Good morning, and welcome to the NovaBridge Biosciences business update call. At this time, all attendees are in a listen-only mode. A question and answer session will follow the formal presentation. As a reminder, this call is being recorded, and a replay will be made available on the NovaBridge website following the conclusion of the event. I'd now like to turn the call over to Sean Fu, Chief Executive Officer at NovaBridge Biosciences. Please go ahead, Sean. Thanks, Tara. Good morning, everyone. I'm Sean Fu, CEO of NovaBridge. Once again, welcome to VIS-101 clinical data and the development plan update. Next slide. In this presentation, we will share forecast about future performances, which are speculative, not guarantees. Actual results may differ materially. Like Tara mentioned, I wanted to reiterate the material presented today will be publicly available on NovaBridge website. Next. During today's call, we'll first walk you through some high-level information about NovaBridge, our hub and spoke business model, and the first spoke company, Visara. Focus on ophthalmology, obviously. Then I will cover a few more topics, including detail the phase IIa clinical data of the first pipeline asset of Visara. We call it the VIS-101. We'll also include important perspectives from respected KOLs on the call, and we'll comment about next phase clinical development plan as well. Finally, we'll be happy to answer some questions from the audience. Next. Joining me today are Visara management team and the guest experts to walk you through phase IIa VIS-101 clinical data. It's my pleasure to introduce today's speakers, Dr. Emmett Cunningham, Executive Chairman and Co-founder of Visara, and also Vice Chairman of the board, NovaBridge. Dr. Cadmus Rich, Chief Medical Officer of Visara, and Dr. Carlos Quezada-Ruiz, Chairman of the SAB of Visara. Last but not the least, Dr. Nikolas London, Managing Partner, President of Retina Consultants San Diego. We are excited to tell you about NovaBridge, Visara, and the VIS-101. All right. Next. Let's start with some intro of NovaBridge. The next slides, please. NovaBridge is a global biotech platform with portfolio of the first and the best-in-class programs. At this moment, we have two lead assets. Let me give you a quick download of who they are. Both demonstrated a compelling clinical proof of concept supporting differentiated positioning. The first one we're talking about today is VIS-101. This is a molecule that's purposely designed and with a differentiated molecular structure targeting VEGF-A ANG-2. Has a favorable safety profile and a rapid durable response supporting a potential best-in-class durability. I'll show you a lot more data in the next hour also. The other asset we have is in the oncology space. We call it givastomig. It is a Claudin 18.2 4-1BB bispecific antibody, which demonstrated a robust and a durable response in patients across broad biomarker expression levels, be it PD-L1 or Claudin 18.2. It is a potential best-in-class molecule that can be bolt on to the current standard of care for the frontline gastric cancer patients. We're super excited about this molecule, just like we are today for VIS-101. Two very impressive, very important molecules. We have a healthy balance sheet talking about our finance. As of last SEC filing, we have $228 million in cash, providing operational runway through 2028. If you look at our upcoming milestones, we expect multiple near-term catalysts from the lead assets VIS-101 and givastomig in those therapeutic areas in the coming months and period of time near term. It's very exciting pipeline. Next slide, please. I wanted to give you a high-level overview of NovaBridge's business model. NovaBridge is a hub and spoke gateway connecting innovation from China and other emerging biopharma ecosystems to global patients. We believe the quality and efficiency of a China biotech industry will continue to create significant value going forward. There are three components of our business model. The first thing we do is to leverage our strong access to China biotech ecosystem to identify and to license in innovative assets in a capital efficient way. We prefer clinical stage or clinical-ready stage programs in order to reduce our exposure to biology risk. In doing so, we take a therapeutic agnostic approach, really focusing on the overall value and the quality of the assets. Subsequently, we build an industry-leading development team around these assets in the U.S., form a subsidiary or a spoke company. The spoke company will then design and implement clinical trials with a goal to demonstrate clinical POC, at which time we expected the asset value to increase significantly 5 times, 10 times, or even more. When we have achieved the clinical POC in some of those programs comes the step number three, which is the value realization. In this phase, we could pursue an out-licensing deal, a co-development deal, or in selected cases where when we feel the circumstances are right, the molecule is right, the team is great, and the therapeutic area is suitable, and the commercial opportunity is right, competitive landscape, the subco in under those circumstances, then we have the option to let subco be in a vehicle to raise additional fund, engage itself in late-stage development in order to capture additional upside. We have flexibility in this particular business model step. NovaBridge, but in doing those three things, really is the only publicly listed company to engage itself in systematically creating value through the bridging of China innovation to global markets, building a differentiated capability based on BD in, BD out capability, as well as industry-leading clinical development capabilities. Next slide, please. What about Visara? What is the relationship between Visara and NovaBridge? NovaBridge invested $37 million cash October of last year. Here I highlighted on the left-hand side the cap table. NovaBridge currently owns 65% of Visara. AffaMed contributed its right and interest in VIS-101 in exchange for 30% of the equity in Visara. The remaining 5% is ESA. Visara is the first spoke company in the hub-and-spoke model of NovaBridge. As I mentioned earlier, our business model combines the strengths of the molecule with the quality of the management team. On the right-hand side, I think you will see that the Visara is a wonderful example of that. The Visara company is led by Co-founder Executive Chairman, as I introduced earlier, Dr. Emmett Cunningham. Give you a little bit more background about Emmett. Emmett is a world-renowned ophthalmologist, also a former senior managing partner of Blackstone Group, with over 25 years of experience as entrepreneur, as an investor, as a drug developer. Co-founded more than five different companies with successful track record exiting IPO or acquisition, published over 450 papers in the field, notably was also one of the leading scientists behind the Macugen, which is the first VEGF-A inhibitor for AMD and DME. Cadmus, as I introduced earlier, is our CMO with over 18 years of experience in ophthalmology R&D with companies such as Lassen, Aura, Elcano, major players, all major players in the field. Great experience working with regulatory agencies, FDA, EMA, MHRA on multiple projects. Dr. Carlos Quezada Ruiz is the chairman of our SAB, again, with over 25 years in experience in ophthalmology R&D. Most recently, I wanted to highlight that the Carlos was the medical lead for Vabysmo at Roche, and he played a pivotal role in the global development and approval of Vabysmo itself, which targets the same two targets that VIS-101 target, and also other drugs like Susvimo. Carlos led the design execution readout filing and launch activity for those product. I cannot think of a better person guide us as SAB chair through the clinical development for VIS-101. We're extremely happy to have such an experienced management team for Visara. Now, to tell you more about Visara and VIS-101, here is Visara Co-founder and Executive Chairman, Dr. Emmett Cunningham. Emmett? Yes, thank you, Sean. Emmett Cunningham here, as Sean said, co-founder and Executive Chair of the company. Next slide, please. Today we're going to hear some pretty exciting results from VIS-101, which was, as you've heard, purpose-designed to be best in class for retinal vascular disease. The molecule schematized here on the left, you can see is tetravalent. It has two anti-VEGF-A binding sites and two ANG-2 neutralizing sites with an Fc modification to limit systemic circulation. These attributes, which you'll hear more about in just a second, make it, we believe, best in class. You'll also hear today the results of our phase IIa trial performed in China, which demonstrate that the drug is safe and well-tolerated. You'll see that it has a very rapid, robust, and durable treatment response with a mean vision and CST response that are, I believe, at least equal to best in class. Notably, the durability, as we saw in this trial, showed that up to two-thirds of patients were retreatment-free at four months, with about half retreatment-free at six months. Again, potentially best in class. Next slide. Now, Sean has introduced Carlos Quezada-Ruiz, so I'll let those words stand for themselves. Carlos will be presenting our clinical data. Dr. Nikolas London was an investigator in the U.S. portion of VIS-101 development and will give some perspective from that experience, following Carlos's presentation. Dr. London is a world-renowned KOL, a retina specialist who practices in San Diego. With that, I'm going to hand this over to Cadmus Rich, my colleague at Visara, to do a brief introduction of the molecule and its properties. Cadmus. Thank you, Emmett. Thank you all for attending today. I'm really excited and feel privileged to be able to introduce our lead program, VIS-101, to you today. Next slide. A few words first about the unmet need and the disease that we are treating with VIS-101. Basically, the main retinal vascular diseases, including, as you see here, wet AMD, which has over 20 million patients. This is where abnormal blood vessels grow under or within the retina from the choroid and cause damage to the vision. Diabetic macular edema in the middle, which is a manifestation of diabetes, sick blood vessels in the retina leak and cause edema of the central part of the retina, which impacts the vision as well. There are 21 million people with this condition. Last, retinal vein occlusion, where a blood vessel is occluded and the backup of the blood flow causes edema of the macula, which VEGF therapy can also reduce. You see 16+ million people afflicted with this condition. Overall, there's more than 57 million people affected globally, and there's a large unmet need to have therapies that could extend the treatment interval to reduce the number of injections needed, which means there'd be less disease fluctuation and fewer injections over time. Next slide. This durability is very important, and we know that the market does have a lot of impact with durability. You see this here on this slide with the graphic you see on the left with Lucentis was the first drug after Emmett's Macugen, the first anti-VEGF drug, which took market share from Macugen. That was every four weeks, as you could see on the right. Eylea was developed with every eightweek therapy and came in and reduced the growth of Lucentis and took over market share. Vabysmo and Eylea were developed recently and have now have a treatment interval of around Q 8- Q 16 weeks and have taken over a large amount of the market share. Now we wanna introduce you to VIS-101, where we feel we will have Q8 to Q24-week treatment intervals, and that we think that this will give us a best-in-class durability as well as a potential in the marketplace. Next slide. Introducing you to the molecule, which Emmett touched on briefly. This is VIS-101, the next generation bispecific, purpose-designed to be best in class with dual VEGF-A and Ang-2 inhibition. This bispecific tetravalent design increases the number of binding sites and has a higher affinity for both the VEGF-A and Ang-2 receptors. You could see on the molecule on the left, the two anti-VEGF sites on the top. These are two times more inhibitory than faricimab. You could see on the bottom, the two ANG-2 receptors on the other side of this traditional antibody molecule. The 18 aptamers that are for ANG-2 that are 17 times the inhibitory activity of the faricimab ANG-2. We touched on the optimized Fc region for shortened half-life with bypassing the FcRn pathway. This combination gives us a purpose-designed molecule that in both our phase I study, which we won't cover today, and our phase IIa study, that we will cover today, where about half the patients remain treatment-free at six months. Next slide. Comparing our drug to the market leader, Vabysmo, you know, how do we compare? You could see on the left the Vabysmo molecule with one site for anti-VEGF and one site for ANG-2 versus VIS-101 on the right, where we have two binding sites for VEGF and two binding sites for ANG-2 or the tetravalent platform. The antibody format is bispecific for Vabysmo and tetravalent bispecific for VIS-101. The molecular weights are similar, but the VIS-101 is slightly larger, which may also confer a slight advantage on the PK profile. The dosing that we compared in this study are similar at 6 mg each. Although in our phase IIb study, we will investigate a 9 mg dose as well. There are three loading doses for VIS-101 versus four loading doses for Vabysmo. I think this is partly because of the tetravalent molecule and the better affinity, giving us longer inhibitory activity, and I'll show you a model of this in just a moment. You could see the durability of response, up to 16 weeks has been investigated for Vabysmo. For VIS-101, we have up to 24 weeks of durability. Overall, this is a purpose-built molecule, bioengineered for rapid, robust, and durable response. Next slide. I'm gonna show you our PK/PD model, which helps to demonstrate the advantage of the inhibitory activity with VIS-101 compared to faricimab. This PK/PD model was developed specifically for faricimab. The reference to that model is at the bottom of the slide. This model was used to estimate the inhibitory potential for VIS-101 and compare that to faricimab. This was developed by the engineer who actually built and designed the VIS-101 molecule, Jeff Lu in China at AskGene. This shows both the VEGF-A on the right axis. If you see on the right side on the Y-axis, predicted free VEGF-A levels in the aqueous humor, and then on the left, the Ang-2 levels. We'll go through this graph together here. With an injection, the level of both the VEGF and Ang-2 with the inhibitory drug dropped down to zero, and you could see that at the bottom left of the slide. As the drugs, both due to PK, but also due to the inhibitory activity and affinity of the binding sites and the number of binding sites, as the drug starts to leave the eye, you could see that the levels of both of these molecules start to increase in the aqueous humor again. You could see on the solid lines to the left in red is the faricimab VEGF activity. In blue, with about a one-week benefit of longer inhibitory activity is the VIS-101. On the dotted lines with ANG-2, you could see in red the faricimab ANG-2 inhibitory activity lasting about 16 weeks, which goes along with its testing interval. For VIS-101, you could see we significantly extend that over four more weeks or longer with our dotted blue line here. This shows that we are able to have longer VEGF and Ang-2 inhibition, which may predict increased VIS-101 durability. We feel that this will also be shown to you by Dr. Carlos Quezada-Ruiz on the next part of the presentation, where he will show the clinical data that supports this. Next slide. Let me turn it over to Carlos. Thank you for your time and attention. Thank you very much, Cadmus. Good day to everyone. I'm Carlos Quezada-Ruiz, and I'm a retina specialist, I'm a drug developer, and I'm the chair of the scientific board of Visara. I'm honored to present to you this morning the top-line data for the phase IIa study. I want to thank the teams of Visara, the investigators, the study staff, and the patients who participated in this study. Next. First, I want to take some time to explain the trial design on this slide. This was a multicenter, open-label, randomized, multiple-dose study to evaluate the safety, the tolerability, the pharmacokinetics, and the pharmacodynamics of VIS-101 in patients with neovascular AMD, important to note, both in treatment-naive and previously treated patients. The key inclusion criteria included patients with active macular neovascularization secondary to AMD who were between 50 and 80 years of age. The total lesion size of up to 12 disc of areas, a baseline BCVA on ETDRS of the study eye that fell between 19 and 78 letters, which represents approximately 2,400- 2040 on the Snellen chart, were the key ocular inclusion criteria. On the exclusion criteria front, we excluded fibrosis or geographic atrophy that involved the fovea, any history of glaucoma or having received any anti-VEGFs within 60 days prior to screening. The primary endpoints of this phase IIa study was the incidence and severity of ocular and non-ocular adverse events, treatment emergent adverse events, and serious adverse events. The selected secondary endpoints include the mean change from baseline in BCVA, CST, and the durability. A total of 38 patients in China were randomized in a 2-1 ratio to either the three or the 3 mg VIS-101 groups with 25 and 13 patients in each group respectively. Important to note, the patients were stratified by baseline BCVA at day zero. Patients then received 3 monthly injections, often referred to as loading or initiation doses. Starting at week 12, the investigators evaluated for disease activity every fourr weeks and gave rescue treatment based on strict and pre-specified disease activity criteria that I will explain a little bit later. The duration of the study was 20 weeks post first dose with monthly follow-up visits. If a patient had not received rescue treatment by that time, then the study would be extended to a maximum of 36 weeks post the first dose or until the disease activity criteria are met and rescue therapy is initiated, whichever occurs first. Next. Here we see the baseline characteristics, and they're generally comparable between the two groups. I wanna point to your attention a couple of topics here. BCVA was a few letters better in the 6-mg group at 54.7 ETDRS letters, which represents approximately 20/80 on the Snellen equivalent, and 52.3 ETDRS letters for the 3 mg group, or 20/90 in Snellen equivalent. The central subfield thickness, or CST, was on the thicker side with about 410 microns at baseline in both groups. As you can see on this table, more previously treated patients were randomized to the VIS-101 6-mg group. This baseline visual and anatomic values, the existence of a pre-treated cohort show here that probably this population represents a sicker patient population that than those that were included in more recent trials for neovascular AMD. Next. Here we see patients treated with VIS-101 at both the three and 6 mg experiencing a rapid and robust BCVA gain during the loading phase. The solid and dotted lines represent the treatment naive and the previously treated groups respectively. As mentioned during the trial design slide, starting at week 12, all patients were assessed every month for signs of disease activity, and if they met criteria, they received supplemental treatment and left the study. You can see this part of the study reflected in the table on the bottom, and you can see this attrition by the number of patients per visit as it's declining as patients receive supplemental treatment and then exit the study. Both the three and the 6 mg groups showed very good treatment response and durability. Next. Here to the right of the slide, you can see the BCVA results from the STAIRWAY study, which was the phase II study of faricimab that was designed to evaluate its durability potential. The STAIRWAY study included monthly 0.5 mg Lucentis arm in addition to the Q12 and Q16 week arms of faricimab, as you can note. The BCVA gains by VIS-101 in the treatment-naive and previously treated patients are comparable to those achieved by faricimab and other anti-VEGFs. Important to note, there's only three loading doses that were given in the VIS-101 study versus four loading doses that were given at the STAIRWAY and the TENAYA and LUCERNE studies for faricimab. Next slide. When we look at the treatment-naive population, we see that about 70% of the patients are treatment free at four months and about 40% are treatment free six months after the last loading dose. Important to note, with a strict pre-specified disease activity criteria. Next. Treatment with VIS-101 also resulted in rapid and robust anatomic improvements with a decrease in central subfield thickness by over 100 microns. This was after the first injection in both the three and the 6 mg arms and across both treatment-naive and previously treated groups. Next. These anatomical results were achieved with about 70% of the patients being treatment free at the four month and about 40% treatment free at the six month after the loading dose. Next. This graph shows the durability over time for the 6 mg arm with approximately half of the 6 mg patients being treatment free out to and past six months, with visual stability as shown in the previous slides. Here to the right, you can see the disease activity criteria that had a combination of visual, anatomical, and clinical criteria to ensure the safety of the patients. You can see that having an increase of 75 microns or more in CST compared to the previous lowest CST in the study, or having a BCVA decrease of five letters or more compared to the mean BCVA of the previous two scheduled visits, or having a loss of 10 letters or more compared to the previous highest BCVA, or having new or recurrent fluid due to neovascular AMD activity, or the presence of macular hemorrhage, that in the criteria of the investigator was due to neovascular AMD activity could trigger a supplemental treatment in these patients. Next. As always, super important, safety. Throughout the study, VIS-101 at both the three and the 6 mg arms were well-tolerated, and there was no dose-limiting toxicities. There were two patients who had treatment-related adverse events. One patient that had three episodes of uveitis. Those were detected on the slit lamp exam. The patient was asymptomatic and did not affect vision. There was one case of vitreous opacities. There was no cases of ocular hypertensive events. Across all patients dosed, there was no patient who lost 10 letters or more during the study. Lastly, there were no cases of occlusive vasculitis or retinitis. Next slide. With that, I now want to hand it over to my dear colleague, Dr. Nikolas London. Thank you. Great, Carlos. That was an amazing overview. This is an exciting molecule, and as a clinician, I'm very excited to see these early results and very hopeful that they are replicated. I think if they're replicated in later phase clinical trials, we're going to have a real great blockbuster on our hands. We can go to the next slide. We've seen this slide before. This is comparing VIS-101 to currently available best in class bevacizumab or faricimab. You can see some of the key differences that have been reviewed. Just to review, we've got about double the anti-VEGF inhibition and about 17 times the anti-ANG-2 inhibition. For faricimab, there are four fixed loading doses compared to three fixed loading doses, we see a post-dosing loading dose durability in faricimab of up to 16 weeks with up to 24 weeks or longer with appears a single dose of VIS-101. Similar BCVA gain and a really strong safety signal. You know, all clinicians are concerned about inflammation. This one case of mild, easily controlled uveitis to me as a clinician is not overly concerning. You know, for me, from a clinical perspective, you know, when faricimab came onto the market, it was fairly slow at the beginning to adopt because we were not at all comfortable with the ANG-2 component. We weren't convinced. We have subsequently become convinced, and you can see the overwhelming increase in the market share that shows that on a previous slide. I kind of think of Vabysmo as a speeding train, we are aggressively adopting it. VIS-101 is not trying to change the direction of that train or compete with that train. It's really grabbing onto that momentum with an improved product. Personally, I can't wait to see my patients benefit from a medication like this. Next slide. Okay. I think we're going to hand over, sorry, to Cadmus at this point to take us through the next steps. Yeah. Thanks, Emmett. I appreciate that. Let's go to the next slide. Just to reiterate what you've heard today, VIS-101 is a purpose-designed, best-in-class molecule for retinal vascular diseases. Our early data here is at phase IIa in wet AMD. The drug was safe and well-tolerated. There was rapid, robust, and durable treatment responses both for BCVA and CST, and we did not really show retinal drying, but also retinal drying. Potentially this is a best-in-class durability with up to 24 weeks or longer, shown now in our early phase I study that Nick was an investigator in and this phase IIa study. Our next steps you see are to begin our phase IIb study in China, which will be initiated in the second half of this year. We're looking forward to beginning our global phase III program, which will begin in 2027. Thank you all for your attention, and if you go to the next slide, turn it over to Emmett for the Q&A. Thank you, Cadmus. I think at this point we're going to try Hollywood Squares-type interaction just to keep it more lively and organic. Yeah. You'll get to see all of our faces. Tara, can you have it such that we can see the Hollywood Squares block template as well? Mm-hmm. Yes. We'll just ask everyone to turn their cameras on that is participating into the Q&A. Great. Now you have several world experts regarding VEGF-A and VEGF-A Ang-2 inhibition. I'm going to take the questions and sort of shuttle them off to others. I would just say to my colleagues, if you feel as though you'd like to add to a comment, please just speak up and let us know. First question, Tara. Great. Yes, please hold for a brief moment while we pull for questions. Our first question comes from Christopher Liu at Lucid Capital Markets. Please go ahead, Christopher. Hey, guys. Thanks for the question. I just wanted to ask, you know, what the key differences are between the study you had here and maybe something like, faricimab. Also, what are your plans or preliminary ideas for the global phase III design in terms of where patients might be coming from and anything else that might be important? There are a couple questions there, Christopher. Thank you for those. The first is, what is the difference between faricimab? As you know, there were more than one faricimab study. There were the phase II, the phase IIIs. What we've done in this presentation is compare directly to the STAIRWAY phase II study. The key difference was that faricimab was entirely treatment naive, where we had a mix, 2-1 mix of naive to pretreated patients. We also think our patients were somewhat slightly more severe in that they had lower vision at entry and a little bit more fluid. Another key difference was we had three loading doses versus their four. Those to my mind are the key differences. Cadmus, do you wanna add to that before we go to the phase III plan? Yeah. I think those were the key differences, Emmett. We showed a comparable vision response to the STAIRWAY study with those advantages you listed. Right. The phase III plan, the traditional phase III plan would be two phase III trials globally, each comparing to a standard of care recognized by the agency, that is typically monthly Lucentis, ranibizumab, or every other month, Eylea or aflibercept. That is the base case plan for us now to have two phase III global studies. It is interesting, as I'm sure everyone has seen, that the agency has said they're moving toward a one phase III paradigm, we will have that discussion with them. We will by that time have a large randomized phase IIb study done in China. We know from other companies doing studies globally, including in China, that the patients respond identically, and so we expect that to be a recognized trial. That could be two trials. In the worst case scenario, we could have one trial that would be centered in Asia and a second centered outside of Asia, which could meet the two-trial rule. All that is sort of on the table, and we plan to have those discussions with the agency moving forward. Cadmus, you're leading that effort. Anything to add there? Yeah, I think that's exactly right. I think we're looking forward to going to FDA and MPA and to MHRA and EMA to get the advice and align the global program. Thank you. Cadmus, one thing that makes me comfortable as a clinician with the clinical trial design is the retreatment criteria. They're good for patients, right? They're or statements. They either have to have a decrease in vision or an increase in anatomic parameters to be retreated instead of an and treatment, which is what some trials require. I think that's great. It makes me very comfortable. Mm. I agree, Nick. I think that, you know, the part of the similarities, I guess, with the or differences with the faricimab trials, as Emmett and Cadmus highlighted, are, you know, on the BCVA, the CST, and the inclusion criteria. The size of the lesion was also smaller in those studies. The or, as part of that, the disease activity criteria is definitely a difference, you know, when it comes to being strict for extension of the patients. Next question, Tara. Yep. Thanks for the questions, Christopher. Our next question comes from Andres Maldonado at H.C. Wainwright. Please go ahead, Andres. Thank you very much for taking my questions. Congrats on the progress. I guess two for me. First, from a vascular biology perspective, I guess how much of the clinical signal observed in the current dataset, you know, would you attribute to VEGF suppression versus ANG-2 pathway modulation? I guess, how should we be thinking about that from an elevated biomarker changes such as TIE2 activation or maybe other vascular stabilization markers to dissect those contributions? Thank, Andres. I'll try to answer that question. If you look back historically at ANG-2 inhibition at Aerpio, which was a company from, I think more than a decade ago, they had a small molecule, which was a direct TIE2 activator. It had a very modest effect. That I think they studied mostly diabetic retinopathy DME. They did have an effect. It was a drug effect. We all believe there was a drug effect. Less than, I believe, what we're seeing with the add-on of faricimab. There, however, when you look at faricimab, you see some of the trials had some vision separation, clearly there appeared to be an enhanced durability, better than, I would say, the Aerpio drug. The point I'm trying to make is that as we get a better inhibitor of ANG-2, and we go from, say, or what Aerpio had to faricimab to now what we believe we have, we believe we can see better performance, I would suspect mostly on the durability side. Mm-hmm ...although there may be numerical add-on, if you will, to both vision and CST. Implicit in your question was what can we expect from a TIE2 activator of the type that others are developing. I'm not sure. We've only seen a handful of patients treated with a TIE2 activator. I have no reason to believe that it should differentiate from a strong ANG-2 inhibitor, but we will see as the studies read out over time. Carlos, did you have anything to add to that? Thanks, Emmett. Yeah, I agree with you. I think where we're seeing really the benefit of the ANG-2 inhibition, which is the most meaningful to our patients, is actually on the durability side, which is again, as noted by the ASRS path survey, the biggest unmet need for patients with AMD. I think when you look at, you know, AKB-9778, I believe was the name of that Aerpio acid, there's definitely signals of activity. We look at the nesvacumab program as well, both in the ONYX and the RUBY trial. There's definitely a signal towards better anatomical benefits which actually do translate to extended durability as well. This is where I think it's the biggest value proposition that VIS-101 actually brings to our patients. One thing that we have not seen, so far has been, you know, and again, bearing in mind the small numbers, and the fact that this is a phase IIa study, but getting half of the patients to 6-month dosing with a biologic is something that we have never seen. This is with sustained BCVA and anatomical, you know, stability as well. That I think is very powerful. Just to add on to that, Carlos, before we go to the next question. What excites me most about the possibility here is that we believe, and the biology would support, that ANG-2 inhibition, TIE2 activation is vasorestorative. You might be in a situation where as you extend the half-life, especially of the ANG-2 inhibition, and we have a pretty long-lasting ANG-2 inhibition, you get this virtuous cycle, so to speak, where you can lower the VEGF-A levels and start to heal the vasculature, and that may be underlying this amazing durability that we've been seeing in this trial. Next question, Tara. Great. Thanks for the questions, Andres. Our next question comes from Kumar Raja at Brookline. Please go ahead, Kumar. Thanks for taking my questions. You touched about the 9 mg dose a little bit in the prepared remarks. What kind of data do we have with that dose, and what are the expectation in terms of duration of response with that dose? In terms of the next steps, is the strategy to find a partner? What needs to be done if, before you can start the next trial? Thank you. Yeah, Kumar, there are a couple questions there. The 9 mg dose was not studied extensively in trials to date. We plan in our China phase IIb study to directly compare 9 mg- 6 mg in safety, efficacy, and durability. We'll pick our dose at that point. As you know, generally in the field, people like to dose as much as they can, recognizing that every increased mole, if you will lead to some enhanced durability. We will do the same. Cadmus, you wanna add on to that? No, I'm excited about the 9 mg dose. I think that, to your point, it may increase the durability. We have in the phase IIb study a very good plan to assess that dose against the 6 mg and then be able to pick the dose for the phase III program. I just wanna add on here a point, maybe it was made indirectly. The structure of this molecule, while it's novel in that it's tetravalent, it's novel in that the binders are, I think, sort of best in class, the inhibitory function of them, it's in all other respects a pretty traditional antibody onto which we've linked these two 18-mers at the Fc. We expect it can be made, we know that it can be manufactured easily, we expect that it can be given at very high concentrations, that's why we're gonna explore the 9 mg, which would be the highest concentration. To your second question about partnership, you know, we're open to all sorts of discussions. As everyone knows, we've kicked off a crossover round now that obviously crosses over to another round later, let us say with, you know, within 6-18 months, and we think between the crossover round now and that future round we'll have more than enough to do the global development of this molecule. We don't need a partnership, but we would always entertain one for the right partner. Next question, Tara. Yes. I believe we have another question from Andres at H.C. Wainwright. Please go ahead, Andres. Thanks again for sneaking me back onto the queue. Just curious if you could talk a little bit more about, you know, how heterogeneous was the patient population in terms of prior anti-VEGF exposure, and more importantly, you know, how does this durability or visual acuity outcomes differ in the treatment naive versus previously treated patients, and how should we be thinking about that in later line trials if that kind of signal further separates or kind of comes together there? Thank you very much. Yeah. All, good questions, Andres. The phase IIa from China was 2 - 1 randomization, so treatment naive to treatment experienced, that's about what we saw. Let me just understand. Your second question, other than the mix of 2 - 1? Correct. It's just trying to parse kind of some of the expectations in the real world versus clinical settings. Right. If you could give us some historical perspective on prior anti-VEGF exposure kind of differences in that efficacy signal from the clinical study, to the real world setting, kind of just setting expectations for the delta there. I think obviously if someone has received some VEGF inhibition and gotten some therapeutic benefit from that, then there's less of a gain one would expect going from some treatment to, let's say, best in class treatment. That's exactly what we think we saw. In the naive patients, we had 10 letters and greater improvement, whereas in the experienced patients we had. I don't wanna misquote the exact number, but it was six, seven letters. Something like that. Still impressive given that these patients have already received treatment. To the point of what we can expect going forward, it's pretty clear that the agency does not want treatment experienced patients in trials moving forward. They would much prefer treatment naive, and that's what we will do. The reason there is that they have very good understanding of what the non-inferiority margin should be for treatment naive patients. For treatment experienced, that they don't quite know how to interpret that. They've come down pretty clearly in recent interactions to say that they want treatment naive moving forward. You know, moving into the, beyond that, let's say post-approval, I think we would expect to be an agent that could be used in virtually any patient. We would expect many patients who have a suboptimal response to existing standard of care to be at least tried with new agents, whether it's ours or others. Great. Thank you very much. Great. Thank you for the questions, Andres. That concludes our Q&A session for today. I'll turn it back to you, Emmet, for some quick closing remarks. Well, I'd just like to thank everyone for sitting through our first presentation of this exciting phase IIa data. We are available. You can reach us if you have additional questions, and we'd be happy to chat. As I said, we're in the midst of a crossover financing and would welcome any or all of you to reach out directly. Thank you. Thank you. Thank you, Emmett. Thank you, everyone. Thank you, everybody.