All right. Afternoon, everyone. My name is Bob Klingenberger with Morgan Stanley. Excited to welcome the Adlai Nortye team here to our conference. Just before we get started, just want to refer everyone to the Morgan Stanley Research Disclosures website. If you have any questions, reach out to your Morgan Stanley representative. Like I said, very excited to have the Adlai Nortye team here. I'm joined by Brittany Stopa, Director of IR, and Alex Yee, the CFO. We'll be diving into some good questions here. Thank you guys for coming. Thank you for having us. Sure. Thank you for Maybe just to start off, you all, I think, described the strategy of the company and really the two pillars, both the Precision RAS pathway targeted therapies, and then next generation PD-L1 pathway modulation. Can you just talk about how you feel like at a high level, those two come together and form the portfolio that you all have today? Yeah, great. Well, thanks for having us, Bob. We are really thrilled to be here at the Morgan Stanley conference. Adlai Nortye is a clinical stage biotechnology company that is targeting RAS from multiple angles. And we have a mission to transform deadly cancer into a chronic and eventually curable disease. We are approaching that with. We have a global team which has operations in the U.S., Singapore, and China. And we have an in-house R&D team that has synthesized over 1,000 RAS(ON) inhibitor molecules. And we have a proprietary RASiCA platform, which is our RAS Inhibitor Conjugated Antibody platform. We are advancing first-in-class and potential best-in-class molecules with our three lead oncology assets. We have two innovative RAS modalities, so that includes AN9025, which is a potential best-in-class pan-RAS(ON) inhibitor oral small molecule, and AN4035, which is a first-in-class pan-RAS(ON) inhibitor ADC targeting CEACAM5. We also have a next generation immunotherapy, that is AN8025. That is a potential first-in-class multifunctional T cell/APC modulator. For now, our focus is squarely upon our RAS programs, which we think could be quite differentiated in addressing the over 175,000 patients diagnosed in the U.S. every year with RAS-addicted PDAC, non-small cell, and colorectal cancers. Great. Well, I think in terms of the RAS platform, we should just start. You introduced AN9025 and AN4035. I'll try and get those right throughout the questions. Maybe just to start on the small molecule pan-RAS AN9025, just maybe give us a little bit of overview of the molecule and where you all sit today in terms of development, and we'll dive into some of the details from there. Yes. AN9025, like I said, is our pan-RAS(ON) inhibitor oral small molecule. That's been developed all in-house, and it's been developed to address multiple RAS mutant solid tumors. The way that we've designed the molecule is that it has about 250x higher potency relative to the first generation pan-RAS(ON) inhibitor, daraxonrasib, and that higher potency is driven by stronger CypA binding and slower dissociation, as well as stronger binding to RAS(ON) and slower dissociation. So you get a more stable tri-complex formation. That is leading to what we've seen in the preclinical setting, including more durable RAS signaling inhibition, deeper tumor regression, and more delayed adaptive resistance formation. We're excited about the potential and what we're seeing in the preclinical profile there, and we're hoping that translates into the clinic. So right now we're in a global phase I trial. We began enrolling patients in the QD arm in February, and in July, we actually activated a QW arm, and that intermittent dosing schedule was enabled by, like I said, that preclinical profile and the durability of signaling inhibition that we saw. What we'll look forward to doing is we're continuing to dose escalate on both arms, but we're looking towards providing an update in the first half of 2027 on that program, which will be the full phase I-A data for the QD arm, as well as an early look at the QW arm. Great. You referenced some of the preclinical data both on potency and durability, and half-life. Maybe just as we think about that first half 2027 disclosure, what should we be looking for to demonstrate that kind of best-in-class potential that you've been talking about? Yeah. I think for the molecule AN9025, if fully translated 100% from preclinical to the clinical, I think we would be expect to see a better safety and tolerability profile, also with better efficacy, compared with the current players. But this need to be 100% translate. I think right now, based on the initial clinical data we see, it's a little bit early, but I would say it's not far away. Probably we need probably two or three months to really understand the profile. Initially, as we briefly mentioned, we already released to public, we just initiated the expansion cohort for our QD dosing for the small molecule, which implies we have been seeing pretty good human PK data compared with. It's highly correlated with what we see from preclinical. We also are being observed and seeing preliminary efficacy with better tolerability profile in the human data. And I know you all have, in your corporate deck too, extensive kind of preclinical package. Any particular kind of data, especially as you think about relative to some of the other players in the space that you want to highlight as we sort of are thinking about expecting the clinical data next year? Yeah. As we always saying, the reason we initiate the human data is we want to really further confirm with the preclinical finding. But if you're just looking for a few preclinical data, we've been demonstrating our corporate deck. We have been doing very extensive preclinical CDX model to compare our molecule with current market players. I think with all those G12X, G13X CDX model, we have been showing very good deeper tumor inhibition in the in vivo level. We also showing potentially in the QD dosing, we have a very comparable therapeutic window with the [audio distortion] in the preclinical, head-to-head study. We're also potentially showing the weekly dosing can further open that therapeutic window while we didn't compromise our potency in improvement. In the animal, we hadn't been able to show over 200 to 250 for more potent, in the animal, in favor data, but we didn't compromise for the therapeutic window, loss. Yeah. And you touched on, I think, where I wanted to go kind of with the next question, just in terms of, excuse me, both the QD dosing and then the weekly kind of intermittent cohort that you started this summer would be really curious to hear a little of how the internal thinking is around which one of those kind of. How you look at both arms playing out and in parallel, and what you're looking for in terms of what you might be taking forward as you advance the program further. The idea we initiate the QD dosing early this year for our oral small molecule is that we hopefully were able to see the differentiate just by the QD dosing, which is very comparable with what other market players is doing, using a once a day of the dose regimen. By the QD dosings data right now, we have been feel very comfortable. We just initiated dose expansion, but we also share to public and investors saying we are not reaching the MTD yet. We are continue to doing dose escalating the QD dosing. Of course, we also initiated weekly dosing about two months ago. But we want to highlight is that we initiate a weekly dosing is not because we are not able to really doing a daily dosing. It's just for the weekly dosing give us additional optionality. We will be able to see by the weekly dosing whether we can further improve the tolerability and also potentially push higher dose in human. In our preclinical data, we are showing the weekly dosing actually was able to further open the therapeutic window. We know in the animal, for the QD dosing, potentially we will reach the MTD in about 0.2 mg in rat in the animal. But for the weekly dosing, we actually could push to about 2.8 mg in animal, which imply a potential at least double of the therapeutic window extension. Everything finding on the preclinical need to be translated in human. So which is right now we are doing in the weekly dosing in human. But I want to highlight our development strategy on the front-line PDAC, which is the most immediately and most time urgency indication. We will probably just starting that combination in a QD regimen. We do not necessarily waiting for the weekly dosings data. We can always testing the weekly dosing while we have a QD dose regimen combination data. I think what you started to touch on, I think what my next question was going to be, which is great. In terms of maybe just, it is obviously early, you are in dose escalation. Help us, right? This is pan-RAS(ON) broadly expressed could be a very broad development plan. Where are you sort of at in terms of thinking through tumor types to focus on, combinations, just maybe kind of help us understand at least the current thinking as we are expecting this data? Yes. We believe as a potential best-in-class profile of the pan-RAS(ON) program. For us, I think the combination is really the very key strategy to moving forward in that development strategy. First I want to say in China, for our Chinese partner, ASK Pharm, they will certainly can follow what we may been doing in the U.S. because China is still relative early days. So they certainly will go with the monotherapy in second-line PDAC, and of course, they can looking for the non-small cell lung cancer in China. For ex-China, which is our going to responsible for development, we are going to focus on the front-line PDAC as the combination strategy because in our development strategy, we always about one and a half years ago, we already know we are going to avoid a second line. In front of the PDAC combination, we actually first going to try the chemo combination. Based on our current data, we believe we are going to moving the QD dosing as initial combination dose regimen with chemo. We are going to try two different chemo. One is the GnP, the other would be a FOLFIRINOX in the front line PDAC as the initial combination. Once we see a very comparable safety, we probably can move into a discussion with the U.S. FDA for the registration pathway. Besides the chemo combo, I know there is multiple precision agent combination is being discussed. For example, like PRMT5 and also other agent in the clinical stage. I think there will be also available option for us to consider combination. When we are talking about a non-small cell lung cancer, I believe the market opportunity is still quite open, especially if you can come up with a better tolerability profile molecule, then you can consider the front line combination with the IO and with the ADC. It is a lot of option layer. I think our strategy is one, to initiate a combination as soon as possible to really showing some combination data, hopefully in 2027. How do you think about the weekly intermittent? Could that be helpful as you explore some of these combinations? Because to some of your earlier points. Yes. The time sensitive indication, like a front line PD or lung cancer, we do not necessarily waiting for the weekly dosing data because the QD dosing data may be good enough for the combination. I think the time to the market is also very important. We are not going to waiting for weekly dosing data. But for some of the indication, like colorectal cancer, we might still have some time. There is not that many panel players showing the colorectal efficacy data or higher response rate yet in the CRC indication. For that regard, potentially, a weekly dosing could be showing some benefit to try those hard to treat indication. We have a decision process at certain point when we are going to view the Q week dosing showing a benefit could really 100% translate from preclinical to human. We are going to look at the MTD or the RP2D dose for Q week dosing or for the QD dosing. If at the time the total weekly dose of the Q week would be larger than total weekly dose of the QD dosing, then we can kind of making a decision and say, "Okay, the Q week dosing really showing a differentiate, and potentially we can maybe testing Q week dosing in certain indication." But right now it is too early to tell. We just initiate a Q week dosing, and time will tell. Okay. Maybe then just kind of back to the overall first half disclosure, right? I appreciate it is ongoing, the trials, but could you start to give us maybe a bit of a sense of what we should be expecting in terms of kind of number of patients, efficacy, safety, initial kind of data that you might expect to disclose? Sure, Brittany. Yes. As you mentioned, they are still in the dose escalation portion of the phase I, so it is difficult to provide an estimate on the number of patients at this stage. Also, because we are doing the backfill, so the number of patients that we will be able to share is still not yet disclosed. But what I can say is that we are aiming to provide a really fulsome update and to give a comprehensive look at what our phase I-A experience is with the QD dosing. So we aim to provide a meaningful number of patients at an interpretable dose level with a meaningful amount of follow-up, because we understand that there are other data sets out there against which our data will be benchmarked, and so we want to tell a compelling story with the data that we are able to share. With the QW arm, with the intermittent dosing, because we are the only RAS(ON) molecule that is exploring intermittent dosing in the clinic, we think that setup is a little bit different, and so if we are seeing some early signals, that could be interesting. That is why we are guiding to sharing an early update on the QW with the first half data. Yeah. I guess as we think about some of the external data sets that exist and are out there today, any in particular that have caught your eye as you think about some of these development strategies and where AN9025 could really differentiate, fit in the paradigm? You mean the current data from other panel? Yeah, just in terms of how you feel like AN9025 can really stand out, differentiate relative to some of what you've seen so far. I think the only thing would be able to differentiate you must to showing your human data. Of course, right now we're showing a great preclinical profile, and the only thing we need to show is the human data, which is not far away from now. I would say if a molecule you really can claim as a best in class or is a better molecule as a next generation molecule, you need to show it's a much better tolerability. Also in the efficacy dose, you will be able to show comparable efficacy which means like overall response rate. Ideally, I don't think next year we're going to show the OS data yet, but at least it's the overall response rate in PDAC indication or overall response rate in a non-small cell lung cancer. We need to at least benchmark with the current market players, which we have two players showing the clinical data, like Revolution Medicines and Erasca. I think we need to show a better tolerability and also compatible or maybe better efficacy to really claim as a better molecule or best-in-class molecule. Again, I want to highlight the current RAS market is very big enough. It is about 20% of solid tumor with RAS mutation. Even come with the mid two molecule, it is the third place, you still have a lot of angle to play. For example, a combination would be a huge opportunity. The current players majority, they are showing the monotherapy data. I believe the combination is really an opportunities there. We also have the potential to show difference as the preclinical profile, showing a potential next-gen, but just want to be conservative here before we release the human data. Yeah, great. I think the second program that Brittany, you mentioned at the beginning too, that I know had some exciting news last week, entering the clinic, so for AN4035, now that the first patient has been dosed and your IND has been cleared, maybe talk a little bit about the thesis behind this molecule. Obviously, we spent a lot of time on the pan-RAS(ON), and what you are sort of hoping the initial clinical data can prove out for that molecule. Yeah. You want me to? Yeah. AN4035, like you mentioned, is our antibody drug conjugate, ADC, but instead of a cytotoxic chemotherapy payload, we use a pan-RAS(ON) inhibitor payload. It is a first-in-class molecule to do that, actually a first-in-class molecule to our knowledge to have a precision oncology payload on an ADC. We are really excited about the potential there. This comes out of our RASiCA platform, and this is the first molecule to come out of that platform. We have selected as our target CEACAM5, which is highly expressed in colorectal cancer. What this mechanism of the ADC allows is more targeted tissue delivery of the payload. In our preclinical experience, we saw that we are able to deliver a higher potency of the, a higher load of the drug to the tumor and provide a better balance with the systemic toxicity. We are excited about the potential for the ADC. Like you mentioned, we just dosed the first patient. We shared that news last week. That global phase I trial is ongoing now, and we are running that trial with two arms. We have a monotherapy arm and a cetuximab combination arm, which will have a staggered start, and our goal is to have the full phase I-A data for that program available in the second half of 2027. Yeah. I guess, I know the goal in the study too is a CEACAM-enriched population. Maybe just if you talk a little bit about how you are going through the patient selection process and how that may interpret some of the early data and maybe just a little bit more about the combination versus monotherapy, where you are focused there. Yes. We are running the phase I as a basket trial, so we are enrolling solid tumors with RAS mutation. For the big three, PDAC, non-small cell colorectal, we are not requiring elevated CEA levels for enrollment onto the trial, but for tumor types outside of the big three, you would just need to have an elevated CEA level. Circulating CEA, it is a common tumor marker, so physicians are able to order that in the clinic. Then, certainly on the back end, we will be looking to better understand how CEACAM5 expression levels relate to the ADC activity, so our scientists would plan to conduct immunohistochemistry studies to understand the CEACAM5 expression levels. Yeah. I know that the platform you all have is this is producing a first-in-class molecule entering the clinic. Maybe if you describe the platform a little bit more for us because I think it's produced obviously a first-in-class, pretty interesting molecule to start. Yeah. I can share a little bit about the platform. The idea with going to design this RAS payload ADC platform is we see there is a great challenge on the first generation of pan-RAS(ON) molecule. They usually have a very limited combination ability because the overlay skin and GI toxicity. We feel it's antibody targeting platform potentially can address those challenges. Also in current ADC therapy, there's a lack of diversity of the payload mechanism, which in this year you see pharma companies starting their acquisition for a lot of novel payload mechanisms company, which has further validated our approach. We have designed an internal linker payload, would be able to conjugate with the pan-RAS(ON) payload, then we can select a certain target antigen. For example, the first program we're choosing is a CEACAM5 ADC. This is the program as AN4035 we designed. Thank you for our great understanding knowledge for our internal discovery team, because we initial working on the pan-RAS(ON) approach is about five years ago, so we built up quite a lot of knowledge. Also we had over a thousand molecule, would be able to allowing us to quickly select the most best profile payload. This platform would be a platform play. Besides the CEACAM5 ADC, we also were working on other type of target antigen, and potentially we could also combine with other payload in the near future for the ADC. I want to do a little bit explain for the CEACAM5 ADC's development strategy. I think the idea is we, of course, recruit all the RAS mutations, solid cancer patient, but with the CEA enrichment. We hopefully were able to see potential responders in the colorectal cancer patient because this indication is very difficult to treat. Of course, we could also seeing some combination data as well. As Brittany mentioned, we initiated EGFR combination in quite early stage. We actually designed it, staggered design for the combination study. Potentially for the ADC study, we will also, potentially in the expansion cohort, we will also enroll post daraxonrasib patient as well, and we want to see what kind of a profile will looks like for those type of patient to receive treatment for our ADC. Yeah. Excuse me. Next year promises to be a pretty data-rich year in terms of the disclosure for AN9025 and AN4035. Maybe as you've done several financings this year, maybe if you just kind of remind us in terms of current cash runway, what is funded with your current cash. Yes. Early this year, we did two financings, a PIPE financing. Of course, thank you for our current shareholder coming from those PIPE financing. They provide a great support for our current two RAS programs development. By end of June 30, we have a total cash of about $232 million cash. This is good for us to get through 2028 and allowing us to really testing the preliminary safety and also preliminary efficacy, potentially a few proof of concept data for our oral small molecule pan-RAS(ON) inhibitor, including the first ADC, CEACAM5 ADC program. By the first half next year, of course, once we are announcing our human data, for the small molecule, we probably also going to initiate some combination data, and then based on those, of course, we would looking to accelerate a registration pathway strategy. Yeah. We've covered a lot on AN9025, AN4035. Earlier pipeline, I know Brittany, you mentioned some of the other programs, and I know that the focus is on the pan-RAS, but maybe just spend a moment on where else you all are excited with some of those earlier programs. Yes. As I mentioned, the CEACAM5, of course, the reason we selected CEACAM5 is because it has overexpressed in the colorectal and also PDAC tumor, while it has a relative lower normal tissue expression. Also CEACAM5 is perfectly avoid skin expression and also they have a very manageable GI toxicity. So CEACAM5 actually proved to be a very perfect combo with the pan-RAS(ON) payload as ADC design. Even it's a perfect combination, but it had a limitation because you might need to looking for CEACAM5 enrichment tumor type outside those big three. You could imagine if we going to target other indication, for example, for breast cancer, for liver cancer, for other type of solid tumor cancer, they might have also coexist with RAS mutation with other tumor antigen. Then we could ideally seeing we may be choosing other tumor antigen to target other indication as the following program. For the payload itself, the pan-RAS(ON) payload has specific address for those RAS mutation tumor. But potentially you could also consider a combination with the pan-RAS(ON) payload with other mechanism of the payload to do as a dual payload program. We're seeing the fast follower from China, they also have some company, they're working on the dual payload. It's not easy, but I think that's something is another mechanism we also are being working internally as well. As a target antigen, you could also consider, for example, like a bispecific. As a target antigen, could be also addressing relative different challenge in the current cancer treatment. This is a platform play, and then we have a lot of ongoing, but of course, we would focus on our resource on that two lead program. Of course, we can consider a potential strategic partnership for a platform of our novel payload ADC. Yeah. No, that's great. Maybe as we're kind of wrapping up here, Brittany, you've been with the company a little bit now, and as you all are telling the story, and we've heard it today, what do you feel like maybe is maybe just not as well understood or appreciated about the story that you'd like to kind of re-emphasize for us as we're wrapping up? Yeah, absolutely. I think understandably, there's a lot of investor focus on the most near-term catalyst, the data readout for the AN9025, the small molecule program, and we're certainly excited to see how that preclinical profile translates into the human data and what we can share with folks there. But we're also really excited about the ADC program. We think the mechanism is really differentiated and could open up a lot of avenues for interesting development. As we enter the clinic with AN4035, we're starting to hear more interest from investors on that front, and we continue to hope that as that story unfolds, we can continue to share that more. Yeah. Alex, anything you would like to add in terms of where you feel like, in terms of the story, what people are missing, where you want investors to be focused? I think right now is we would hopefully investor focus our clinical data. Of course, it's not far away from now. As we all a drug developer, I think really showing the differentiate profile you need to use in the human data to really prove the idea. Yeah. I think the first half 2027 will be exciting time to really the first showing our data. Of course, I think the execution is also very important for our current development strategy for our pan-RAS(ON) program. Yeah. We like to focus on the execution in 2026 and of course in the data year 2027, then we would be able to report the data at that time. Yeah. Great. Well, we'll be watching closely. Thank you both for joining us. We're just out of time, and thanks for being here. Great. Thank you, Bob. Thank you, Bob, for the invitation.