CytomX Therapeutics Inc (CTMX) 2020 Q4 法說會逐字稿

Good afternoon, ladies and gentlemen. Thank you for standing by. Welcome to the CytomX Therapeutics Fourth Quarter and Full Year 2020 Financial Results call. (Operator Instructions) I would now like to hand the conference over to your host for today, Chau Cheng, CytomX's Vice President, Investor Relations and Corporate Communications. Please go ahead.

Thank you, Victor. Good afternoon, and thank you for joining us. With me today are Dr. Sean McCarthy, CytomX' President, Chief Executive Officer and Chairman, 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 cytomx.com.

During today's call, we will be making forward-looking statements. Because forward-looking statements related 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'd like to turn the call now over to Sean.

Thank you, Chau, and good afternoon, everyone. Thanks for joining us today. 2020 was a highly productive year for CytomX in spite of the COVID pandemic as we continued 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 II work on our lead conditionally activated antibody drug conjugates, CX-2009, or praluzatumab ravtansine and CX-2029.

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. CytomX is blazing the trail of conditional activation, and we believe this can lead to important advances in oncology, perhaps in other therapeutic areas. CytomX has demonstrated versatility of conditional activation across multiple antibody modalities, including immune checkpoint inhibitors, antibody-drug conjugates and bispecific antibodies.

Our robust clinical pipeline now comprises 5 Probody therapeutic candidates, 4 of which are in Phase II evaluations across 9 cancer types. We have purposefully applied our Probody technology to 2 different but complementary therapeutic strategies that we believe offer an appropriate balance of risk. Firstly, we have advanced Probody 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 anticancer therapies.

Secondly, and in contrast, we have challenged ourselves to drug the un-druggable, 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 CX-2009 and CX-2029. Antibody-drug conjugates against novel tumor antigens, CD166 and CD71, respectively.

Moreover, our 2 therapeutic strategies dovetail into novel combination approaches, such as our ongoing Phase II study combining CX-2009 with CX-072, 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 Probody therapeutic pipeline before handing it over to Amy for some additional detail. CX-2009 is a wholly owned conditional antibody drug conjugate targeting CD166; currently in a 3-arm Phase II 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 CX-2009 is significant. The target of CX-2009, CD166, is a collective protein 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. CX-2009 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 CX-2029, a conditional antibody drug conjugate that targets CD71, which is also now in Phase II. 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 over-expressed 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, make CD71 an intensively studied target for the delivery of drugs into malignant cells, it remains an elusive and un-druggable 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 AbbVie, we are now exploring this asset in Phase II expansions in 4 different tumor types with initial data anticipated in the fourth quarter of this year.

In addition to our progress with CX-2009 and CX-2029, we're also very pleased to report that our partner, Bristol-Myers Squibb, continues enrollment in its ongoing randomized Phase I/IIA study of the anti-CTLA-4 Probody BMS 986249 in patients with previously untreated unresectable stage III/IV melanoma, and BMS has expanded the scope of the Part IIB evaluation to include 3 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 I study of a second anti-CTLA-4 Probody, 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 Probody 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, CX-2043, which targets EpCAM, also known as TROP-1. 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, CX-2043, designed to be delivered systemically, as shown in preclinical studies, potent antitumor activity across multiple cancer types and superior tolerability in animal models compared to the corresponding unmasked conventional ADC. CX-2043 is currently and IND-enabling studies, and an IND application is anticipated for late 2021.

Another preclinical candidate, which we continue to advance towards [the clinic], is CX-904. Our T-cell engaging bispecific Probody that we're developing in partnership with Amgen. CX-904 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 un-druggable 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 IND 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?

Thank you, Sean. Hi, everyone. I'm going to start with CX-2009 or praluzatumab ravtansine and lay out our strategy for demonstrating the value we believe is inherent in this asset. CX-2009 as a potentially first-in-class conditionally activated ADC with the potential to address 2 major subsets of breast cancer.

At the 2020, San Antonio Breast Cancer Symposium we provided clinical updates from our Phase I work in patients with HER2 non-amplified breast cancer as well as translational data. The clinical update reinforced data previously reported at ASCO. 2 confirmed responses occurred in patients with hormone receptor positive disease and compelling but unconfirmed responses were observed in 3 patients with triple-negative breast cancer; including one patient who had progressed on paclitaxel pembrolizumab and subsequently progress on sacituzumab govitecan.

Encouragingly, our data to date suggests that CX-2009 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. CX-2009 was generally well tolerated with manageable adverse event profile at the recommended Phase II dose of 7 mg per kg every 3 weeks, and ocular toxicity was the most frequently observed adverse event.

Also at San Antonio, we provided data from exploratory translational study. In circulation, CX-2009 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 4 days following the first infusion. Furthermore, the concentration of activated intratumoral CX-2009 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 CX-2009 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. CX-2009 will be investigated in 3 parallel enrolling arms. Arm A will evaluate monotherapy CX-2009 in patients with hormone receptor positive HER2 non-amplified breast cancer. This is the largest subset of breast cancer, representing over 2-thirds of all patients with breast cancer. Arm B will evaluate monotherapy CX-2009 in patients with triple-negative breast cancer. Arm C also enrolling patients with TNBC will evaluate CX-2009 in combination with pacmilimab or CX-072, 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 Probody/Probody 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, [CVR-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 and greater than 80% of hormone receptor positive breast cancer, thus, we will not select for CD166 expression in Arm A. High CD166 expression has been observed in approximately 50% of triple-negative breast cancers. So we will require that patients 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 CX-2029, 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 4 patients with squamous non-small cell lung cancer and 8 patients with head and neck squamous cell carcinoma. That analysis highlighted that of the 4 patients enrolled with squamous lung, one achieved a best response of stable disease lasting approximately 6 months and 2 had confirmed partial responses. One with the duration of response approaching 6 months. The fourth patient was enrolled at 1 mg per kg, a dose not expected to be clinically active and progressed on study.

For head and neck squamous cell carcinoma, all 8 patients received 2 or 3 mg per kg. We observed a best response of stable disease or better in 7 of the 8 patients including one patient with a confirmed partial response, who remained on treatment for 9 months and one patient with stable disease who remained on treatment for 8 months. Of these 12 patients, none discontinued treatment due to an adverse event.

In all patients, the most commonly occurring Grade 3 or higher adverse event was anemia, which was predictable and manageable using one of 4 interventions; red blood cell transfusion, growth factor support, dose delay or dose reduction. No patient discontinued CX-2029 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 ADC's, and we're continuing to work with experts in the field to investigate the mechanisms contributing to this toxicity which could include CD71 biology and [Redwood] cell production as well as the effects of various interventions so that we may better mitigate the side effect in the Phase II expansion study.

Taken together, the exciting results from our Phase I dose escalation for CX-2029 have led us in collaboration with our partner, AbbVie, to launch a Phase II multi-cohort study, evaluating patients with squamous non-small cell lung, 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.

Thank you, Amy. We have continued to successfully finance CytomX' 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, cash equivalents and short-term investments we had as of December 31, 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 antibody to introduce new product candidates from our Probody 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. The total revenues were $16 million and $100 million for the quarter and full year, respectively, compared to $8 million $57 billion for the corresponding period in 2019. The 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 Sean.

Great. Thanks, Carlos. So 2020 was a highly productive year for CytomX, in which we saw our clinical stage pipeline advance to now encompass Phase II evaluations of 4 Probody therapeutics across 9 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, and we continue to execute on our strategic plan to deliver on the promise of our technology by 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 II data sets with CX-2009 and CX-2029, 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 3 additional tumor types beyond melanoma. In addition to deepening, broadening and advancing our unique pipeline of Probody therapeutics throughout 2020, we continue to build strength throughout the company. Including the appointments of Miss Halley Gilbert and Dr. Mani Mohindru, 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 CytomX board member, Dr. Charles Fuchs, for his valuable guidance of friendship over the years. Effective April 1, Charlie will step down from CytomX 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 CytomX came out stronger in every dimension. I'd like to convey my gratitude and appreciation to our entire CytomX 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.

(Operator Instructions) Our first question will come from the line of Terence Flynn from Goldman Sachs.

Maybe 2 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 and 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 is -- 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 Trodelvy. And just wondering how you expect 2009 to be positioned there, if it's approved?

Yes. Terence, thanks for the question. Let me make a couple of general comments on our experience at sites and enrollment then I'll hand over to Amy, who may want to add. And then Amy will address the 2009 question as well. So 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 I expansion, we did slow that down. We paused enrollment, and we took advantage of that pause to rewrite the study as a formal Phase II study, which is what we've launched at the end of last year.

We have, I would say, seen like others, that enrollments 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 remain -- we feel pretty good about our guidance on data for the 2009 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 negative.

Yes. Got it. So regarding the recent entry entrance of PD-1, yes, we are aware of that in the front line. And what we actually are excited about is that CX-072, when we looked at the data in the Phase I 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 innovation works. We know our checkpoint inhibitor works. We know that right now, the best partner with checkpoint inhibitor happens to be chemotherapy. ADC's 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, he 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 2 cycle -- really, I want to say, 16 weeks on treatment.

So as we think about positioning 2009, in triple-negative breast cancer, sacituzumab, we're well aware, has accelerated approval. We understand what accelerator 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 sacituzumab 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 front line and sacituzumab potentially thereafter. And we'll be looking to see how we position it further as we get data. I hope that answers your question.

And our next question will come from the line of Peter Lawson from Barclays.

This is Mitchell on for Peter. 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 CX-2029, 4Q 2021? And how many patients of data about could we expect?

Yes. Thanks for the question, Mitchell. Let me give a couple of 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 in terms of scope of data, so just to recap, those 4 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 2 cohorts, by the end of this year. Does that help?

Our next question comes from the line of Boris Peaker from Cowen.

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?

Sean, you want me to answer that or --

Yes. Go ahead, Amy, please.

Okay. Yes, 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.

Got you. That's helpful. Also, I'm curious on BMS. You mentioned that they started enrollment of a second CTLA-4 Probody. Just curious, can you comment what's the difference between the first one and the second one?

Yes. Sorry, certainly -- 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 Probody 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 Treg's. 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 enhance 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.

Our next question will come from the line of Mara Goldstein from Mizuho Securities.

This is Gabriel on behalf of Mara Goldstein. 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 2 of the tumor types are prioritized? Or was it just that they have happened to enroll faster, probably the head and neck in the [hot spots] and lung group? And another question here on, again, the BMS expansion into the 3 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 [lead] them there?

Yes, great. Thanks for the questions, Gabriel. Let me comment on the 2029, and then I'm sure Amy will 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 yes, with regards to the 2029, it's a pretty straightforward answer, really, which is that we -- the first 2 cohorts of lung and head and neck, where we saw such promising activity in the Phase I dose escalation, it's the kind of signal that you look for in Phase I. So we're just kind of making an assumption, I suppose, that, that will carry the enrollment into those 2 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, yes, comments on BMS 249?

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 ipi/nivo combination that they have accelerated approval on and so I think they know what success would need to look like there. So I think it's a -- these are 2 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.

Our next question comes from the line of Robert Burns from H.C. Wainwright.

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 the overwhelming majority where CD166 is high and with the monotherapy efficacy of 2009 in this population, it appears that it may demonstrate a lower response rate to that seen in TNBC. Are you considering any potential combinatorial strategies to potentially enhance the response rate of 2009, for example, in combination with SERD? And if not, how do you view the potential of SERDs in that relapsed/refractory sort of setting? And I've got one more after that.

Let me ask Amy to comment on that one. Great question. Thanks.

Happy to do so. So if I got it right, the questions were the 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, right? 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 II.

When it comes to -- 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, with SERDs 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 cytotoxic light chemotherapy. And so they may not go back to SERDs or hormonal based therapy.

With the other thing that drives the physician to think more towards chemotherapy is the disease in the patient. So while I said most of the time, they have hone disease, that's usually how it will start, but once they get 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 based chemotherapy, and that's what we would expect where CX-2009 would be positioned initially.

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 hormonal, 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.

Okay. That's completely fair. And my last question for now, so have you done any additional correlative studies regarding CD71 expression and the antitumor efficacy seen with 2029? And if so, what has that shown to date?

Yes. Really early on that, still, Robert. Great question. It's certainly an important question from the data we presented so far, really is a little early to tell, but we're highly interested in understanding more about that. It's an abundant target in many different tumors. It's also a rapidly internalizing target. And so the properties of this target we just need to study more. So there's not really a whole lot we can say right now.

Our next question will come from the line of Etzer Darout from Guggenheim.

This is Paul on for Etzer. I'm hoping to get a little more color on what we can expect from the Analyst Day in April -- in April? Is there potential to see any sort of clinical update for 2009 or 2029 at that time or at any other conferences ahead of the plan for fourth quarter disclosures?

Yes, Paul, thanks for the question. No. So the goal of the Analyst Day that we're planning for April will be really more of 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 ADC's 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, that'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.

Great. 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?

Great question for Carlos.

Sure. So as we stated before, this additional rate positions us really well to continue to fund our clinical space pipeline. But also allows us to introduce new programs that are currently in per 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.

And our last question will come from the line of Mohit Bansal from Citigroup.

Congrats on all the progress. I was just wondering, so Amy, you mentioned that -- and Sean you also mentioned, but basically, CD166 is a novel target. So expectations, probably, it is hard to understand at this point. But just looking across the board, ADC's as a monotherapy treatment have come a long way and the kind of responses we are seeing in the like of Trodelvy and other ADC's out there, they are getting even late lines of therapy, they're getting 30% plus kind of responses.

So to that extent, do you think that could be an expectation as a monotherapy, you kind of had to get to that kind of mark to make a mark in these kind of tumors? And if -- to that extent, you may have to get that, can you [enrich] the patients with some way to make sure that you select the patients who benefit the most from these drugs?

Yes. Thanks for the question, Mohit. And you're dead right, ADC's 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 CytomX. 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 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 our 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 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.

And at this time, I would like to hand the conference back over to Chau Cheng for his closing remarks.

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.

Ladies and gentlemen, this does conclude today's conference call. Thank you all for participating. You now disconnect, and have a great day.