Zai Lab Limited (ZLAB) Earnings Call Transcript & Summary

Good day, and thank you for standing by. Welcome to the Zai Lab 2025 ASCO Investors Call. [Operator Instructions] Please be advised that today's conference is being recorded. I would now like to hand the conference over to your speaker today, Rafael Amado, President and Head of Global R&D. Please go ahead.

Hi, everyone. Thank you so much for joining us today. I'm 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 2 for further details. Moving to Slide 3. During today's call, we will be discussing the updated monotherapy Phase I dose escalation and dose expansion clinical data of ZL-1310, our investigational DLL3 targeted ADC. Dr. Patel, one of the lead researchers for this trial, is here to present the data and will be presenting the poster at ASCO later this afternoon. Dr. Patel is a hematologist, medical oncologist and serves as the Director of Drug Development for Florida Cancer Specialists and is an Associate Director of Drug Development for Sarah Cannon Research Institute. Following Dr. Patel's presentation, I'll discuss next steps for the program and then open the line for question and answers. Dr. Patel is unable to stay for the Q&A portion, but we are pleased to be joined by Dr. Spira, who is the Director of Clinical Research and CEO at NEXT Virginia, Co-Director at the Virginia Cancer Specialists Research Institute and a Clinical Assistant Professor at Johns Hopkins. I will now pass it to Dr. Patel.

Well, thank you, Rafael. My name is Dr. Manish Patel, I'm the Director of Drug Development at the Florida Cancer Specialists and Sarah Cannon Research Institute. And on behalf of my co-investigators, I'm excited to share the latest findings and insights from our ongoing Phase Ia/Ib multicenter study evaluating ZL-1310 in patients with recurrent small cell lung cancer. Later on this afternoon, we'll be presenting our poster at the 2025 ASCO meeting in the session entitled Developmental Therapeutics— - Molecularly Targeted Agents and Tumor Biology, poster #356. So small cell lung cancer accounts for approximately 15% of all lung cancers, affecting around 372,000 patients worldwide and resulting in approximately 270 deaths annually. It is characterized by a high proliferation index and early metastases with up to 70% of patients developing brain involvement. The prognosis remains poor with a median overall survival of around 13 months, and there is an urgent need for novel treatment modalities and targets. Recently, DLL3 has become a validated target for small cell lung cancer and other high-grade neuroendocrine tumors. ZL-1310 is a DLL3 targeted antibody drug conjugate consisting of a humanized anti-DLL3 IgG1 antibody with a topoisomerase 1 inhibitor payload with a cleavable linker that demonstrated promising clinical activity in patients with relapsed/refractory extensive stage small cell lung cancer as previously reported. In particular, Zocilurtatug pelitecan, we'll call it Zoci going forward, has some unique characteristics that may portend potential best-in-class treatment for recurrent small cell lung cancer, namely the high antibody affinity, relatively prolonged half-life and clean and frequent DLL3 expression in tumors allow for targeted killing. In addition, the cleavable linker and high DAR of 8 allows it to have a strong bystander effect, leading to good clinical activity across a wide range of DLL3 expression, as you will see. On to Slide #6. This is a study design for our Phase I trial designed to evaluate the safety and efficacy of Zoci monotherapy in patients with recurrent extensive small cell lung cancer following at least 1 prior platinum-containing regimen. Patients with asymptomatic brain metastases, both treated and untreated were allowed as well as patients who failed prior DLL3 targeted agents. The trial has evaluated 6 monotherapy dose cohorts with additional patients treated in expansion cohorts of 1.2, 1.6 and 2.0 milligrams per kilo of 1310 to optimize dose selection for pivotal studies. We highlight the 1.6 milligram per kilo dose to draw attention to those results in multiple slides going forward. In this update, 89 patients have been enrolled across 6 dose cohorts. Of these, 47% received 1 prior line of therapy and 53% of patients have failed at least 2 prior lines of therapy. Notably, the 1.6, 2.0 and 2.4 milligrams per kilo arms included 23%, 24% and 29% of patients, respectively, and these patients all had 3 or more prior lines of therapy. 90% of patients received prior anti-PD-L1 therapy, 11% received prior DLL3 targeting therapy and 30% of these patients have brain metastases documented at either target or nontarget lesions, 8 of which were untreated at the time of study entry. 74% of patients are available for efficacy assessment across doses and lines of therapy. Turning to safety on Slide 8. The safety analysis set includes 89 patients who have received at least 1 dose of zoci. In general, zoci demonstrates a remarkably well-tolerated and manageable safety profile. We are presenting the safety data in 2 cohorts, those receiving less than 2.0 milligrams per kilo, that is 0.8 to 1.6 milligram per kilo or those receiving 2.0 milligrams per kilo or higher to highlight the remarkable safety profile. Of note, only 16% of patients in the low dose group required dose interruptions for any cause and only 2 patients required dose reductions and no patients discontinued treatment due to adverse events. The dose reductions were due to low-grade pneumonitis, fatigue, hyponatremia and neutropenia. The data are even more impressive when we look at grade 3 or greater adverse events with only 6% experiencing this level of toxicity. Overall, however, there were 5 patients who discontinued treatment, all at the higher doses and 1 patient who died due to interstitial lung disease. This patient had previously received a high dose of chest radiation therapy. While initially responding to therapy, the patient withdrew from the study and opted to forgo further care. On Slide 9 is a table of treatment-related adverse events that occurred in greater than or equal to 10% of patients. The most common treatment-related adverse events of all grade included anemia at 40%, neutropenia at 30%, nausea at 26% and leukopenia at 23%. Grade 3 or greater heme toxicity was less than 5% in a lower dose group and only 26% in the higher dose group, indicating low systemic exposure of the TOPO1 payload in plasma. Overall, there were 9 patients who developed pneumonitis or interstitial lung disease. The low-dose group had 2 Grade 1 ILD cases and both of these recovered and were able to restart 1310 therapy. Now we turn to efficacy, beginning with the dose escalation results on Slide #10. In October 2024, we presented initial results of the triple meeting in Barcelona for 25 patients enrolled in the dose escalation, of which 19 were efficacy evaluable. At ASCO, we presented efficacy data on 28 patients enrolled in the dose escalation. These patients demonstrated a confirmed ORR of 68% and a disease control rate of 93% with strong efficacy across all dose levels. Of the 19 responders, 10 remained in response between 2.8 and 9.1 months. So half of these are still in response now greater than 6 months out. Turning to Slide #11. We are presenting efficacy by lines of therapy across dose escalation and expansion. Of the 89 patients treated as of April 1, 74 patients have had at least 1 post-baseline tumor assessment. The ORR remains quite robust at 67% in second-line patients with a disease control rate of 97% and decreases not unexpectedly in later lines. 29 of the 38 responders remain on study with the longest surpassing 9 months on treatment. The median follow-up of this group is 3.4 months and the median duration of response cannot be estimated. Interestingly, 87% of patients with stable disease also remain on study, highlighting the potential durable benefit in these patients. On Slide #12 is the efficacy by dose level in patients treated with 1310 in the second-line setting. Across all dose levels in the second-line setting, unconfirmed ORR was 67%. Even more impressive were the results from the 1.6 milligram per kilo arm, where patients achieved an unconfirmed ORR of 79% and a disease control rate of 100%. Together with a favorable safety profile, these data would support 1.6 milligram per kilo as a reasonable Phase III dose, pending the completion of dose optimization, longer follow-up and discussions with the FDA. The waterfall plot on Slide 13 includes the 74 efficacy evaluable patients treated across all dose levels, demonstrating 89% of patients experienced a reduction in their tumor burden. Interestingly, 55% of patients with stable disease and tumor reduction continue on study. Indeed, the vast majority of patients had tumor reductions and remain on study, some with stable disease and deep decreases in tumor dimensions, hence, the mature ORR may change over time. This next slide with a spider plot shows that most people achieved a response by their first tumor assessment, including 1 CR. This is unlike other mechanisms of action and results in rapid onset of activity in patients with bulky disease and in those with brain metastases with a median time to response of 5.6 weeks. In addition, frank progression is rare and some patients continue on study past 11 months. In second-line patients treated with Zoci, patients achieved response by their first tumor assessment, typically plateau. However, there are a few who continue to deepen in their response. The longest ongoing patient is approaching 48 weeks and the longest responder at the 1.6 milligram per kilo dose is over 36 weeks on trial. Turning to Slide #6, an interesting slide. Brain metastases are very common in patients with recurrent small cell lung cancer with up to 70% of patients experiencing such. Thus, activity in patients with brain metastases is an important factor for the treatment of these patients. In our study, we had 22 patients or 30% of patients who had either a target or nontarget lesion in the brain at study entry. The ORR of this cohort was 68%. However, the response in patients without prior cranial radiation was 86%. While intracranial disease response regardless of target lesion is ongoing through scan reviews, at least 4 patients with measurable target lesions and either no cranial radiation or cranial radiation longer than 6 months prior to study entry experienced intracranial tumor shrinkage of up to 70%. While we continue to evaluate intracranial activity in all the patients, we are highly encouraged by the data we observed. So in conclusion, ZL-1310 demonstrated an acceptable safety profile with low rates of drug withdrawal and low rates of high-grade adverse events. It presented clear evidence of high antitumor activity in patients with relapsed or recurrent extensive stage small cell lung cancer, including those with brain metastases. Responses were particularly notable among patients who had undergone one line or prior platinum-based systemic therapy at the 1.6 milligram per kilo dose and the stable disease rate may result in an increase in deepening of the responses as a follow-up is immature. Based on these findings, a Phase III pivotal trial assessing ZL-1310 in extensive stage small cell lung cancer patients is planned to start later this year. Thank you for your attention. We look forward to your questions and further discussions.

Thank you, Dr. Patel. Moving to Slide 19. The safety and efficacy profile of ZL-1310 continues to be compelling with a great opportunity to significantly improve outcomes of patients with small cell lung cancer. While the dose optimization study is still ongoing, the 1.6 milligrams per kilogram dose shows the most promising combination of response and tolerability thus far. With an unconfirmed response rate in second-line small cell lung cancer of 79%, a well-tolerated safety profile and efficacy in brain metastases, ZL-1310 has significant potential in this setting. While it is premature to assess the durability of response as the median follow-up in all patients is only 3.4 months, we note the longest ongoing response is 9.1 months with 29 of 38 responders still on treatment. Based on these results, we will be initiating a registrational study in second-line small cell lung cancer later this year. The study will be a randomized 2-arm study comparing ZL-1310 at the selected dose against investigators' choice of therapy. The trial is designed with overall survival as the primary endpoint. For accelerated approval, we'll also assess confirmed overall response rate. Secondary endpoints include duration of response, progression-free survival, time to response, safety and quality of life. Eligible patients will be those with extensive stage small cell lung cancer who have progressed after first-line platinum-based therapy and received only 1 prior line of systemic therapy. Key certification factors include the presence of brain metastases, chemotherapy-free interval and choice of chemotherapy in the control arm. We expect to initiate this registrational study in the second half of this year with a planned interim readout next year, which could potentially set the stage for an accelerated approval in 2027. Beyond second-line small cell lung cancer, we will also be pursuing opportunities in first-line small cell lung cancer and neuroendocrine carcinomas. Slide 20 summarizes the clinical development strategy and key catalysts in the next 12 months in these areas. Given its favorable safety profile, ZL-1310 is particularly well suited for use in the first-line setting, either to enhance maintenance treatment or as a potential replacement for chemotherapy. These strategies are designed not only to improve outcomes, but also to reduce treatment burden for patients with extensive stage small cell lung cancer. We've begun enrollment in the combo dose escalation portion of the study, which will be followed by dose optimization and then a pivotal combination trial after a defined follow-up period. We're also expanding the reach of ZL-1310 into other DLL3 expressing solid tumors, particularly poorly differentiated neuroendocrine carcinomas. The estimated global prevalence of DLL3 expressing in NEC is roughly 350,000 to 400,000 patients. These are aggressive tumors with poor long-term survival outcomes and very limited treatment options. We're aiming to accelerate a Phase I/II potentially registrational study this year. Together, these programs provide us with an opportunity to expand the reach of ZL-1310 across multiple high-need tumor types with the first regulatory submission targeted as early as next year. In conclusion, we are pleased with the promising data thus far for our DLL3 ADC program. Taken together, the profile we've seen with ZL-1310, high response rates, early and durable activity and CNS activity support its competitiveness in the second-line setting. Importantly, we're achieving this efficacy with a highly manageable safety profile. Beyond these results, we're advancing into a randomized pivotal trial in second-line small cell lung cancer in the second half of this year using the 1.6 milligram per kilogram dose pending FDA agreement. I look forward to providing further updates on our DLL3 ADC program in the second half of this year. And now operator, please open the line for questions and answers.

[Operator Instructions] Our first question comes from the line of Yigal Nochomovitz from Citigroup.

Congrats on the data. I was just curious with respect to the therapeutic window, if you could comment on what you saw perhaps at some of the higher doses in terms of efficacy and how confident you are that 1.6 is the right dose to take forward into the pivotal studies.

Yes. Thanks for the question. We started based on the therapeutic window that we had seen comparing 2 MPK with 1.6 MPK. And as Dr. Patel said, there was more ILD at 2 MPK and above, although only 2 of them of the 7 that were observed at 2 MPK and above were grade 3 plus. With 1.6 MPK and below, particularly with 1.6 MPK, we only saw 2 grade 1 that were able to be treated. So there is, as you saw in the dose response, a slight attrition as you go up with the dose. And that is particularly due to the fact that, one, there's a plateau in the response curve, but also some of the patients need to be discontinued or interrupted. And so if you look at also hematology toxicity, there's a difference where we only saw a 6% grade 3 plus with 1.6 MPK. So you're right, the therapeutic window may still be narrow, but we have what we think is a good dose of 1.6 MPK. We've been asked to study a lower dose, which is not unusual. FDA oftentimes does that. And we are putting patients in 1.2 MPK as well. And then we will very carefully look at these patients and make sure that they're measuring up both efficacy and safety-wise with 1.6 MPK. And as we announced, we got fast track, we will also apply for BTD and hope to have a pretty fluid dialogue with FDA to be able to land on that dose. So I mean, so far, it appears based on the totality of the data that particularly in second line, 1.6 MPK is highly active with actually a very mild safety profile, particularly when compared with other ADCs and other classes. So that's what I can say as to where we are now. We will complete the randomization expansion and then present the entire package with some durability to FDA and make the decision. And we hope to do that before we start the Phase III.

Our next question comes from the line of Jonathan Chang from Leerink Partners.

This is Albert Agustinus dialing in for Jonathan Chang. So my question is, what is the dosing strategy and safety consideration for your combination trial, given what we know from the monotherapy profile to date?

Yes. So as you know, there's been already precedence of ADC supplanting chemotherapy in other diseases and some of the very effective ADCs out there are moving into frontline as well with chemotherapy-sparing regimen. We wanted to be methodical in terms of combinations. Cisplatin/etoposide is active and it's active fast. So in order to be able to discontinue chemotherapy and just use checkpoint inhibitors plus 1310, we have to demonstrate, a, combinability but also that the activity is competitive and superior to the standard chemotherapy regimen that's available now. We are confident that, that will be the case because in second line, we are seeing numbers that compare very favorable with chemotherapy upfront. And what I can tell you is that we are finishing the atezolizumab combination and have started the carboplatin combination along with atezolizumab in frontline patients, and we will expand that as well. And as the field evolves because of the entrance of new agents like the T-cell engagers, we will explore as well the possibility of combinations with T-cell engagers if those end up being part of the frontline regimen. But our initial going in is that probably the frontline combination will include carboplatin, atezo and 1310. So that's where we are now. We will continue the dose escalation and collecting efficacy data and safety data. So far, the safety has been remarkable and the efficacy has been quite good. And we'll make a decision after we collect all that data. And meanwhile, we're really focused on the second line.

Our next question comes from the line of Anupam Rama from JPMorgan.

This is Priyanka on for Anupam. Can you quickly put the durability of ZL-1310 into context of the competitive landscape of the refractory SCLC?

The follow-up, as Dr. Patel mentioned, is not very long. That's why we isolated the dose escalation because that's the one that has the longest. And just to reiterate what you heard, the median follow-up for that group of 28 patients was 6.9 months. The response rate was 68%. So that's mature response rate. Everybody is confirmed. And the disease control rate is 93%. This is across lines of therapies. And we have still 10 patients remaining in response. So just above 50%, 53%. And half of those responses are at 6 months or above. So with that median and the number of patients still in response that can give you a sense of what that durability may be, at least in that group. You know the durability of other agents in this class, whether it's 5.7 or lower response rate, but durability more in the 9 months with TCEs. So for us, I think the durability is around 6 or above would be considered clinically meaningful. And for the rest of the patients of the entire 74 patients for whom we have efficacy, the follow-up is 3.4 months and the median has not been reached. But if you look at the waterfall plot, you can see that many of these patients are continuing -- or close to 30% are still early in the study and the response and durability will continue because many of them are still continuing to be treated. But we can't unfortunately give you a number now. We just have to wait and obviously, the longer, the better.

Next question comes from the line of Michael Yee from Jefferies.

Maybe just 2 questions also for the doctor. How are you thinking about using this potential drug if approved in second line as it relates to the competitor tarlatamab, which has survival data here -- although I think this morning here at ASCO, I think published in the New England Journal, the durability came down. But maybe you could compare and contrast those 2 and particularly the opportunity in first line for both of these agents given tarla versus this ADC.

It's Alex Spira. So I mean I just put up a New England Journal article this morning. So tarla is a great drug. You can't belittle it at all. The challenge is in the administration. The clinical trial, obviously, was a very selected site. And what that basically tells us and the utilization is much lower just because it's really hard to give. Most physicians outside [indiscernible] trial sites and the big academic centers can't really do it that well. I mean obviously, I'm a researcher and I do a lot of things and even our hospital can't do it and can't administer it just because of logistical implications, hospital reimbursement, et cetera, plus all the toxicity. It's obviously a good drug, but I think for the general small cell community, which real world, of course, is sicker, older than a lot of these patients on study, I think an easy to administer outpatient drug will likely be given. Even as tarla gets to be administered as an outpatient and certainly, Amgen is finally studying it, it's still significance of cytokine release syndrome and ICANS events that happen at all hours of the night, making it challenging to give in an outpatient scenario. So I think it will largely be used because of ease of administration going forward. And certainly, you didn't ask the question, but in other patients right now comparing versus topotecan and others, there's not even a question. Topotecan is just another drug we like to give.

Dr. Spira, I would just simply add that there are different mechanisms of action. And even though still anecdotal, we, I think, treated up to 4 patients post tarlatamab. And we've seen a complete response, a partial response and some decrease in tumor diameters in a couple of other patients. So there will be combinations between ADCs and this modality, I think, as people start sort of working out how to treat this disease. But there are clear differences in toxicity, although it's a highly active drug as you saw.

Our next question comes from the line of Louise Chen from Scotiabank.

Congratulations on the data. I wanted to ask you, what gives you confidence in a potential accelerated approval for ZL-1310? And what do you think the FDA needs to see for accelerated approval?

Yes. So we've been having discussions with FDA about this potential. They have been unambiguous about the fact that accelerated approval is an option in the context of the randomized trial that we described earlier and that would be based on comparisons of response rate. So I think the agency and us are discussing what the number should be between both the control and the test arm. They obviously do want every patient to be accrued by the time the analysis is done, and they don't just want a number of patients. They want them followed for a period of time, probably around 8 months or so. That number of patients will probably be around 100 per arm. So we think that we could have that data in 2027 and file. So we don't expect the agency to change its mind. Obviously, there will be an approved drug with full approval, but I think they really realized that we need more drugs in this disease that this is a different mechanism of action, different ease of administration. And we've received no signal that accelerated approval is a viable option for the drug.

And I had just one quick follow-up question. What do you hope to see in your combo data later this year? And any positive read-through from the data today to that data coming up?

I think it's early days for the combo data. I mean it's -- all the patients are responding and the responses are high. And what we expect is that we'll see upwards of 75% or so response. And then we'll obviously have to have sufficient number of patients and sufficient durability to make sure that, that study will be positive. So we also will have to do some dose optimization, although the [indiscernible], the doses are fixed. We don't think that we will have to do as many doses as we did with monotherapy in second line. So it will go a little faster. But time to progression will be important. I think we've learned today that it's in the 4s or so for tarlatamab. So we will be waiting for a period of time of 7 months or so to see whether -- what percent of patients are still in response. So it will take some time. We hope to be able to show some data towards the end of the year, but we will wait until we have a clinically meaningful data set that's informative.

Our next question comes from the line of Li Watsek from Cantor Fitzgerald.

I wonder if you can just talk about the remaining items that you still have to align with FDA before you initiate the pivotal study? Is it just a going-forward dose? And then just curious, is there a dose de-escalation protocol for the Phase III trial? And then can you clarify if you expect to enroll patients may be pretreated with tarla into the trial, just given you require only one prior line of therapy?

Yes. All very good questions. And some of them we still need to agree with FDA. It's a second-line study. So these patients will be tarlatamab naive. Now in the control arm, the question is whether tarlatamab will be required. The FDA has not asked us to include it. And there are other studies out there for ADCs where they only include a single chemotherapy. We plan to include dealer choice with 3 chemotherapy. There will be dose modification guidelines for patients that have toxicities that call for resumption of the drug at a lower dose level. We hope that, that won't be very high because we have seen that in very few patients at 1.6, if that ends up being the final dose. I think the important -- the most important thing is to land on the dose. We plan to update FDA on where we are with the totality of the data soon, and we're putting that together and then understand from them what else, if anything, is required for us to choose the dose. And if they ask us to increase the number of patients or any other variation, then we will complete that. Accrual has not been an issue for us. And so we think that we'll be able to have those data available before the initiation of the study. Of course, the sooner we can do it, the better, but that is really the main issue with regards to what's left with FDA in terms of agreeing on the study design. And yes, the issue of tarlatamab that hadn't come up, I'm sure it will come up in the next discussion. And tarlatamab is unfortunately not approved in many countries. So patients in the United States may see tarlatamab. But overall, the use of tarlatamab, if we start the study soon in the control arm, we don't expect it to be overly high.

Our next question comes from the line of Linhai Zhao from Goldman Sachs.

Congratulations on the great data. I have 2 questions. The first question is about, can you elaborate more on the ILD occurrences, particularly on the two Grade 3 and above ILD cases? What are the dose levels for those 2 cases? And also, did you do any more detailed data in terms of helping to understand the differences in the safety profile for the high dose versus the low dose? For example, maybe the analysis on free payload concentrations, the correlation of the AE occurrence versus the duration of treatment? Any color to help us understand the differences here.

Yes. Good question. And I'll focus on those 2 Grade 3 and above. One was a Grade 3 patient and the second ended up being a Grade 5 patient. I think as Dr. Patel mentioned in his remarks, the patient was initially treated and then withdrew treatment. The thing about ILD is that it requires some time to -- for it to manifest. So we have treated a number of patients at doses at 2 and above. And then we saw these 2 events at 2 MPK and the other one was at 2.4 MPK relatively sort of concomitantly on time. And that's what led us to institute guidelines for follow-up for these patients. And that -- the more you look for this, the more you see it obviously. So we'll review the scans for fibrosis very thoroughly prior to patients entering. We've learned that patients that had high doses of fibrosis -- of radiation, for instance, above 35 gray or 40 gray are higher risk. And then obviously, dose is a factor and then be very vigilant with questioning the patients and performing CAT scans. And if we see grade 1, then stop immediately and then resuming when the patient recovers. ADC is seen -- there are -- all of them associated with ILD. And I think we just have to be vigilant about this. So I would just sort of echo that it's been seen as well in -- with B7-H3. And also our study was multicenter and multi-country. So when you have multiple centers and patients with multiple lines of therapies, et cetera, you may see this more often. But in general, we don't think that high-grade ILD is any different than anything that's been seen with other ADCs. I don't know, Dr. Spira, if you want to comment about your experience with ILD and ADCs in this field?

Yes. I mean you said it very well. Bottom line is it happens with all ADCs, especially in lung cancer patients. Anybody may have changes, but obviously, lung cancer patients that have been treated before with radiation, with COPD or just having cancer in the lung, obviously, the levels seen here in my mind are not unexpected because we do see it in all. And it does take investigators and physicians diligence to monitor closely for signs and symptoms. But in the studies, we're all used to it and clinicians are used to it as well. And if you look at other drugs that have been approved in the lung cancer space that are ADCs, T-DXd as being the major example, it is certainly seen there as well at a similar frequency at a minimum.

Yes. And as I said before, it doesn't manifest right away. It generally takes about 60 days or so. A number of patients at 1.6 have passed that threshold, and we're not seeing very many. We just see a couple of them with grade 1. So we think that, as I said before, dose matters and that, that dose should be associated with a low dose, a low rate rather of interstitial lung disease.

There are no further questions at this time. So I'll hand the call back to Rafael.

Thank you, operator, and thanks to everybody that were on the call today. We will be presenting the poster later on today. Again, thank you for your attention. And operator, you may disconnect.

Thank you. This concludes today's conference call. Thank you for participating. You may all now disconnect. Speakers, please stand by.