Ladies and gentlemen, thank you for standing by and welcome to Zai Lab's 2026 AACR Investor Call. At this time, all participants are in listen-only mode. Later, we will conduct a question and answer session, and instructions will follow at that time. As a reminder, today's call is being recorded. It is now my pleasure to turn the floor over to Dr. Rafael Amado, Zai Lab's President and Head of Global Research and Development. Please go ahead, sir. Hi, everyone. Thank you so much for joining us today. I am Rafael Amado, Zai Lab's President and Head of Global R&D. Before we begin, we will be making forward-looking statements today, and I ask you to review slide two for further details. Moving to slide three, I'm joined today by two outstanding clinical investigators. Dr. Luis Paz-Ares is a leader in lung cancer. He chairs the Medical Oncology Department at the Hospital Universitario 12 de Octubre and Head of the Lung Cancer Unit at Spanish National Cancer Research Centre in Madrid. Dr. Rohit Thummalapalli is an Assistant Attending Physician and Gastrointestinal Medical Oncologist at Memorial Sloan Kettering Cancer Center. He specializes in GI and neuroendocrine cancers. On the next slide, the disclosure information for both doctors. Moving to slide five, here's our agenda. Dr. Paz-Ares will present first-time intracranial data with zoci in small cell lung cancer, followed by Dr. Thummalapalli in neuroendocrine carcinomas. Both posters will be presented tomorrow at AACR. I will conclude with an overview of zoci's clinical development plan and additional AACR highlights, followed by Q&A. Now with that, I will pass the call to Dr. Paz-Ares. Hello, this is Luis Paz-Ares. I'm a medical oncologist at Hospital Universitario 12 de Octubre in Madrid. Over the next few minutes, I'm going to report to you on the intracranial activity of zocilurtatug pelitecan in extensive-stage small cell lung cancer with brain metastasis. Extensive-stage small cell lung cancer is a high-grade, very aggressive carcinoma characterized by early metastatic spread and a very aggressive clinical behavior, and poor prognosis. One of the characteristics is the propensity to develop brain metastasis, which are actually impacting the survival, but also in quality of life. Some 20% of the patients really present brain metastasis at the initial diagnosis. Over the time of the disease, so the natural history of the disease, some 30% of the patients do develop brain metastasis. As I said, that is really a very relevant clinical condition. Far, the treatments are not the most effective therapy for that particular issue. At present, when a patient is having symptomatic brain metastasis, we typically deliver radiotherapy, stereotactic, or whole-brain irradiation. The problem is that often you have to stop systemic therapy while you're giving the brain metastasis irradiation. You put the patient at risk of rapid extracranial progression. For asymptomatic patients, often, we administer brain radiation as well, and the risk being as well to develop into the future some cognitive deterioration. Overall, the survival impact is very clear for those patients. The real-world data suggest that typically, the median OS for those patients is in the range of eight months, being particularly bad for patients that really present brain metastasis and are treated with whole-brain irradiation. The rationale to use the zoci ADC into the brain is because it allows a target delivery of the payload on those tumor cells that are expressing DLL3, which is most of the cells. The payload is actually producing direct cytotoxic killing, and the good theory is that each ADC will have a good number of payload molecules of the Topo 1 inhibitor, is actually having a DAR of eight, and it's having a strong metastatic effect that really enhance the activity in the various tissues. In the next few minutes, I'm going to provide you the data that are being presented at the AACR meeting this year. Pretty sure that you are aware of the background, what is zocilurtatug pelitecan, which is an ADC directed to DLL3 with a very efficient payload, a Topo 1 inhibitor with a DAR of eight. It has a very relevant bystander killing mediated by the payload, as I mentioned, as the drug is typically released and accumulated into the tumor microenvironment thanks to the TMALIN platform that is being used to produce this ADC. The data from this study on brain metastases are coming from the dose escalation and expansion phase I study, ZL-1310, using the ADC as monotherapy or in combination with Atezolizumab or Atezolizumab plus carboplatin in extensive stages of small cell lung cancer, with a data cutoff of February 2026 and a median follow-up of some 8 months. The anti-cancer activity has been actually assessed with an independent radiology committee, using the mRANO brain metastasis. With this criteria, you may measure up to five brain lesions, and they should have been studied using the contrast enhancing, and importantly, the diameter should be at least in the longest 10 mm and at least five in the perpendicular diameter. Included patients in these trials were patients with extensive stages of non-small cell lung cancer with asymptomatic brain metastases, and archival biopsy was collected to retrospective DLL3 testing, good PS, and importantly, prior DLL3-directed therapy was allowed. You see here on part one and part two what was the dosing used, and from 0.8 mg per kg to 2.8 mg per kg in the part A1, and the second, the part two, the patients were randomized to receive 1.2 or 1.6 mg per kg. As you see here, 136 patients were included on this study, and importantly, brain metastases were seen in 49, 36%, and out of those, about 1/3, 30.2% overall, didn't receive prior irradiation. That means 2/3 received prior irradiation and 1/3 didn't before entering the study. As you see, 2/3 of the patients had received one prior line of therapy, and 1/3 had received two or more lines of systemic treatment, and more than 90% received PD-L1 therapy, and about some 10% of the patients received DLL3 inhibitors. The overall response rate that we have seen was 34%. 22 out of 41 patients responded, and responses were particularly high on those patients treated at 1.6 mg per kg. That was 62% responses. 50% were assessed responses in cases treated with 1.2 mg per kg. Importantly, responses were seen in 50% of the patients treated with prior radiotherapy and in 60% of those that didn't receive radiotherapy before entering the study. Out of the 22 responders, 21 responses were already seen at the time of the first tumor assessment. That means some six weeks. The other issue important is that 14 responders, that means 2/3 of the responses are still ongoing with a median time of nine months. You see here two illustrative cases. The first case on the top is a 60-year-old female treated with carboplatin etoposide Durvalumab plus that developed a brain metastasis, as you see here, during the induction treatment in the first line. patient received without prior irradiation, ZL-1310 at 1.6 mg per kg, and as you see here, the time of the initial evaluation, the patient was on complete response and still on complete response six months later. The second case was another female, 65 years old, that progressed while on initial therapy with carboplatin etoposide Atezolizumab, developing multiple brain metastases. Importantly, the patient didn't receive before entering into the ADC study, radiotherapy. As you see here, a clear response was already seen at the time of the week six that was evolving over time to a scar remaining at week 24. Safety-wise, the drug was reasonably well tolerated, and the typical side effects we have seen related to the drugs were typically seen consistent with the topoisomerase inhibition mechanisms of the drug. You see here, some about 1% of the patients at all those levels had some grade three or four treatment emergent side effects. You restrict to those related to the treatment, you see that the doses that 1.2 and 1.6, only about 16% or 2% of the patients really had treatment emergent adverse events related to the drug. Typical side effects, particularly cytopenias, as you see here, are mainly myelosuppression. Others include, of course, nausea, fatigue, asthenia, so on, typically only grade 1 or 2. As a conclusion, let me tell you, the drugs ZL-1310 has demonstrated a quite relevant high intracranial response rate in patients with extensive stage small cell lung cancer with brain metastases at baseline. As you remember, the overall response rate was in the range of 54%, including complete responses in 17% of the cases. Responses were observed in patients without prior radiation, 60%, but also in those with prior radiation, 50%. The higher response rate was observed at the 1.6 mg per kg dose level. At this dose, the treatment was pretty well tolerated. Remember, side effects grade 3 or more were in the range of 15%, and we didn't identify new signals of safety, including no hemorrhages at the intracranial level. This study is still ongoing, enrolling now patients that haven't received DLL3-targeted therapy before study entry. In addition, there is an ongoing phase III study, the DLLEVATE study in second-plus lines of extensive stage small cell lung cancer, where patients that have progressed to platinum-based chemo with or without durvalumab are to be randomized to zoci versus the investigator's choice of therapy, topotecan, irinotecan, or amrubicin. This is very much what I have to say today. Thank you very much for your attention. Thank you, Dr. Paz-Ares. I'm excited to be here to present the updated data for ZL-1310 or zoci in extrapulmonary neuroendocrine carcinomas and other DLL3-expressing tumors. Extrapulmonary NECs are highly aggressive malignancies with very poor outcomes. Five-year survival in patients with metastatic disease is less than 15%, and median overall survival in these patients is only five to eight months. Extrapulmonary NECs share key biological features with small cell lung cancer, including frequent expression of DLL3. However, treatment options remain very limited, particularly after progression on platinum-based chemotherapy. While initial responses following frontline etoposide and platinum-based chemotherapy can be observed, durability is limited compared to small cell lung cancer. Most notably in the second-line setting, there is no established standard of care. Physicians can use different single agent or combination chemotherapies with response rates of around 20%, but short median progression-free survival. In addition, different from small cell lung cancer, there is no established role for DLL3-targeted T-cell engagers in extrapulmonary NECs and no established role for new checkpoint inhibitors. Hence, there really is an urgent medical need for more treatment options for these rare and aggressive cancers. This is a global phase Ib/II study of zoci in patients with extrapulmonary NECs and other DLL3-expressing solid tumors who have progressed on or after platinum-based chemotherapy. The study included two cohorts, one in gastroentero-pancreatic, or GEP-NECs, and the other in other extrapulmonary NECs, including large cell neuroendocrine carcinoma of the lung, genitourinary or gynecologic NECs, Merkel cell carcinoma, and other DLL3-expressing solid tumors. For extrapulmonary NEC patients, DLL3 expression was evaluated retrospectively by immunohistochemistry, but was not required for eligibility. Initial cohorts of 10 patients were enrolled with expansion triggered by observed responses, and the phase II part is a single-arm study, which is currently enrolling. The study enrolled evenly in the U.S. and China. As you can see, the majority of patients had advanced stage disease at enrollment. These tumors were highly proliferative, as reflected by the majority of patients having high Ki-67 levels. At baseline, nearly all patients had received prior platinum-based chemotherapy. About a quarter of patients had prior immunotherapy, of course, although the role for checkpoint inhibitors in extrapulmonary NECs is still debated. Five patients received prior irinotecan. These were all in Cohort 1, consistent with the common practice of using FOLFIRI or FOLFIRINOX in GI neuroendocrine cancers in the second line. Overall, we feel the study population represents a typical extrapulmonary NEC population that we see in clinic. In terms of efficacy, we saw encouraging antitumor activity with zoci. Among response evaluable patients, the overall response rate to date is 38%, with a disease control rate of approximately 56%. We feel these responses are clinically meaningful in these aggressive tumor types with few treatment options after platinum-based chemotherapy. Tumor reductions were observed across multiple extrapulmonary NEC subtypes. The response rate in Cohort 1, enrolling gastroenteropancreatic or GEP-NECs, was 33%, and in Cohort 2, which enrolled extrapulmonary NECs other than GEP primaries, the response rate was 44%. As shown in the waterfall plot, we saw substantial target tumor shrinkage in patients both in Cohort 1 and Cohort 2, although we did absorb more patients in Cohort 1 with primary progression. When we break down the data in more detail, we see responses were observed across a spectrum of extrapulmonary NECs. Interestingly, in the five patients who received prior irinotecan, which is another TOP1 inhibitor, no patients showed a response. All of these five patients had gastroenteropancreatic NECs or GEP-NECs. Whereas a patient with NEC of the cervix who received prior topotecan, which is another TOP1 inhibitor, did achieve a partial response with zoci. More data is being generated to understand factors that impact response to zoci. We are also seeing early signs of durability with multiple cases of durable responses across different origins of NEC. These data are still immature, but taken together, these data suggest clinically meaningful efficacy with zoci. Similar to what we saw in small cell lung cancer, we have not yet observed a clear relationship between DLL3 expression and response. Importantly, responses have been observed in DLL3-negative patients, and we have seen activity across a broad range of DLL3 expression levels. While preliminary, this data does not support excluding patients from zoci treatment in the case of negative DLL3 expression. Taking a look at safety and tolerability, overall, zoci demonstrated good safety and tolerability in extrapulmonary NEC, consistent with the safety profile of small cell lung cancer. Most events were low grade. The most common events were hematologic and gastrointestinal, including anemia, leukopenia, and nausea. There was only one case of grade 2 ILD among these 46 patients treated to date. We have limited data so far, but the ILD rate in patients with extrapulmonary NEC seems to be lower than the small cell lung cancer, and this may be related to difference in tumor burden in the lung and lower frequency of prior radiation to the chest. In summary, we believe ZL-1310 or zoci is well-tolerated compared to other treatment options in extrapulmonary NECs. To bring this to life, I'll walk through a representative patient case. This is a 52-year-old patient with small cell neuroendocrine carcinoma of unknown origin. He exhibited primary progression on first-line platinum-based chemotherapy, and then initiated ZL-1310 and achieved a partial response within six weeks. We saw a large tumor reduction at week six, with one of the target lesions nearly disappearing. The tumor shrinkage is deep and nearly 75% by week 18, and the patient is still benefiting at time of data cutoff, with a very encouraging durability of response of more than six months. In summary, zoci is demonstrating clinically meaningful activity in a very difficult to treat population. We're seeing responses across multiple extrapulmonary NEC tumor types and primary origins. While cross-trial comparisons must be interpreted with caution, these response rates to date appear favorable relative to historical chemotherapy outcomes. The safety profile is consistent with what we observe in small cell lung cancer, and the study is ongoing with expansion to phase II and continued follow-up in the phase I-B ongoing to better characterize efficacy. With that, I'll turn it back to Rafael. Thank you, Dr. Thummalapalli. This next slide outlines our broad and comprehensive development strategy for zoci across both small cell lung cancer and extrapulmonary neuroendocrine carcinomas. Starting with small cell lung cancer, we are advancing across multiple lines of therapy. In the second-line and third-line setting, our global phase III DLLEVATE study is ongoing. We expect to complete enrollment in the first half of 2027, followed by an interim analysis positioning zoci monotherapy for potential accelerated approval in 2028. At the same time, we are expanding into first line. Here, we have multiple ongoing combination strategies. First, we're evaluating zoci in combination with a PD-L1 inhibitor plus or minus chemotherapy. We expect to present combination data, including first-line data, in a conference later this year and expect to initiate a pivotal trial by end of the year with the selected combination. Additionally, we also recently announced a collaboration with Amgen as well as Boehringer Ingelheim, which I will discuss in an upcoming slide. Turning to EPNEC, we're advancing zoci monotherapy in the second-line setting, where there is significant unmet need. The ongoing study is generating registration-enabling data. In parallel, we're exploring combination strategies, including obrixtamig, through our collaboration with Boehringer Ingelheim, to further expand the opportunity in this population. Overall, this strategy reflects our goal to position zoci as a backbone therapy across both small cell lung cancer and EPNEC, spanning monotherapy and combination approaches and across multiple lines of therapy. I wanted to briefly touch on the recently announced collaboration with Amgen and BI to pursue combination strategies in small cell lung cancer and neuroendocrine carcinomas. The rationale is grounded in complementary mechanisms. zoci delivers rapid cytotoxic tumor debulking, while T-cell engagers activate immune-mediated killing to drive durability. Together, this approach has the potential to both deepen and extend responses. Importantly, these agents are expected to have minimal overlap in toxicity. Combined with zoci's favorable safety profile and compelling systemic and intracranial activity, we believe it is well-positioned as a backbone for combination therapy. We've initiated a global phase Ib study with Amgen evaluating zoci in combination with tarlatamab. The study includes dose exploration and dose expansion in both tarlatamab naive and tarlatamab-exposed patients. We plan to also evaluate a triplet in the first-line setting. We also plan to initiate a global phase I-B/II study with BI evaluating zoci in combination with Abraxane in neuroendocrine carcinomas, as well as a triplet combination with Atezolizumab in first-line small cell lung cancer, and depending on emerging data, in first-line EP-NEC as well. Amgen and BI will sponsor and lead their respective global studies. Overall, we see zoci emerging as a differentiated DLL3 ADC with the potential to become a new standard of care across small cell lung cancer and extrapulmonary neuroendocrine carcinomas as monotherapy in previously treated population and as a backbone in the frontline combinations. With that, let me turn to the broader pipeline we're advancing at AACR. ZL-1222 is our IL-12 PD-1 immunocytokine. It is designed to overcome the key limitations of current immune checkpoint blockade, which has had limited activity in cold tumors, and systemic IL-12, which could result in significant toxicity. It combines PD-1 targeting for tumor localization. It silenced Fc for half-life expansion and a potency reduced IL-12 to improve tolerability. This enables localized activation of IL-12 signaling in the tumor microenvironment, reprogramming the TME and activating T-cells to drive durable antitumor immunity. We see clear antitumor activity. ZL-1222 inhibits tumor growth in the ICV-resistant model, EMT6, with good tolerability, and shows dose-dependent efficacy that tracks closely with exposure in CT26 model. Together, these data show that ZL-1222 can drive meaningful antitumor responses in a biologically predicted profile. Our pilot toxicology study in non-human primates showed tolerability up to 10 mg per kg. We're currently conducting a dose range finding study and are preparing GLP toxicology study to establish its safety profile. We're now advancing towards IND-enabling studies in 2026. Turning now to ZL-6201, our LRRC15 targeting ADC. ZL-6201 combines a humanized anti-LRRC15 antibody with a protease-cleavable linker and a camptothecin-based Topo 1 payload. Mechanistically, this enables efficient internalization and payload release in targeted cells, leading to DNA damage and tumor cell death. Importantly, LRRC15 is broadly expressed across sarcomas and in cancer-associated fibroblasts within the stroma of many epithelial solid tumors with limited expression in normal tissues, making it a highly attractive ADC target. Collectively, these findings highlight the potential for ZL-6201 to address significant unmet need across both mesenchymal and epithelial malignancies. Looking at the efficacy data, ZL-6201 demonstrated dose-dependent tumor growth inhibition across multiple LRRC15-positive sarcoma patient-derived xenograft models. We also observed robust antitumor activity in non-sarcoma CDX models, where LRRC15 is expressed on cancer-associated fibroblasts rather than in tumor cells. In these models, CAFs facilitate the release of C24 payload to deplete neighboring antigen-negative tumor cells, demonstrating potent efficacy driven by a strong bystander effect. Together, these data support the dual mechanism of action involving both direct tumor cell killing and stromal targeting. Based on this profile, a global phase I study is now underway, with enrollment acceleration planned in 2026. With this, I will end the highlights from AACR. Now please join me, Dr. Luis Paz-Ares, and Dr. Rohit Thummalapalli for questions and answers. Thank you. We will now begin the question-and-answer session. To ask a question, please press star one and one on your telephone and wait for your name to be announced. To withdraw your question, please press star one and one again. Please stand by while we compile the Q&A roster. We will now take our first question from the line of Jonathan Chang from Leerink Partners. Please ask your question, Jonathan. Your line is open. Hi, guys. Thanks for taking the question. Dr. Paz-Ares, how should we be thinking about the intracranial activity of zoci relative to standard of care in development stage treatment options in small cell lung cancer? How should we be thinking about the impact of this intracranial activity on overall survival? Thank you. Well, of course, today is still early days, because we haven't got, let's say, very robust data in terms of phase III trials. The only thing I can tell you is that the response rate we have seen, you remember 54% overall intracranial response rate being 62% on those patients that actually were treated at a 1.6 mg dose. I think this is quite impressive in this setting as compared to standard of care drugs, which are more on the 20%-30%. That is at least encouraging data, thinking into the future about the possibility of impacting survival. At the same time, you're able to really get responses in the brain, very likely, I would assume that you have good possibilities of getting better or improvement in quality of life. Having brain metastases, particularly asymptomatic brain metastases, are really impacting very much on what you're able to do and your quality of life. I would say the early data are really encouraging, but still, of course, it's going to be needed randomized phase III trial. I'm fairly sure the trial we just described in the pre-treated setting is going to give us a more robust data. Early data are very encouraging. Understood. Thank you. Thank you. We will now take our next question from Michael Yee from UBS. Please ask your question, Michael. Your line is open. Thank you. Good morning. We had two questions. One was just thinking about the enthusiasm about this data in intracranial tumors and how that would drive a robust response in the phase III frontline small-cell study, where obviously it's much better to treat earlier. Could you talk a little bit about what type of results you would expect to then see in the first-line study and how that would compare versus, say, tarlatamab, which has a first-line label? The second question then is, I guess you're going to combine the two. How would that be envisioned if the two of them are combined? Thank you. Okay. Related to the first question, I would say, typically at diagnosis, about 20% of the patients are having brain metastases. It's not only important to treat those 20% of the patients, but also to prevent brain metastases to happen in the future. That is a very frequent site of disease progression. Having a drug which is very effective into the brain, likely is going to prevent brain metastases to happen or at least delay that progression to happen. Of course, durvalumab is an amazing therapy with a clear impact on survival and in other endpoints. The ideal here would be to be able to combine those drugs. My anticipation would be that there are a couple of trials in the first line setting, induction and maintenance. I would assume in the near future, the result of those trials are going to be positive, and tarlatamab is likely to be part of the standard of care. The way I envision this ADC against DLL3 in the first line setting will be in combination with tarlatamab. Hopefully that could have at least there are good rationale to really have a synergistic effect between both of them. I think, it's been commented by Rafael that combination data are going to be produced, and I suppose frontline would be a quite urgent strategy into the future. Thank you. Thank you. We will now take question from line of Anupam Rama from JP Morgan. Please ask your question. Anupam, your line is open. Hey, guys. Thanks for taking the question and congrats on the update. One for the company. In the phase III DLLEVATE study in second line plus small cell lung cancer, can you walk us through the rationale to stratify based on having brain mets or not? Isn't the activity that you're seeing today here at AACR, ultimately within brain mets, that's going to be key for PFS, right? In the overall population as de-risking? Thanks so much. Yeah, that's a very good question. Thanks for asking. Generally, these studies are stratified by brain metastasis because they pertain a poor prognosis, as was remarked upon the beginning by Dr. Luis Paz-Ares. The difference in second line on survival may be between five to nine months for those that don't and those that do have brain metastases. Stratification ensures that the number of patients with brain metastases is equal in both arms. Now, the point that you're making, I think, is that if brain metastases patients do appear to do equally well as those that don't when they're treated with zoci, why stratify? Well, in the control arm, that will not be the case, and we wouldn't want there to be an unevenness in the control arm whereby one preponderance of patients with or without brain metastases occurs, and then the comparison wouldn't be apple-to-apple comparison. I think in spite of the good data that you've heard today, because it's a randomized trial against chemotherapy, the stratification is necessary. Thank you. Do you have any follow-up question on the plan? No, thanks for taking my question. Thank you very much. Our next question comes from the line of Yigal Nochomovitz from Citigroup. Please ask your question. Yigal, your line is now open. Okay, thanks. I thought I heard my name. One for Dr. Paz-Ares, one for Dr. Thummalapalli, and one for Rafael. Dr. Paz-Ares, I'm wondering with the 10 patients that had responses intracranial, could you describe whether they also responded systemically? What was the concordance? Because I recall with tarlatamab in their intracranial data, I believe the concordance was quite high. Okay. Again, here the concordance is pretty high. I mean, those data have been already reported in, I think, in prior trials, and the response rate is over 50% as well. The important thing would be what, because there are a number of drugs that induce a reasonable response rate systemically, but they fail to produce the same type of activity in the brain. The reason for this presentation here at the AACR is specifically to highlight that the responses you're seeing in the brain are similar. There is no problem to access into the brain and to induce responses here. That is very much the reason. Okay, thanks. For Dr. Rohit Thummalapalli, I'm just curious, do you have any theories as to why you're not seeing a differential response with respect to DLL3 expression? Yeah. Yeah, it's a great question. I think we have limited data so far. I think there could be a number of reasons. In extrapulmonary NECs, DLL3 expression is not as universal as it is, or at least as prevalent as it is in small cell lung cancer. There also could be some heterogeneity. There also could be other factors that are DLL3 independent that could be associated. Of course, the drug also kind of invokes a bystander effect as well, and so you may not necessarily need to have high level homogeneous DLL3 expression. You could potentially respond to the drug even with lower levels. I think a lot of different possible reasons, but I think that data will bear out with time. Okay. For Rafael, quickly, you have the interim coming up next year, as you mentioned. What more can you tell us today about that interim? The sorts of questions we'd want to know would be the% of PFS maturity, what you can say about the bar, meaning the critical hazard ratio. How much can you tell us today about what would be necessary for that study to report a positive interim next year? Thank you. Yeah. The critical endpoint for conditional approval or accelerated approval is response. It's not PFS. FDA will be looking at durational response, and the analysis will be done when patients have been able to or have had an opportunity to be followed for at least six months after the first scan. The agency will be looking at the durability of that response as well. It won't be based on PFS or survival, but rather on differential response rate, and the durability of that response. In terms of the type of difference that needs to be seen, this is not something that we've commented in the past, and I think it will be probably something that FDA will deem clinically relevant. I can tell you that we are tracking very well for that endpoint. We plan to have approval by the end of the next quarter, and shortly after, we will be able to do the analysis. Fingers crossed and stay tuned. Okay. Thank you. Thank you. We will now take our next question from Li Watsek from Cantor. Please ask your question. Li, your line is open. Good morning. This is New Benon for Li. Question about the next Jesse update. It seems like the next update is going to be in the second half of 2026, and that's going to be the combination of chemo and PD-L1. Can you guys set the expectation there? What kind of data we should expect to see? Thank you. Yeah. I think you're asking about the frontline data with chemotherapy and PD-1. We treat a number of patients with both PD-1 in second line as well as in first line, and then in first line with carboplatin as well. All that data is maturing. The majority of patients are with PD-1. I can tell you that the toxicity does not seem to be overlapping, and we're being able to advance the doses as expected. We obviously are observing data that is very encouraging to us, but we need more time to see what the durability of that data is going to be. Our hope is that with good data sparing chemotherapy, we will be able to treat longer than with chemotherapy alone. The majority of patients with chemotherapy alone tend to stop after about four cycles or so. Given the tolerability that you've seen with ZY, and the one that we're seeing with ZY plus PD-1, that the treatment to progression or toxicity will be longer with ZY. I think that is the underpinning of that phase III study. We're in discussions with regulators at the moment as to the actual details of the design. As I said in the prior remarks, we plan to present the data in the second half of this year, sometime in one of the meetings in the fall. That sounds good. Thank you. Thank you. As a reminder, before we take our next, it is star one one on your telephone keypad if you wish to ask a question. We will now take our next question from Linhai Zhao of Goldman Sachs. Please ask your question, Linhai. Your line is open. Thanks for taking my question. This is Linhai Zhao. Very exciting results. Congrats. I have two questions. The first question is how do you think about the potential confounding effect from the prolonged intracranial efficacy from the previous radiotherapy? What is the time gap between the last radiotherapy to the first dose of ZY? That's the first question. Second question, I would appreciate some clarification, as I see in the page nine of the deck, it was showing that ZY was able to penetrate the blood-brain barrier and enter within the brain tissue. That was somehow the reason that it can generate the high intracranial efficacy. Just want to clarify if is my understanding correct? Thank you. Sorry. Yeah. I was just going to say that the protocol requires at least a seven-day washout for radiotherapy. Dr. Luis Paz-Ares, please go on. Yeah. I mean, for sure, a washout were required. The only thing I can say with this limited data is that among those patients that didn't receive radiotherapy before, the response rate was 60%. In nine out of 15 patients, and it was very similar, I would say 50% response rate in patients that have been treated with prior radiotherapy, 13 out of 26. The number of patients are too small to really dissect on the time elapsed since last radiotherapy, always knowing, as Rafael mentioned, that anyway, it's going to be at least two weeks from last radiotherapy dose. You need to have a control image before starting baseline post-radiotherapy. That means the effect you're observing is not due to the radiotherapy, but is due to the drug. Anyway, that is the maximum we can say about those data, I have to say. Follow-up question, Linhai? Yeah, just on the second question, is the ability of ZY to penetrate the blood-brain barrier. Let's say the idea here being that the way the drug is working, is brain metastasis, of course, because our small cell lung cancer express quite uniformly DLL3 in the surface of the cell, and that facilitates the entrance into the tumor and into the microenvironment the drug is actually delivered with a high number of molecules of the payload per se. Of course, we know that when brain metastases are there is disruption of the brain barrier. Actually, the fact that we have observed such a high response rate somehow validates that concept, I would say. I don't know, Rafael, would you like to add on something based on the preclinical data? No, nothing else. I think the disruption of the blood-brain barrier is at some point, and also this is a very avid antibody with very low nanomolar affinity. Binding to DLL3 is with very high affinity. Perhaps that is one differentiating factor that makes it possible to have such high activity. Yeah, that's very helpful. Thank you. Thank you. Once again if you wish to ask a question please press star one one on your telephone keypad now. Thank you Thank you all very much for your questions. I'd now like to turn the conference back to Dr. Rafael Amado for his closing comments. Thank you so much, Dr. Thummalapalli and Dr. Paz-Ares. We believe that the data presented today reinforces the potential of zoci as a differentiating agent in DLL3-positive tumors and supports our strategy to advance it into multiple lines of therapies and in combination settings for both small cell lung cancers as well as neuroendocrine carcinomas. We are executing against the comprehensive global development plan, as I outlined, including the current ongoing phase II study, and we look forward to sharing additional data with you as the program progresses. We appreciate your time and interest today, and we look forward to keeping you updated. Thank you so much. Have a great day, and operator, you may now disconnect.