CytomX Therapeutics, Inc. Q4 FY2021 Earnings Call

Good afternoon everyone. Thank you for standing by. Welcome to the CytomX Therapeutics Fourth Quarter and Full Year 2021 Financial Results Call. Please be advised that today's call is being recorded. I would now like to hand the call over to your host today, Chau Cheng, CytomX's Vice President, Investor Relations and Corporate Communications. Please go ahead.

Thank you, Michelle. Good afternoon and thank you for joining us. With me today are Dr. Sean McCarthy, CytomX' Chief Executive Officer and Chairman; Dr. Amy Peterson, President and Chief Operating Officer; and Chris Ogden, Vice President, Finance and Accounting. Earlier today, we issued a press release that includes a summary of our fourth quarter and full year 2021 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 recording of this call can be found under the Investors and News section of our website at cytomx.com. 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 uncertainty surrounding the COVID 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 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.

Thanks, Chau, and good afternoon, everyone. Thanks for joining us today for an update on recent progress at CytomX. Before I begin, I'd like to note that on February 14, we issued an 8-K announcing that our Chief Financial Officer, Carlos Campoy, has begun a temporary personal leave of absence. We very much look forward to Carlos' return. In the interim, our Vice President of Finance, Chris Ogden, who joins us on the call today, has assumed the role of Principal Accounting Officer and will oversee day-to-day operations of our finance functions. I would also like to congratulate Amy on her recent promotion to President and Chief Operating Officer of CytomX, an expanded role in which she will have responsibility for all aspects of product development as we advance towards potential registrational studies and beyond. I would like to start today's call by taking a step back to comment on our overarching corporate strategy as I reflect on our many accomplishments over the past year, resulting from sustained and relentless execution by the CytomX team. I'll then hand the call over to Amy to provide updates on our broad and increasingly mature therapeutic pipeline. CytomX is a clinical-stage oncology-focused biopharmaceutical company dedicated to destroying cancer differently. We are utilizing our industry-leading proprietary Probody platform to create biologic therapeutics to make the biggest possible difference we can to the lives of people with cancer. Our ambition is to build a long-term multiproduct commercial biopharmaceutical company. Our innovative platform is designed to enable conditional activation of therapeutic candidates within the tumor microenvironment, minimizing drug activity in healthy tissues, resulting in more selective targeting of tumor tissue. We have established conditional activation as a strategic area of current biologics research and development in the industry. We believe our innovative approach has the potential to improve cancer treatment in three ways: firstly, allowing the pursuit of high potential targets that were previously considered undruggable due to their ubiquitous expression on normal tissues. Secondly, enhancing a potential product's therapeutic window, the balance between tolerability and antitumor activity with a particular focus on potent immunotherapy. And thirdly, enabling the development of new combination therapies, including immunotherapies, by improving tolerability. We are employing our platform to address some of the biggest challenges today in oncology biologics R&D. These include the validation of potential new targets for antibody drug conjugates, opening solid tumor opportunities for T cell engaging bispecific antibodies, and increasing the therapeutic window for immune modulators such as cytokines and checkpoint inhibitors. We have utilized our multi-modality Probody platform to build a deep clinical pipeline that now encompasses six novel product candidates, four of which are currently in multiple Phase II clinical studies across nine cancer types. The breadth, depth, and range of our pipeline are unmatched in the field of conditional activation. We have treated more than 400 patients with Probody therapeutics and we have proved key translational questions in the clinic to validate the performance of our platform and we continue to add to our strong intellectual property portfolio which now comprises over 550 issued and pending patents. Our product candidates include the conditionally activated ADCs and praluzatamab ravtansine which targets CD166 and CX-2029 which targets CD71. These Phase II clinical programs highlight our strategy of leveraging our technology to pursue high potential previously undruggable targets. Our pipeline also encompasses the anti-CTLA-4 Probody, BMS-986249, and the Probody immune checkpoint inhibitor, ipilimumab, targeting PD-L1, both of which are also in Phase II studies. These product candidates highlight our strategy of using the Probody platform to improve therapeutic window for potent immunotherapies, broadening the clinical utility of these important pathways. In addition to our Phase II programs, our versatile and tunable platform has continued to deliver new product candidates for advancement into the clinic. CX-904 is our first conditionally activated T-cell engaging bispecific antibody targeting EGFR on tumor cells and the CD3 receptor on T cells. In January 2022, the IND for this program was cleared by the FDA and we're in the process of initiating a first-in-human Phase I study in patients with advanced solid tumors. Our integrated corporate strategy has and continues to encompass the formation of major partnerships with pharmaceutical and biotechnology companies. To date, we have formed multiple strategic alliances with major multinational pharma companies, including AbbVie, Amgen, Astellas, and Bristol Myers Squibb. These alliances not only broaden the impact of our technology platform by increasing the number of Probody therapeutic candidates being advanced into clinical studies but they have also added considerable financial resources in the form of non-dilutive capital, enabling us to consistently maintain a strength over the years. Today, we have reported a 2021 year-end cash balance of $305 million which provides funding well into 2023 without taking into account any potential cash flows from existing or new partnerships. Chris will provide you with an overview of our financials momentarily. Our successful financing of CytomX, coupled with our prudent financial management, has allowed us to aggressively advance our pipeline to key upcoming milestones and value inflection points and to build a broad early-stage pipeline that extends beyond our six clinical stage assets as we continue to innovate and reinforce our lead in the field of conditional activation. Let me now hand the call over to Amy to walk through our many exciting achievements in the pipeline in 2021 and also our outlook for 2022.

Thank you, Sean. I am very excited about the progress we are making at CytomX and look forward to continuing to deliver on our goal of building our company for the long term and making real our promise to positively impact the lives of people with cancer. In 2021, we made significant advancements despite contending with the COVID-19 pandemic. Let me begin with praluzatamab ravtansine, our wholly owned Phase II asset. As Sean mentioned, praluzatamab is a CD166 directed conditionally activated ADC with first-in-class potential in breast cancer and we recently published full data from our Phase I monotherapy dose escalation study in clinical cancer research. In this paper, we reported encouraging anticancer activity in patients with either triple-negative or hormone receptor-positive HER2 non-amplified breast cancer. In particular, the clinical benefit rate, defined as any partial or complete response or stable disease at 16 or 24 weeks, was 41% and 28%, respectively, despite a median of seven prior therapies. The treatment landscape in breast cancer continues to evolve, especially in the area of ADCs with the recent results from the DESTINY-Breast03 study evaluating trastuzumab deruxtecan in patients with HER2 low breast cancer and, of course, the anticipated Phase III results from sacituzumab in patients with hormone receptor-positive breast cancer. ADCs are clearly making an impact in breast cancer and we are excited about the potential for praluzatamab. Let me discuss the design of our ongoing Phase II study in a bit more detail. The tolerability and activity of praluzatamab monotherapy is being assessed in arms A and B in approximately 40 efficacy evaluable patients with either hormone receptor-positive disease or triple-negative disease, respectively. Our enrollment criteria in all arms exclude patients with HER2 amplified breast cancer meaning we are enrolling patients with either HER2-low or HER2 negative breast cancer, the latter being a sizable population that is not addressed by trastuzumab deruxtecan. The primary endpoint in all arms is response rate by central radiology review and the key secondary endpoint, particularly important for Arm A, is CBR24. The definition of efficacy evaluable includes high expression of CD166. Of note, our Phase I experience with hormone receptor-positive disease showed high CD166 expression in more than 90% of patients in Arm A as an unselected population. For TNBC, we saw more heterogeneous expression levels in Phase I. And for this reason, we're selecting patients for CD166 expression. Enrollment into the trial continues at over four sites globally and we anticipate having initial data in Arms A and B in the second half of 2022. Let's now move to Arm C which is evaluating the combination of praluzatamab and pacmilimab, our PD-L1 Probody in patients with PD-L1 positive, CD166 expressing triple-negative breast cancer. Each agent has shown single-agent activity in triple-negative breast cancer and we are excited to see what this combination can do for patients. Enrollment is ongoing and we expect results from this arm to be available in 2023. I would now like to discuss CX-2029, our program assessing the anti-CD71 ADC in partnership with AbbVie. To briefly recap, in December 2021, we reported encouraging results for our ongoing Phase II expansion of this program in patients with late-stage metastatic squamous non-small cell lung cancer, an area of high unmet clinical need. Specifically, we reported a preliminary response rate of 18.8% and a disease control rate of 87.5% in 16 patients with squamous lung cancer who had received both prior platinum-based treatment and checkpoint inhibition. This is a growing patient population with a high unmet need. To put these preliminary monotherapy results into context, several randomized studies conducted in the second or third-line squamous lung setting report a response rate to checkpoint inhibitors between 8% and 11%. This response rate is in patients who are checkpoint inhibitor naive. As an additional reference point, nivolumab was approved by the FDA in 2015 for the treatment of patients with previously treated metastatic squamous non-small cell lung cancer as monotherapy reported a response rate of 12.8% in the third-line setting. Given the prior treatment regimens in our study and the unselected nature of the study population, we are encouraged by the activity. Enrollment continues towards our goal of 25 efficacy evaluable patients and we expect to provide a data update on all efficacy evaluable patients in the second half of 2022. To briefly recap, both praluzatamab and CX-2029 are first-in-class, conditionally activated ADCs directed against tumor targets that were previously deemed undruggable, a core element of our strategy to destroy cancer differently. I'd like to now turn our efforts to use our platform to improve the therapeutic window for potential immunotherapies, starting with CTLA-4 and BMS-986249, the Probody version of ipilimumab we created with our partner, Bristol-Myers Squibb. CTLA-4 targeted therapy is a foundational immuno-oncology strategy and treatment with ipilimumab as a monotherapy or in combination with nivolumab has resulted in clinically meaningful antitumor activity in a variety of malignancies, highlighted by the recently updated median overall survival of 72.1 months for the combination in the Phase III melanoma CheckMate 067 study. The durability of responses to anti-CTLA-4 therapy continues to highlight the importance and uniqueness of this target. However, CTLA-4 blockade has a narrow therapeutic window and we believe that broader potential of CTLA-4 therapy could be realized through the application of our Probody platform. We believe our CTLA-4 targeting Probody therapeutic may be able to effectively localize the anti-CTLA-4 antibody's activity to the tumor microenvironment, thereby limiting systemic toxicities often seen with ipilimumab, potentially improving the benefit/risk profile of an anti-CTLA-4 containing regimen. The Phase I study conducted by BMS and previously reported at ASCO 2020 evaluated doses of BMS-986249 monotherapy that were equivalent to up to 30 milligrams per kilogram of unmasked ipilimumab. And in combination with 480 milligrams of nivolumab, doses that were equivalent to up to 15 milligrams per kilogram of unmasked ipilimumab. This is remarkable in that a dose of 3 milligrams per kilogram of ipilimumab was not tolerable in combination with an equivalent dose of nivolumab as shown in the 2013 Phase I study reported in the New England Journal. Our partner, Bristol-Myers Squibb, is currently evaluating BMS-986249 plus nivolumab in a randomized Phase II study against ipilimumab plus nivolumab in patients with untreated advanced melanoma. This novel combination is also being evaluated in advanced hepatocellular carcinoma, castration-resistant prostate cancer, and triple-negative breast cancer. In addition, BMS is conducting a Phase I study with BMS-986288, our Probody a non-fucosylated version of ipilimumab, again, as monotherapy and in combination with nivolumab in patients with advanced solid tumors. Continuing with our work on potent immune modulators, the tremendous versatility of our platform is allowing us to expand the reach of Probody therapeutics to T cell engaging bispecific antibodies or TCBs. Unmasked TCBs, even at very low concentrations, can bind to normal tissue, even with low antigen expression of the target. This results in significant and sometimes quite harmful side effects and has limited the dose and applicability of this extremely potent antitumor immune mechanism, particularly for solid tumors. We believe our Probody platform has the potential to meaningfully widen the therapeutic window for TCBs by localizing their therapeutic activity and target engagement to the tumor microenvironment. We have demonstrated this concept in nonclinical models and are now moving into the clinic in collaboration with Amgen with our first Probody T-cell bispecific CX-904. CX-904 is a conditionally activated TCB, targeting the epidermal growth factor receptor, or EGFR, and CD3, and is our most advanced program utilizing the modality. We submitted the IND in December of 2021 and, as noted by Sean earlier, we are in the process of initiating the first-in-human Phase I study in patients with advanced solid tumors now marking the sixth therapeutic candidate and the third treatment modality to enter the clinic from our Probody platform. Another exciting and emerging application of this powerful and versatile platform is in the field of cytokines. Our interest in this area stems from the fact that systemic toxicity and poor exposure have limited the clinical success of this important and highly potent class of immune modulators. By leveraging our deep understanding of the tumor microenvironment and our masking technologies, we have engineered a protease-activatable version of interferon alpha-2b that incorporates both affinity-based peptide and steroid masking technologies. In preclinical studies, we have already seen that the dually masked interferon alpha-2b provides an improved therapeutic window and we are driving this program towards clinical candidate selection. From my comments today, I hope I have conveyed to you the breadth and depth of our platform and pipeline and the progress that we are making towards our commitment to destroying cancer differently. With that, I'll turn the call over to Chris for a financial review.

Thank you, Amy. CytomX entered 2022 with a strong balance sheet. As of December 31, 2021, as Sean mentioned earlier, we had $305 million in cash, cash equivalents, and investments which we project will fund the operations of the company well into 2023. For the fourth quarter of 2021, revenue was $20 million compared to $6 million for the corresponding period in 2020. The increase was largely related to the CD71 collaboration with AbbVie. R&D expenses increased $15 million to $37 million during the three months ended December 31, 2021, compared to the corresponding period in 2020. The increase was driven by personnel expenses, clinical trial activities, and consulting and contract services to support our preclinical and clinical portfolio. G&A expenses were $9.5 million during the three months ended December 31, 2021, an increase of $300,000 compared to the same period in 2020, due mainly to increased personnel-related expenses. Before I hand the call back to Sean for his closing remarks, I want to reiterate Sean's point earlier on prudent financial management at CytomX. As we advance our pipeline to key inflection points, we will remain judicious with our capital and continue to marshal our cash resources thoughtfully.

Thanks, Chris and Amy. To wrap up, CytomX had a very strong 2021 and we have entered 2022 intensely focused on continued pipeline execution. Across multiple targets and within our broad and deep therapeutic pipeline, we have clearly demonstrated that conditional activation is a versatile approach to enhancing or indeed creating a therapeutic window for high-potential cancer treatments and we see enormous opportunity for our technology. We have much more work to do to destroy cancer and our different approach, leveraging our industry-leading Probody platform offers unique opportunities to make a real impact. As our pipeline continues to grow and mature, we are working in increasingly defined areas of unmet medical need as evidenced by the encouraging clinical activity of CX-2029 in lung cancer and our ongoing Phase II studies of praluzatamab in breast cancer and of our anti-CTLA-4 Probody in melanoma. The substantial investments we have made in recent years in our platform and in our pipeline position us well to build long-term value as we drive towards key milestones in 2022 and for our most advanced programs, whilst also advancing many new product candidates towards the clinic. I want to extend my sincere thanks to the CytomX team for their ongoing dedication and commitment to our vision and mission. And in closing, our thoughts are with everyone impacted by the unfolding events in Ukraine and we hope for a peaceful solution to the crisis. With that, operator, we can now open the call up for Q&A.

And our first question comes from Gavin Scott with JPMorgan. Your line is open. Please go ahead.

Hi, thanks for the update and thanks for taking our questions. Question on CX-2009 and Arm B in the TNBC breast cancer population. I'm just curious on the opportunity in the CD166 positive TNBC. And is there any stratification criteria in the protocol to see, I guess, prespecified analysis across CD166 expression levels?

Yes, thanks for the question, Gavin. Let me start by addressing that. As Amy pointed out earlier, in Arm A, we have observed high expression of CD166 in the majority of patients during Phase I and in public databases. Therefore, for Arm A, we are not using target selection as a criterion for enrollment. In contrast, for Arm B, based on our Phase I experience and data from public sources, we see that CD166 expression is more varied, so we are implementing a patient selection strategy for Arm B. We do require that patients in both Arms A and B have high CD166 levels for the definition of efficacy evaluable. We're not discussing the specific cutoff at this moment, as we need to learn more about the target, especially in triple negative cases, which have a diagnosis of exclusion and a fairly varied histological definition. More information will be shared as we progress through the year.

Great. Thank you.

Thank you. And our next question comes from the line of Kaveri Pohlman with BTIG. Your line is open. Please go ahead.

Yes, good afternoon. And thanks for the update. For TNBC Study again, are you enrolling patients who have prior experience and will we see any data for that?

Yes, Kaveri, thanks for the question. So if I could just repeat it. So are we enrolling patients who have experience on Trodelvy? The short answer is yes, we do expect to see some patients for sure, having experienced Trodelvy. I want to remind everyone that in our previously reported clinical study, we did see a very intriguing response in a patient who had progressed on Trodelvy on sacituzumab. So we have evidence that praluzatamab can work in that patient population. We are enrolling in the U.S. and ex U.S. and so we would expect, given the approval in the U.S. and the pending approvals ex U.S., that we would end up with a somewhat mixed patient population, some of whom have and some of whom have not been treated with Trodelvy.

Got it. That's useful. And regarding the EGFR CD3 bispecific, the triple meeting poster shows a two plus two design for this molecule. Can you talk about your rationale for using a two plus two format because I believe that format is mostly used for better safety, but 904 is already masked to provide tumor-directed activity.

Yes. Good question and thank you for referring to some of our earlier work on the program. Just to clarify, the two plus two you mentioned is the dual antigen for both CD3 and two EGFRs, correct?

Correct.

Yes. So we haven't disclosed the actual molecular anatomy of 904 to this point. We have done a considerable amount of additional optimization of that program to ultimately reach 904 as the clinical candidate, in collaboration with our partner, Amgen. And so actually, the structure of 904 is not yet disclosed.

Got it. Thank you. And thanks for taking my questions.

You're welcome.

Thank you. And our next question comes from the line of Joe Catanzaro with Piper Stanley. Your line is open. Please go ahead.

Hey, thanks for taking my question. Maybe the first one for me. I think for CX-2029 initial Phase II readout. Ahead of that, you characterize the size of the data set that's going to show meaningful progress towards the planned patients per cohort in that study. So maybe with that, at this point, I guess, how would you characterize expectations for sample size for 2009's initial Phase II monotherapy readouts? And I have a follow-up.

Joe, thanks for the question. So just to recap the goals of the Phase II, the 3-arm study. The goal is to enroll 40 efficacy evaluable patients in each arm. And we are making very good progress with enrollment. As you may recall, we had a few bumps in the road last year, but the team has done an amazing job, and we are making progress. Our guidance at this point is from data from Arms A and B initial data this year. We do expect it to be meaningful numbers of patients. We're not quite ready to comment on a specific number at this point.

Okay, got it. And then, if I could just ask a follow-up. I was scanning through the 2009 publication and I noticed the figure that showed a strong correlation between unmasked antibody and the tumor and expression of CD166. And I'm trying to understand what the cause-effect relationship there is if you could help with that, that would be great.

Yes, it's a great question, and thanks for studying the publication in detail. There's a lot in there that we wanted to report. I don't want to get to too many details here but I mean there's a lot still to learn about the sequence of events with regard to Probody functionality. One can imagine this derives from a relationship between activation and target level and the order in which the Probody actually becomes converted into the active form. So it's an intriguing observation, there's a little bit written in the paper about that but we think it provides some interesting translational insight into how this platform functions.

Okay. Got it. Thanks for taking my questions.

You're welcome.

Thank you. And our next question comes from the line of Mara Goldstein with Mizuho. Your line is open. Please go ahead.

Hi, thank you for taking my questions. This is Supawat for Mara Goldstein. My question is about CX-2009, which now has data expected in the second half of 2022. Since it was previously indicated for 2022, could you consider this a slight delay? I would appreciate any additional details you could provide.

Good question. I would not characterize it as a delay. It's obviously a refinement of our guidance that we wanted to provide today. Given that this is a fairly substantial Phase II study, we are working towards providing meaningful updates. By giving ourselves a little more time to gather data that will guide us in the next steps of product development and allow us to share that with external stakeholders, we believe it's the right approach. We see no need to communicate data that is too premature.

Got it. Thank you.

Thank you. And our next question comes from the line of Roger Song with Jefferies. Your line is open. Please go ahead.

Great. Thank you for taking our questions. Just quickly to confirm some of the logistics for 2029, you are expecting the non-cell lung cancer update in the second half, any comment around the other cohort like DJ and the DLBCL data readout. Similarly, for the four. Any color around the data timing will be helpful.

Thank you for your questions, Roger. Regarding CX-2029, we have a substantial amount of data that we aim to disclose in the second half of this year, which will be a crucial period for our pipeline. At this point, we cannot provide further details on the additional cohorts for 2029, but enrollment is still ongoing in esophageal and gastroesophageal junction cancers, and DLBCL is also part of that expansion phase. We will share more updates throughout the year. As for 904, we are in the early stages of getting it operational. The team has successfully cleared the IND, but we do not expect to have any data from 904 this year. We need time to start dose escalation, especially since initial doses for T-cell engaging bispecifics tend to be lower. Therefore, we are not ready to provide guidance on the data for 904 at this time.

Got it. Thank you.

You're welcome.

Thank you. And our next question comes from the line of Mitchell Kapoor with H.C. Wainwright. Your line is open. Please go ahead.

Hey, there. Thanks for taking the questions. The first one, I just wanted to ask on Arm C of the Phase II of praluzatamab. What kind of added benefit could we expect from pacmilimab to show in TNBC? And how should we think about it being positive when we compare to separation from monotherapy?

Yes. Thanks for the question, Mitch. Let me hand that one over to Amy.

Mitch, thank you for your question. I want to highlight that we have shown monotherapy activity with each of these agents in triple-negative breast cancer. We reported monotherapy activity with pacmilimab in the Phase I expansion for triple-negative breast cancer, particularly in the challenging subset known as inflammatory breast cancer. We did see activity there. Additionally, we observed activity in triple-negative breast cancer with 2009. As for what you might expect from the combination, it’s not entirely clear yet what we need to see. We know that checkpoint inhibition is effective when combined with chemotherapy, as evidenced by pembrolizumab maintaining its approval in frontline triple-negative breast cancer. We have an idea of what we might expect, but we can't provide specifics about what we are hoping to see. We are considering response rates with sacituzumab as monotherapy in this setting to be in the mid-30s. We would like to observe a compelling response in a patient population that may be refractory to sacituzumab.

Great. And then just thinking about any potential milestones we could see this year, could you talk about any of those that we could see from collaborators?

Yes. Thank you, Mitch, for your question. We haven't disclosed any additional milestone structures in our alliances at this point. As I mentioned earlier in my comments today, our cash runway projection extends well into 2023 and does not factor in any milestones or new business development activity. I have consistently been able to finance the company through a combination of dilutive and nondilutive capital, and I expect that trend to continue.

Great. Thank you very much.

You're welcome.

Thank you. And our next question comes from the line of Peter Lawson with Barclays. Your line is open. Please go ahead.

Thanks for taking the questions. Just as regards to the update, thanks for the timing around updates in the second half. Anything you can say around kind of the number of patients or time on therapy for the triple-negative and HR-positive HER2-negative arms?

Peter, this is Amy. Thanks for the question. So for Arm A, which is hormone receptor-positive breast cancer, one of the key secondary endpoints is going to be CBR24 which is a stable CBR stable disease through 24 weeks. And obviously, that takes six months to get if you're going to get to 24 weeks. So there's a time component to this. Response rates are not necessarily the strongest indicator of activity in this particular disease. We'll see what the details of the data are with deruxtecan. And of course, we're interested to see what happens with sacituzumab in this setting with regard to response rates. But we're really focusing on CBR24 and then, of course, PFS because if you think about what might be the next study, it's going to be depending on what the data show us. If they're hinting in a way that favors activity with this, it would be a randomized study where PFS might be the endpoint. So we'll be looking at those endpoints very carefully in Arm. For Arm B, we're talking about a patient population of approximately 40, 4-0 efficacy evaluable patients. So a population that we can look at that we can get our heads around and that we can begin to define the point estimates for the pivotal study. That's what we're talking about when we say a meaningful patient sample size. The same thing for triple-negative breast cancer. Here, of course, response rates can be the basis for accelerated approval. However, as you already know, we need durability of those responses. You can't just get the first confirmation and report the response rate. So response rate, durability of response are going to be the two key endpoints that we're focusing on in that patient population. And again, a meaningful patient population. And what do I mean by meaningful? Something where we would know how to take this molecule into the next study with the next study having an eye towards registration.

Got you. Same question really for 2029 in non-small cell lung cancer, kind of how much of an update we're going to get? Is that going to be predominantly non-small cell lung cancer?

So too early to comment on any specific indication, I would just observe that EGFR is a widely expressed tumor antigen with a lot of unharnessed potential, I would say, across many different tumor types. So we're excited about this product candidate. And as we mentioned, the Phase I design is a dose escalation in solid tumors initially and together with our partner, Amgen, one could envisage some further focusing of that study over time into specific tumor types, obviously, that express EGFR, of which there are many.

Okay. Thank you so much.

You're welcome.

At this time, I would like to hand the call back over to Chau Cheng for his closing remarks.

On behalf of the executive team, I would 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.

This does conclude today's conference call. Thank you all for participating. You may now disconnect. Have a great day.