Great. Welcome, everyone. I'm Max Skor, a biotech analyst with Morgan Stanley. Before we get started, I just have to read some brief disclosures. For important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. With that, I'm happy to welcome Mickael Chane-Du, Chief Strategy Officer with Adagene Inc. Thank you very much for attending this year. For those in the audience who are new to Adagene, could you briefly explain your SAFEbody® platform and how it enables a differentiated approach to targeting CTLA-4? Hey, thanks for having me. Thank you very much for the question as well. At Adagene, we are very focused on protein engineering, antibody generation. We are leveraging AI to give birth to new, to novel, innovating antibodies. Most notably, recently, we have been putting in the clinic masked antibodies. Thanks to AI, we can really interrogate, explore conformational diversity of protein sequences. We can really interrogate a lot of epitopes. Our lead compound is called ADG126, so masked anti-CTLA-4, number one on the antibody side. The antibody is differentiated in the sense that it's an anti-CTLA-4 that binds to a different epitope compared to ipilimumab and tremelimumab, the first generation of anti-CTLA-4. Thanks to that different epitope binding, we end up with very strong potency, much stronger ADCC compared to ipilimumab, up to 10 times, according to our experiments. That's point number one. Point number two, on the masking side, our proprietary masking technology allows us to expand significantly the therapeutic window of anti-CTLA-4. Anti-CTLA-4 is known to be highly dose-dependent in terms of response, survival, etc. It's a very hard target to address. The antibodies cannot be dosed very, very high. A number of pharmacies do recognize that they wish they could dose very high their antibodies, but they cannot. It's because not as monotherapy, but when you combine with what is a strong backbone of anti-cancer therapy, anti-PD-1, you end up with synergistic toxicity. The discontinuation rates due to toxicity are very, very high, sometimes north of 40%. It's very hard for the patients to tolerate, harsh on the quality of life, harsh also on the data. Thanks to this antibody, we believe, again, that we can expand the therapeutic index and proof it into pudding. We can dose very, very high safely. We can really unleash the true potential of anti-CTLA-4 at a high level. Great. I think that's a great introduction. Thank you. You address ADG126, the lead program. Maybe could you please set the stage for us in microsatellite stable colorectal cancer, the main indication you're going into? What's the core value proposition for ADG126? Which parts of the profile are getting the most traction with physicians? How do you see it slotting into the treatment landscape? Thank you. Let's start with MSS-CRC, a few very, very important data points because we talk about ADG126. MSS colorectal cancer is a very prevalent indication, as you know. MSS, microsatellite stable colorectal cancer, represents 95% of all CRC cases. Importantly, immunotherapies such as PD-1 or anti-CTLA-4 have not been able to make a bridge into MSS-CRC. It is far from a low-angle in food for immunotherapies. It's a very core tumor. There's significant T-cell exclusion, number one. Number two, high T-regulator upregulation. Number three, high prevalence of PD-1 negativity. Just a very, very hard tumor type for immunotherapy. There is really a reason why, unfortunately, anti-PD-1 therapies have not been able, again, to get a label for that. That's really the first point that I wanted to emphasize. MSS-CRC without liver metastasis is the first step. We have proof of concept data in this setting. It is still a significant market in our view because we are still talking about more than 10,000 patients in the U.S. It does represent a significant opportunity for us. Non-liver mets, MSS-CRC is a subtype, a subgroup where a number of companies, including one of our competitors, have generated data. The data strongly suggests that, number one, it is, here again, not an easy subgroup to address, be it with standard of care, because even the fruquintinib or the Sanofi regimen, part of the standard of care today, have very poor efficacy data. They are not easy to tolerate a regimen. Now, when we switch to patients without liver metastasis, immunotherapy seems to have a much stronger potential benefit compared to standard of care. This is the subgroup that we are targeting right now. It doesn't mean that the patients with liver metastasis will be left behind. MSS-CRC, non-liver mets. Your question is, you had a question about what makes physicians excited. Yeah. The number one thing that CRC physicians and QP and leaders are excited about is having an immunotherapy regimen potentially for the patient. You know that immunotherapies, the promise of immunotherapies is potentially to help patients survive for a longer time. Right, and having ADG126, our lead program, in combination with Keytruda, so chemo-free regimen, that's number one. So far in our phase 1B data, has this really high response rate. At the high dose right now, we're standing at a confirmed response rate of 29%. It is very exciting. That's number one. Number two, as mentioned earlier, combining CTLA-4 and PD-1 is not an easy task. As we speak, even at very, very high dose, up to 20 times higher dose levels compared to the first generation of anti-CTLA-4 or even some of our competitors, we are able to maintain patients on treatment. Very few of them discontinue due to toxicity. We have a very low incidence of grade 3. If you look more specifically at 20 milligrams per kilogram every six weeks, we have less than 20% of patients with grade 3, no grade 4, no grade 5. Bottom line, having a very highly dosed, up to 20 times higher anti-CTLA-4, safely with NCPD-1, with a high response rate, hopefully, we can help with the patients to survive longer. As we speak, we presented that data at ASCO from the lower dose. I've been talking about the high dose 20 mpK-Q6W, most notably. Even from the lower dose cohorts, we have seen very interesting data, in my opinion. When you look at 10 mpK-Q6W every six weeks plus 10 mpK every three weeks, we combine these two cohorts, and we have 41 patients. Our confirmed response rate is 10%. The overall response rate is still in the low teens. We have generated a median overall survival of 19 months. You will ask me, how does it compare to standard of care and competition, et cetera? 19 months compares very nicely, we believe, with the current standard of care. If you take, for example, fruquintinib, which is a very relevant control, potentially, the median overall survival for such compound is between 10 and 12 months in their phase 3 in patients without liver metastasis. If you look at the TAS-102 plus bevacizumab regimen, we're talking about something close to the mid teens in terms of months in terms of median overall survival. 19 months is really a really strong number. Yet, from the cohorts that have generated the lower response rate in our data set, if you look at the two cohorts at 20 mpK, we have two cohorts. One is what we call the loading dose cohort. We start with 20 mpK, followed by 10 mpK every three weeks. We have a second cohort, which is 20 mpK every six weeks. Both cohorts at ASCO have generated confirmed response rates of 29%. What we have been saying very publicly is that we are not only seeing a higher response rate with these higher doses, so, we're seeing dose-dependent response. This is something that we expected, we hope to see, because this is something that you normally see with anti-CTLA-4. With a safe anti-CTLA-4, it's more apparent. These two higher dose cohorts both have a confirmed response rate of 29%. Not only is it a higher response rate versus the lower doses, we are seeing a trend towards better duration of response, better PFS. Let's see how the data further matures in terms of OS. The trend is positive. Great. I think this is an important point I'd like to just drill down a bit more on. Mechanistically and clinically, how is ADG126 differentiated from, let's say, ipi and other emerging anti-CTLA-4 programs? I'm going to start with ipilimumab first, and then we can go from there. So ipilimumab is first the very first generation of anti-CTLA-4, great therapy, which, again, unfortunately, has some synergistic toxicity when combined with anti-PD-1. We do bind to a different epitope. We believe that it does help the naked antibody, ADG116. In terms of potency, it's also very well tolerated. We apply our proprietary masking capacities to this antibody, hence ADG126. ADG126 is very safe compared to some other anti-CTLA-4, newer generation anti-CTLA-4. I really want to emphasize the fact that we have very few discontinuations in our phase 1B data due to adverse events, serious adverse events, however you call it. This is a very important first step of differentiation. The second step, now comparing our masked anti-CTLA-4 to other masked anti-CTLA-4, very importantly, our technology is protease sensitive. Like other technologies, some are pH sensitive, others are protease sensitive. Our antibody, to be activated, to be unmasked, we not only need a high concentration of these proteases in the tumor microenvironment, leading to this higher concentration of an antibody that can bind to its target. You can have a very high concentration in the TME and much less in the periphery. We also need a second condition for activation. We need also high expression of anti-CTLA-4, so high protease expression levels, high levels also of anti-CTLA-4 the target. We believe this is very important for the therapeutic index. Last but not least, compared to some of the other masking antibodies, we have a very strong masking efficiency, up to three to four times compared to one of them. When I talk about masking efficiency, I talk about the fact that when the mask is present, the antibody is not going to bind. It's not going to bind to its target. To recap, different epitope binding, masking technology that the masking technology proprietary, and we need two levels of activation and very strong masking efficiencies. This is how we are different. Perfect. Just stepping back and talking about, OK, we've highlighted the data to date. Now looking forward, how will you confirm the MSS-CRC signal? Are you going to be leveraging a loading regimen? What's the regulatory path ahead? Is there a potential for accelerated approval, or are we going to go with the traditional approval path? Thanks for the question. Accelerated approval, if you ask for accelerated approval in the sense that can we file a BLA based on the phase 2 single arm or phase 1B single arm? The answer is no, unfortunately. These days are gone. We have two other points now. We have a randomized phase 2 trial looking at two dose levels of ADG126 in combination with Keytruda® (pembrolizumab). One dose level is 20 mg/kg. Second dose level is 10 mg/kg. In this phase 2, the primary endpoint will be response rate. This randomized phase 2 will be used as a way to answer the question of what is the relevant dose to be moved forward in the pivotal trial, number one. That's actually the main reason we do that study. Then moving to phase 3 trial, this is where we will have a control. This is where we will have a control arm. We have so far a pretty good idea of what it could be based on current discussions with the FDA. Standard of care can always change over time. We will confirm that with the FDA. That's point number one. I do want to emphasize something about contribution of components. It's a question that we get a lot. The FDA so far is suggesting that we do not need a PD-1 monotherapy arm or CTLA-4 monotherapy arm in any of our studies, be it the phase 2 or the phase 3. The agency seems to recognize that PD-1 single agents, CTLA-4 single agents are not really effective in the setting that we are initially targeting. Now, going back to the phase 3 trial, the primary endpoint is more likely to be overall survival. You have seen recent guidance from the FDA. Overall survival is really the gold standard, really the gold standard for the FDA. That's what I want to say. When we look, I'm trying to be factual here. This is not a strong guidance. If you look at what other companies have done recently in the first-line setting, second-line, etc., some companies have been able to use ORR as a co-primary endpoint in a randomized setting. You can do an interim analysis looking at the delta in terms of ORR between one or two or three arms and potentially go to the FDA and get accelerated approval. Overall survival is a very important component of the equation. OK, so if I understand correctly, you have a phase 2, which will then inform the pivotal phase 3 trial. Could you just talk about timelines, when we can expect the initiation and potential data readouts? Sure. The randomized phase 2 trial, again, we will test two different dose levels. We don't have a control arm. We want to be very efficient and fast. 60 patients. This phase 2 trial will be initiated before the end of this year, sooner rather than later. After that, let's see how the enrollment goes. I can assure you that we have a number of very motivated investigators. We have new investigators involved, such as MD Anderson, Fox Chase Cancer Center, et cetera. Again, we're working with more and more U.S. sites, also South Korean sites, et cetera. It's really a global study. We want to leverage all the potential benefits of different jurisdictions, different countries. We hope to see a very nice, very nice enrollment in this phase 2. I cannot give you a strong guidance in terms of completion of enrollment. Let's say that H2-2026 could be potentially something to keep in mind. OK, but when it comes to data readout, I don't want to give a guidance yet. OK, that's helpful. Additional question in regards to a potential biomarker or patient enrichment strategy. Is there anything you're utilizing to raise the probability of success? Addressing first patients without liver metastasis is a very important strategy for us because, as mentioned earlier, immunotherapy seems to do better. It is far from a low-hanging fruit. This is something I really want to reemphasize. Patients without liver metastasis are not super easy to treat patients. The unmet medical need is absolutely significant. Going after patients without liver metastasis, and we do include patients with peritoneal metastasis. Right, remember, we have had this discussion. We are not excluding such patients right now. We do have activity in patients without liver metastasis, but with peritoneal mets. This is the first, and we believe that this is a good strategy first. When it comes to patients with liver metastasis, we want to be smart on how to address this subgroup. One potential option is having a broader regimen. We have a company-sponsored phase 1B evaluating a triplet. We are testing ADG126 plus Keytruda® (pembrolizumab) plus standard of care, standard of care, in this case, being fruquintinib. We like the PD-1 CTLA-4 VEGF combination. Other options could be potentially on the table. We are considering a lot of things. I want to say that patients without liver metastasis and MSS-CRC, this is not the end game for ADG126. OK, can you just talk to the overall patient population, the TAM, in a sense? What percentage have liver metastasis diagnosis? What do not? Yeah, patients without liver metastasis typically account for roughly a third of all MSS-CRC patients. Again, a pretty sizable patient population. We believe that there are a bit more than 10,000 patients just in the U.S. OK, now let's move on to financials. I know you announced a SNOWPEA collaboration. Could you just flesh out your current cash position, runway, any details around that? Sure. We had roughly $63 million at the end of June 2025. That was right before our equity investment announcement from SNOWPEA. Our cash runway, as a result, accounting for the SNOWPEA equity investment, goes into 2027. If that's OK, I want to talk a bit about the SNOWPEA equity investment because it does have some financing components and others. SNOWPEA agreed to invest up to $25 million in Adagene. We received the first tranche of $17 million. This is really helping us to fund our randomized phase 2 trial. SNOWPEA, something that I think now people are, therapy people are realizing this more and more. SNOWPEA actually does know masking technologies very, very well for two reasons. Reason number one, you may remember that they acquired Immunix back in 2021, a company that developed some masked antibodies for a total amount of $1 billion circa. They sold the rights of the company to VIA in 2024. You can imagine that they've done a lot of due diligence. They're very familiar with what's going on when it comes to masking. That's point number one. Point number two, we have had a discovery collaboration with SNOWPEA since 2022. We were very happy that, concomitantly to the equity investment, SNOWPEA exercised an option on a third SAFEbody® antibody in oncology from our platform. SNOWPEA seems to like something from our platform. Not only that, they're supporting the advancements of ADG126 by helping this phase 2 in non-liver metastasis, MSS colorectal cancer. The other point I want to emphasize, SNOWPEA is going to sponsor and fund a phase 1/2 evaluating a novel combination involving ADG126 with one of their core oncology assets. They want to enroll more than 100 patients with solid tumors. I cannot say too much about this trial collaboration. It is an important one that could potentially further, you know, that can expand the potential addressable market for ADG126. That can be very helpful for SNOWPEA. OK, and before moving on to a few survey questions that we've been asking companies, I just want to open up to you. Are there any key data sets you'd like to highlight that potentially get investors up to speed? If we think about the next 12 to 18 months, what do you think are the main headlines we should keep an eye out for? Yeah, thank you. I'm going to start with the catalyst and then highlight some of the key clinical data that investors should keep in mind. Number one, we will update our phase 1B data set, looking at different dose cohorts, but with a particular focus on the higher doses, 20 mg/kg every six weeks, as well as the loading dose cohorts, 20 mg/kg followed by 10 every three weeks. We will have a little bit more patients from the 20 mg/kg-Q6W cohort, a total of roughly 12 patients from that cohort. For the loading dose, it's 14 patients. The number is unchanged compared to ASCO. The street should expect durability data, so more patients, as well as durability data from this cohort. Keep in mind that from the lower dose cohort, 10% ORR, 19 months overall survival. Let's see where it goes for the higher dose cohort. We want to show that to the market in the very coming months. Number two, we will show at some point some initial data. Cannot promise you when. We hope maybe that we can present some data from the triplet combination of ADG126, pembrolizumab plus fruquintinib. We may try to present more data in the coming months. So far, I don't want to give any guidance. We're working on a number of things. Last but not least, business development, as you can hear, has been very important for Adagene. We announced this equity investment from Sanofi, a significant trial collaboration. Something that we are working really, really hard on is expanding. We really want to unlock a lot of value. We really want the true potential of ADG126 to express itself. Again, non-MSS-CRC without liver metastasis is not, this is not the end. I believe that this is not the end game for Adagene and 126. If you have a safe anti-CTLA-4 that can be dosed very, very high and that has shown differentiated efficacy compared to a lot of different anti-CTLA-4, I believe that you should be able to address other tumor types, other settings, etc. Talking about the different data points, clinical data points that people should remember, number one, it's the response rate. We so far have a response rate in the 20%, 30% range, confirmed ORR of 29% from the 20 mg/kg cohorts, with very encouraging durability of response as we speak. We hope to see very encouraging overall survival, phase 1B data. Not randomized. People will do their own cross-trial comparison. The 19 months that we're seeing from the 10 mg/kg is already a very important, significant data point that physicians and investors are really appreciating these days. Point number two is on the safety. I mentioned it earlier. Our discontinuation rate is very, very low. So far, so good. We have no discontinuation from the high dose, despite the 20 mg/kg dose level. Our incidence of grade 3, looking at the 20 mg/kg-Q6W cohort, the incidence of grade 3 is lower than 20%. No grade 4, no grade 5. It's very apparent to me that this is a very different anti-CTLA-4. At such dose level, if you were to give an ipilimumab at 20 mg/kg, I'm not sure you would get that kind of safety. What else? That's on the data point side, I would say. We talked about the SNOWPEA equity investment. I want to reemphasize the fact that this alliance with SNOWPEA is not only a clinical validation because SNOWPEA obviously has looked at our data for ADG126. It is also a validation of our masking technology capacities. I really want to emphasize that also. OK, great. Now moving on to a few questions we've been asking all of our companies. With China's rise in biotech innovation, how are you thinking about your competitive position here? Will it influence your R&D or BD strategy? Thank you for the question. I just want to go back to, I forgot to mention that we have been reinforcing and strengthening the leadership team, or rather people around the leadership team. You remember that we have John Maraganore, the former CEO of Alnylam, as an executive advisor. Very recently, we announced that we hired, also as an executive advisor, Axel Hoos. Axel Hoos, who's the former CEO of Scorpion, but also the former global head of oncology at GSK, and a very important person for the world of immuno-oncology. He's actually behind this term, immuno-oncology. Axel has joined us. Axel, for people who don't know him, was also a very important person for the development of ipilimumab at BMS. He's another person in the team of Adagene that has very strong historical ties to anti-CTLA-4. I wanted to reemphasize that. Sorry, now going back to your question about China. In regards to Chinese rise in biotech innovation, how are you just thinking about your competitive position here? Will it influence your R&D or BD strategy? Thank you. I believe that now people are realizing that China has become a very important player both within the biotech industry and for research and development. Chinese players, and we are a company with a global footprint, but with a significant Chinese heritage. Our headquarters are in Suzhou, China. Pharmas, if you look at year-to-date data, have done close to 40% of their deals, licensing and M&A in China. Down the road, 2035, 2040, a lot of drugs will be on the market originating from China or will have some Chinese DNA. Pharmas and the big pharmas and big biotechs do understand the fact that you can have very innovative assets. We believe that ADG126 is one of them. Very innovative assets, very fast pace of execution at a very good cost, if I may say, as well as very attractive valuation levels. Adagene, again, has a global footprint. Our clinical trials are done in the U.S., South Korea, China, et cetera, et cetera. We have a very, very strong Chinese DNA. We have a lot of people working in China, and they're really helping us to move very, very fast. We believe that we are very well positioned to catch this trend. Great. I think you also noted it at the beginning. How are you currently leveraging AI or thinking about AI's future disruption potential? I guess we are the disruptors. Yep, because we are using AI to help our decision-making and the design of our antibodies. We do leverage AI to explore, again, diversity of conformational changes, epitope coverage, et cetera. AI has been extremely important for the generation of our candidates. I guess we are part of the disruptors. OK, and then last question. What has been most impactful from the regulatory side? Would you say the FDA, MFN, or tariffs? Tariffs are not really impacting us. MFN, let's see. We're not on the market yet. We thought that the FDA could have, I wouldn't say would have been, we could have encountered some challenges. As a matter of fact, the FDA has been extremely helpful. Our end of phase 1 meeting was very positive. We went in this meeting with different scenarios in terms of how the phase 2 would look like for us in non-liver mets and MSS-CRC. It turns out that we ended up with a best-case scenario. FDA said, listen, we understand we need a clinical package of ADG126. We agree with you. You need 30 patients at dose level 1, 30 patients at dose level 2. No need so far, no need for assessment of contribution of components or PD-1 monotherapy or CTLA-4 monotherapy. We agree with the kind of control arm that you are asking for. They said, we give you the option to not have a control arm in the phase 2 because the purpose of the phase 2 is to pick a dose for a registration or trial. We ended up with a 60-patient randomized between two dose levels, phase 2. It's on the smaller side, something that we can execute very nicely. We can be very fast. We were very happy with that. The FDA has not been really an issue. We're happy. OK, great. With that, I think we're up on time. Thank you very much. Thank you, Max. Thanks for the time.