or is it just that they happen to enroll faster, probably the head and neck and not spots along group? And another question here on, again, the BMS expansion into the three different tumor types. To the extent that you can comment, what do you think would have prompted BMS to choose those specific tumor types and if they did any additional studies to leave them there? That's a thank you.
spk06: Yeah, great. Thanks for the question, Gabriel. Let me comment on the 2029 and then I'm sure Amy would be happy to comment on the BMS question. We're really very pleased about the additional work that BMS is doing in these additional tumor types. So, yeah, with regard to the 2029, it's a pretty straightforward answer, really, which is that, you know, the first two cohorts of lung and head and neck are where, you know, we saw such promising activity in the phase one dose escalation. You know, it's the kind of signal that you look for in phase one. So, we're just kind of making an assumption, I suppose, that that will carry the enrollment into those two cohorts with a little bit of initial momentum. So that's really the thinking. It's not really based on anything else at this point in time. So Amy, any comments on BMS 249?
spk01: Sure. I can't say exactly what led them into this. I can speculate on this, which is Certainly, they know what a signal would look like, would need to look like. They have the randomized study going on with melanoma, right? That's the killer experiment in a way. And with hepatocellular, they know what responses look like given the ipinevo combination that they have accelerated approval on. And so I think, you know, they know what success would need to look like there. So I think these are two indications that will give a clear picture of what the combination can bring to the table. And I would imagine that castrate-resistant prostate cancer and triple negative breast cancer is yet other areas to expand into that have not yet reaped the benefits of IO-IO combos.
spk11: Great. Thanks for the details.
spk10: Our next question will come from Robert Burns from H.C. Wainwright. You may begin.
spk12: Hi, guys. Thanks for taking my question. Just two if I may for right now. So although I recognize the highly advanced nature of the patients in the HR-positive, HER2-negative breast cancer, metastatic breast cancer cohort in Phase I, considering that the overwhelming majority were CD166 high and at the monotherapy efficacy of 2009, in this population appears that it may demonstrate a lower response rate to that seen in TMBC. Are you considering any potential combinatorial strategies to potentially enhance the response rate of 2009, for example, in combination with a CERD? And if not, how do you view the potential of CERDs in that relapse refractory sort of setting? And I've got one more after that.
spk06: Let me ask Amy to comment on that one. Great question. And hi, Robert. Thanks.
spk01: Happy to do so. So if I got it right, the questions were a potentially lower ORR in hormone receptor positive than in triple negative. I want to take a step back and just say having responses in hormone receptor positive disease is actually encouraging, period. When you think about their disease and where it's located, they have bone disease, and you don't actually always get resist responses in these patients. So the other surrogates of activity that we look at are things like clinical benefit rate at 24 weeks. And those are the things that we will be looking at in the phase two. So we're equally encouraged by the data that we've observed in both cohorts or in each cohort. Let me say it that way. When it comes to combinations, you know, with SIRS being hormonal-based, typically what will happen is patients will exhaust hormonal therapy, however it is delivered. And at the time that they've been refractory or progressed on 2, 3, and with a CDK4, 6 inhibitor, for example, and they're continuing to progress, oftentimes the physician will start to think about more traditional cytotoxics like chemotherapy. And so they may not go back to SIRDS or hormonal-based therapy. The other thing that drives a physician to think more towards chemotherapy is the disease in the patient. So while I said most of the time they have bone disease, that's usually how it will start. But once it gets aggressive or more aggressive, it will involve the lung and the liver. And so visceral involvement is something that physicians will often use as a guide to start more traditional cytotoxic-based chemotherapy. And that's what we would expect where CX2009 would be positioned initially. Okay. In combination, I think right now we're in the beginning phases. I'd love to be able to figure out how to move this into earlier lines of therapy, be it in combination with a hormonal agent or other. But right now it's first things first and look for the monotherapy in this setting.
spk12: Okay, that's completely fair. Thank you, Amy. My last question for now. So, have you done any additional correlative studies regarding CD71 expressions in the anti-tumor efficacy seen with P029? And if so, what has that shown to date?
spk06: Yeah, really early on that still, Robert. Great question. It's certainly an important question. Yeah, from the data we've presented so far, yeah, really it's a little early to tell, but we're highly interested in understanding more about that. It's a It's an abundant target in many different tumors. It's also a rapidly internalizing target. And so the properties of this target, you know, we just need to study more. So there's not really a whole lot we can say right now.
spk12: Awesome. Thank you. Thank you.
spk10: Our next question will come from Edser Darao from Guggenheim. You may begin.
spk02: Hey, this is Paul on for Edser. Thanks for taking our questions. Hoping to get a little more color on what we can expect from the analyst day in April. Is there potential to see any sort of clinical updates for 2009 or 2029 at that time, or at any other conferences ahead of the planned fourth quarter disclosures?
spk06: Yeah, hi, Paul. Thanks for the question. No, so the goal of the analyst day that we're planning for April will be really more the outlook for the year ahead. So we'll be talking more about the platform, our approach to conditional activation, which I think is of increasing interest to a lot of people, given the broad emerging interest in these types of approaches to localize antibody activity. We'll be talking about our strategies for conditional ADCs and how to really think about these novel agents, and we'll talk about in more detail the design of our ongoing studies and insofar as, so I wouldn't expect any new data at this update. It's really more the outlook for the year ahead. We have not yet communicated on specific timing or venue for our Q4 data updates. That will be coming a bit later in the year.
spk02: Great, thanks. That's really helpful. And then just one more. With your recent raise, I'm wondering if you could provide some comments on how you're currently thinking about capital allocation versus pipeline priorities.
spk06: Great question for Carlos. Sure.
spk09: So as we stated before, this additional raise positions us really well to continue to fund our clinical programs clinical stage pipeline but also allows us to introduce new programs that are currently in for clinical stage into human testing and that takes us into 2023 so that's about the extent of the guidance of where we're investing our money great thank you thank you
spk10: And our last question will come from Mohit Bansal from Citigroup. You may begin.
spk08: Thank you for squeezing me in and all the progress. I'm just wondering, so Amy, you mentioned that, and Sean, you also mentioned that basically CD166 is a novel target. So expectations probably it is hard to understand at this point. But just looking across the board, ADCs as a monotherapy treatment have come a long way and the kind of responses we are seeing with the lack of Tredelvi and other ADCs out there, they are getting in like even late lines of therapy, they're getting in 30% plus kind of responses. So to that extent, do you think that could be an expectation that immunotherapy, you kind of have to get to that kind of mark to make a mark in these kind of tumors. And to that extent, you may have to get that. Can you enrich the patients in some way to make sure that you select the patients who benefit the most from these drugs? Thank you.
spk06: Yeah, thanks for the question, Mohit. And you're dead right, ADCs have come a long way, and we and others, of course, continue to see an enormous amount of potential if we can continue to unlock novel targets such as we've been doing at Cytomics. Again, just to reiterate some of our earlier comments, we're not in a position to comment on specific expectations for these ongoing studies. We are in this business to make a difference, of course, and so we're You know, that is our objective. We want to make the biggest difference we can in the tumor types we're looking at. And we, of course, will be continuing to look at enrichment strategies over time because we all want to make sure we get the right drugs to the right patients. And as Amy mentioned, we have ongoing strategies, particularly in the triple negative setting, to be prospectively selecting patients for target for CD166. We think that's going to help. And we don't think that's necessary necessarily at this stage in the hormone receptor positive setting because of just how high the target is expressed in that patient population. But enrichment across the board is something that we continue to think about a lot. Thank you, Sean. Thank you.
spk10: And at this time, I'd like to hand the conference back over to Chao Cheng for his closing remarks.
spk05: 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.
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