Thank you for joining Jefferies China Biotech Summit. For this company presentation, we have Adagene. We are very pleased to have our Chief Executive Officer, Dr. Peter Luo, for this session. Peter, welcome, and pass it to you. Thank you, Kennyy, and thanks everyone. Today, I'd like to give a company overview and with the latest update. There's a disclaimer. I like to always emphasize our goal at Adagene here is really use the computational power to drive the directed evolutions process. By leveraging our AI-powered Dynamic Precision Library approach, we like to bring highly differentiated antibody-based drugs to cancer patients worldwide. As in Adagene, we are really leveraging this platform to make things very differently with a lot of differentiations. We really believe life is emotions, and so are the proteins and the antibody we are working with. In this way, we'll be able to engage the target and antibody in very different ways. Our strengths, I'd like to share with you. First of all, this is our AI-powered. We call it Dynamic Precision Library platform. Specifically, we focus on three-body technology, which are the NEObody, SAFEbody, and the POWERbody approach. This platform allow us to create our clinical pipelines. For NEObody approach, we have two program in the clinics, including the agonist antibody, ADG106 against CD137 or 4-1BB. Another program we call the ADG116, is against CTLA-4. You will notice we want to show you some technologies. We can hit those targets, for example, 4-1BB or CTLA-4, which are known for safety issues. Our NEObody approach allow us to come up with a novel epitope, which give us a very different safety and efficacy profile compared to, you know, others, either in the market or in the clinics. We hope this kind of differentiations and the data we show pre-clinical and clinically will allow us get a new insight and of course a new you know product profile for our patients. For our SAFEbody platform is our you know we have one program right now in the clinics. That's against CTLA-4 again and ADG126. We recently announced another exciting program in the SAFEbody that's against CD47. We have bringing a lot of differentiated features for this hard targets. This we've already getting the abstract accepted by the ASH and I'd like to touch some of the key differentiating points in today's talk. I hope you will stay tuned for our news release and the abstract releasing pretty soon. For our POWERbody approach, we announced the full program in IND-enabling approach. Again, this is a POWERbody, give us a lot of power in our future pipelines, and including bispecific T-cell engagers on our proprietary bispecific platform together with our masking technologies. Again, we have one program abstract accepted by ASH against liquid tumors. We also have a program going against solid tumors. We hope those transforming pipelines will give you a lot of, you know, excitement to the field. Also, we'd like to share those differentiated products, pipelines and our abstracts in the future. Of course, we'll discuss some partnership for the validation to our platform. This is going strong with already those partnership going on and a new partnership. We'll also bring new leadership to the company across all part of what we're doing from platform, pipelines, clinics, and the business and all this, so we can, you know, help our patients better, our partner better, and to build a good company for our investors. This is the platform I'd like to introduce, is a tailor-made antibody therapeutics. Our NEObody approach shown on the far left. As you can see here, the blue color is a 4-1BB target, and the brown and the green color is our antibody. As you can see, the crystal structure we show you here is coming from a dynamic engagement from our targets and the antibody we designed. You can see that kind of dynamic engagement really bring new dimensions for the diversity of antibody and the engagement between the antibody antigens. If you look at the SAFEbody in the middle, this is the only activity conditioned in tumor microenvironment through our precision masking technology. This allows us to come up safety margin so much higher than the parental antibodies. Of course, gives us a safer profile for target, for example, the CTLA-4 and the CD47 and our T-cell engagers, including the solid tumor targets. The POWERbody I show here on the right, they can come in different flavor and the format, including Fc Engineered, T-cell Engagers, and the ADC. This technology are those powerful modality in combination with our masking technology, allow us to target the tumors with very strong efficacy, still have a good, very good safety profiles. About platform validations and through the partnership and the collaborations, we have announced our collaborations early this year with Exelixis. This is a deal actually that we believe is one of the largest platform-based deals in any China-related biotech companies. The total deal size is close to $1 billion, with $11 million upfront and $780 million in milestones and high royalty rates. Adding together close to $1 billion. ADC Therapeutics is another top large ADC company from Switzerland. Again, we are helping them to market their ADC modality so they can achieve safety otherwise very difficult to achieve. They will show that in the preclinical studies about the safety margin and the potency they can achieve, with the packaging deals. We are also working with Mitsubishi Tanabe from Japan on their solid tumor ADC technology, drug products. We are making progress in all those programs. Our DPL technology could also help our partners to discover antibodies against those very challenging targets, including for NIH, the HERV targets, very challenging antigens. We'll be able to come up, you know, specific design for those antigen and antibody, very specific for those primary tumor cells. Our partners at the NIH and, you know, Dr. Richard Childs, the clinical division head, and on those targets, he works for years and for, you know, potential CAR-T therapies. Of course, we are all on the biologics. We also work with BMS or Celgene and GSK for antibody discovery in very challenging space and therapeutic areas for either agonist antibodies or for, you know, antibodies against some very difficult targets. We also work with Chinese domestic partners and for example, like Hengrui, to make agonist antibody with co-stimulatory activities. We also license our pipeline to Sanjin and including PD-L1, which is a phase II, and the CSF1R in phase I. This year we launched three clinical trial collaborations with Merck, and basically the collaboration for each of our three clinical programs. These three phase I-B/II open-label, dose escalation or cohort expansion trials which include KEYTRUDA, our ADG116, ADG126, and ADG106. In fact, Merck has assigned the clinical lead to those trials. We still have the freedom to collaborate with other partners in the space. Merck is going to provide KEYTRUDA for global combination trials conducted in multiple sites across Asia and the U.S. We're going to run the clinical studies with the important clinical input from the Merck clinical team about the trial design. Let's look at our three tailor-made antibodies in the clinics in our pipeline. Again, I'd like to emphasize, we've chosen a target known to have outstanding safety issues, such as the CTLA-4 and the CD137 clinics, right? If you look at our NEObody, for example, against CTLA-4, the green colored one, there's small difference in epitope. The crystal structure will show differentiation from the ipi in purple colors. Could it make a big difference in terms of mechanism of actions and the safety efficacy profiles. To build on that antibody, we further masking the binding site using our SAFEbody technology to push the safety margin much higher, right? Where we show GLP tox data at even 200 milligrams per kilogram, we still have a very good robust safety profile in the monkeys. For 4-1BB agonist, again, we show the green colored in crystal structure with the 4-1BB, which are differentiated from the BMS antibody on the top and the Pfizer molecule in the bottom in crystal structure. Again, this novel epitope, it gave us a nice balance in terms of safety and efficacy for our agonist antibody programs based on about 100 patient data from both U.S. and China. I like to dive in a little bit about our anti-CTLA-4 therapies. There's a paradox in the field which people believe you have to trade in the efficacy for safety or vice versa. If you look at currently, unlike PD-1 or PD-L1, even the CTLA-4 target has been known for more than 25 years now. So far, there's only one product called ipilimumab being approved with one indication for monotherapy and a sixth indication for combination with PD-1, where those are more common for the combinations. This is highly unusual because this so far is still the only checkpoint target other than PD-1 or PD-L1, shows monotherapy efficacy, of course, in combination with PD-1. Why there's only one product being approved for this drug? I should say, people really try hard on these targets. Until recently, the safety still a big concern for this limited efficacy and the usage for anti-CTLA-4 therapies. You have seen news last month from Merck, for example. Late last year, KEYTRUDA in combination with ipi failed in phase III. AstraZeneca has revoked a lot of failed phase III programs. The good news is recently AstraZeneca has tried to achieve some first-line therapy to lung small cell cancers and also most recently in the HIMALAYA in phase III trial in first-line HCC. Those exciting news. We are yet to see those data, but apparently the safety concern for the treatment has been a deep problem for this drug against these targets. What we can do if we will be able to create a differentiated anti-CTLA-4 antibodies. I like to share our platform here or the example, how we'll be able to do something different here, differentiate. For example, for ADG116, starting with a dynamic binding interface. The same sequence, different conformation, as I show you here. The binding pocket change. Then you go to the second step. You see how our antibody colored in, right, cyan and green are engaging this gray color CTLA-4. This is the crystal structure we show you here. Before they have engagement, they change this conformation from both to have this dynamic engagement. This really allow us to engage this target at its epitope, specific epitope, in a new way, a new dimension. We pioneer this approach for the first time in the world. What this allow us to target this epitope we show conserved between human, mouse, and monkeys in this conserved epitope. Even though the human and mouse CTLA-4, the sequence identity is below 60%. We know in antibody engineering, this is very challenging job. We can do that, target this conserved epitope. Not only we get this novel epitope, we also get a cross-reactivity to study this antibody from mouse, monkey to human, with the same molecules. What allow us is a very robust translational program. We're doing this for many of our programs here. We can use this cross-reactive antibody, look at the mouse tumor models, syngeneic mice, complete immune system, and then we show you can achieve complete response at a dose of 1 mpk. We know this molecule is very important. We show in the monkeys, we can go to the HNSTD to 30 milligrams per kilogram in monkeys, which already shows a safety margin over what's reported for ipi at 10, means we can have dose in the monkey higher without serious damage. Armed with this efficacy and the safety data, then we move confidently go to the human trials. What I was going to share with you in details later, right now we observe very robust dose-dependent PD activations. What dose in the patient right now is at 10 mpk. We are doing cohort expansion at a 6 mpk. Higher than what Yervoy approved original at a 3 mpk to myelomas. How can we do this? Why by changing the Fc by small step can achieve such a striking efficacy and safety? We basically will share with you here our mechanisms of actions, because this allow us to come up with very strong ADCC effect to deplete the Treg, and also allow us to safely activate the T-cells through a novel blocking effect. The end result is a five times more potent efficacy in a head-to-head comparison with Yervoy in preclinical testing. This very strong differentiated profiles which shows preclinically and is right now are showing consistently clinical verification. I'm gonna show you in a minute. Before I show you the clinical data, you'll see here very potent activation in the 0.1 complete suppression. We show for 80 tumors by 80 stage. For big tumors, 500 compared late stage, six out of eight complete response. We show the comparison with ipi head-to-head. 0.2 with complete suppressed tumor. For the ipi, you have to do the 501 mpk. If you look at the 1 mpk here, it's only in the tumor microenvironment you can see the Treg depletion from 40 to below 20 shows this result, and the ipi cannot. Of course, the mechanism, a strong ADCC effect compared to the ipi, and also the blocking is not as strong as ipi, which leaves some safety margin to these products. This is the clinical program I'd like to share with you. This global trial, 116, both Australia and the U.S., we're expanding to other regions. So far we enrolled 25 patients. We finished eight cohorts up to 6 mpk, no DLT. We observed strong dose dependent PD markers and normal PKs, and with dose in patient of 10 mpk. The cohort expansion at 6 mpk are ongoing, and we're also approved by the CDE committee for combination at 6 mpk with PD-1. As you can see, we do have a combination at the bottom line here. First initial with toripalimab, and then also with our 4-1BB agonist and novel combinations. Against this, you know, indications we've chosen which are highly promising for monotherapy or in the combinations, because we know this Tregs play a big role in those indications. We got approval from the Chinese CDE for doing the monotherapy starting at a 3 mpk high dose for that. We're very excited for this. Of course, our collaboration with Merck, with KEYTRUDA, has been approved for that protocol and submitted to the FDA. How about SAFEbody with this masking technologies? I'd like to share with you the masking technology, we can GOP, we can achieve 200 mpk, and we finish the dose escalation at a 3 mpk, no DLT, and we are basically approved for dose in patient at the 10 mpk, now from both U.S. and Australia. This is the preclinical data. As you can see, this SAFEbody is active by itself against different tumor models on the left-hand side. In combination with PD-1, with this SAFEbody or the NEObody ADG116, they show very potent combination against the cold tumors because our construct antibody allow us to do very robust testing here. You can see complete response here. Check the box for Treg depletion in the tumor microenvironment again. Those are the GLP tox data I just shared with you for both program. About our 4-1BB agonist, we have updated the data about our, you know, monotherapy for 100 patient data at a dose level at 3 mpk and 5 mpk, very high than other agonists we used for those cohort expansions. We also observe those interesting biomarkers related to this pathway and the activation. We also have the combination with toripalimab in China for dose escalation. We also submit abstract for both ADG106 and ADG116 and accept by ESMO IO. Stay tuned for those informations. Due to skip those biomarker you already knows, and then welcome to look at those data we presented previously. In the end, I'd like to share with you the excitement for our pipelines. I already shared with you our ADG106 and ADG116 in the current phase I-B/II, and the two abstracts submitted to ESMO IO accepted in the poster form at the end of this year. Please stay tuned for the latest progress for both programs. The other thing is about our SAFEbody programs and the ADG126 are going very well. We'll get a comprehensive release about the progress of the program approval, regulatory approval, and all other things, and its combination and all those things. But also, I'd like to highlight it here for the CD47, highly differentiated programs. Except for ASH for these programs, and I think I'll be happy to talk to Kenny about what's the differentiation there. Of course, we have other program in the POWERbody, two Fc-enhanced SAFEbody, well advanced in our IND-enabling process. Stay tuned for those abstracts. Also, two bispecific T-cell engagers, including one for liquid tumor, accepted by ASH for liquid tumors. Of course, I'll follow up with Kenny for that differentiation. Also, our ADC SAFEbody program with partners. Those are the catalysts and major events for those programs. I basically will put it there, and I'm happy to answer the questions here. Thank you for your attention. Thank you, Peter, for a very comprehensive presentation. I only have one question. Leveraging on your proprietary technology platform, NEObody, SAFEbody and POWERbody, seems like you're building a broad early-stage pipeline. In terms of future development plan, how do you think about assuming that you'll be very active on BD front? How do you prioritize the internal pipeline versus the assets to find partnerships? Yes. Of course, Kenny, that's a very good question. Of course, for our internal program, as you can see, our goal is to push the program to get the early clinical proof of concepts. For example, our ADG116, ADG126 is a great example. It gives the same target two programs because the product profile are differentiated, either for mono or for the combinations. Therefore, we do find partners are very interested in those differentiation, like Merck, right, and other big partners we're talking to. I still say for our partnership and, we like to show those clinical proof of concept. Therefore, we'll be able to do the transactions to enable our partners quickly get into those important pivotal trials or whatever trials in their mind and, right, the key interest. Of course, while doing that, we will continue to develop some of them, say in Greater China, either in partnership with them or by ourselves, choosing those indications that are highly promising based on our early clinical data. Of course, for some early programs, we are also hearing from partners who are interested in those. Of course, it depends on the value inflection for those programs. We'll decide how to do this deal, either in an early stage or a little bit later stage. That all depends on how well we can bring in our investors, right, our investors for the investment in the company and the trust in us. Great. Thank you very much. Looking forward to your update at ESMO IO and ASH. Thank you everyone online joining us for this session. Thanks, Kenny. Thank you, Peter.