Afternoon, everyone, and welcome to the Jefferies Global Healthcare Conference in New York. My name is Jonah Scherl with the Jefferies Investment Banking Healthcare team, and it's my pleasure to introduce Sean Fu, CEO and CMO, Phillip Dennis of NovaBridge Biosciences. Thank you. Thank you very much. Welcome to NovaBridge's presentation. My name is Sean Fu. I'm the CEO of the company. Pleasure to be here to introduce you the story of NovaBridge and our strong pipeline. This is the disclaimer forward-looking statement. We will be talking about projections into the future, and past performances does not necessarily indicate future directions. I'm going to walk you through the company highlights. NovaBridge is a biotech platform that we are organized to accelerate access to innovations globally, to patients globally. Right now we have an exciting pipeline that consists of best-in-class and first-in-class assets in oncology as well as ophthalmology. We have two, what we call the core assets or leading assets. The first one is givastomig or giva. This is a Claudin 18.2 x 4-1BB bispecific antibody that we are developing it as a bolt-on to the current frontline gastric cancer standard of care, which is nivo/ chemo. This particular asset showed strong efficacy, great safety in the phase I-A combination study with the current IO -chemo standard of care. We're excited to report that after consultation with FDA, this asset is phase III-ready. We have a clear regulatory pathway, and we have a clear guidance when it comes to the potential to achieve accelerated approval. We plan to bring this asset into clinical study, pivotal phase III clinical study as early as end of this year, 2026. The second asset we are actively developing is ophthalmology assets. It's also a bispecific biologic, and this particular molecule targets VEGF-A and Ang-2, and it is indicated for wet AMD. We just disclosed phase II-A data, very strong efficacy comparable to some of the best class leading molecules in this space. Solid safety profile, well tolerated. Very excitingly, if you look at the differentiating properties of this molecule versus some other molecules, for example, Vabysmo, it is in its durability. Compared to Vabysmo, the durability for patients on our study is 50% longer if you measure the time between doses where patient can benefit, continue to benefit from therapies without the need to be rescued. Right? This is very exciting molecules in the ophthalmology space. It's a $20 billion market size, and we have this potentially best-in-class differentiated molecule. We also enjoy a very strong financial position. We have $210.8 million on our balance sheet as of last reporting, which is end of the year, last year. We will be able to finance many of the clinical study readout milestones in the near future. Our business model starts with a strong systematic access to global innovations. In particular, I would point out that the company was formed, founded in China back in 2016, and since we had active operation in that part of the world and built out U.S. operation as well. By now, this company is largely a U.S.-based company listed on Nasdaq, but we have strong roots in China, which gave us a strategic advantage when it comes to licensing and sourcing, have visibility into the ecosystem of innovative biologics in China and in Asia at large. This is the Step number 1, gave us access to innovative assets in a capital efficient way. The second step in our business model is really to develop those assets in U.S. and reposition these Asian or China molecules as global products. You increase the value for those molecules as you develop those assets according to FDA regulatory requirement, tailored toward the market requirement in U.S., E.U., and in Japan, and position the molecule in a global market, therefore significantly increase the value of those molecules. The third step in our business model involves finding the right path forward to realize the value that we build now in those molecules. You can think about a license deal, you can think about the co-development, and in some cases, obviously, there is an opportunity for us to continue, especially in a subco structure, continue to develop those assets in a pivotal clinical study settings to capture the complete upside of those molecule if we have strong conviction of the data and have been able to build a strong team around those molecules. These are the three steps of our business model. Under that framework, we have built two verticals. One is oncology. As I mentioned earlier, our Claudin 18.2 x 4-1BB bispecific is the lead asset for the oncology vertical. We also have formed an ophthalmology vertical. We call it Visara. We own 65% of Visara, and VIS-101 is the leading asset within our ophthalmology vertical. This is our pipeline. Obviously, most of the value for any biotech companies will be driven by pipelines. We have exciting pipeline. Givastomig, I mentioned, is positioned in the frontline gastric cancer as a bolt-on to the standard of care. This molecule has potential to grow way beyond the frontline gastric cancer. You can think about indications where the tumor cells express Claudin 18.2, so it could be biliary tract cancer or pancreatic cancer. Those cancer, 60 or plus patients, they express Claudin 18.2. This molecule, when added to the current standard of care for those indications, there is a potential for patient to benefit. These are significant and important future growth areas. We have two more IO oncology assets, and we have VIS-101, our ophthalmology assets, in addition to wet AMD, also indicated for DME. Those huge markets, great growth potentials. I just wanted to give you an overview of our business model, our pipeline, and the near-term focuses. With that, I'm going to pass it over to our CMO, Phillip Dennis, to walk you through pipeline data. Phillip. Thanks, Sean. It's a pleasure to be here, and it's always exciting to talk about giva. I start with the unmet medical need, which is we are developing giva in frontline metastatic gastric cancer. Gastric cancer, as a medical oncologist, is a really underappreciated solid tumor. It's the fourth leading cause of cancer death. The five-year survival is less than 10%, and it's just a horrible disease. There have been a couple of advances, however, and they're shown in the middle of this slide, showing the results from CheckMate 649 that led to the approval of nivolumab, a checkpoint inhibitor in frontline metastatic gastric cancer with, I would argue, very meager improvements, a 10-point improvement in ORR, less than a month improvement in PFS, shown in the slide. The other study is SPOTLIGHT. This led to the approval of the first 18.2 asset to be approved in frontline gastric cancer. This is zolbetuximab. Zolbetuximab did not improve ORR. You can see the ORR there at 40%, even with the addition of what I'll call zoby to chemo, and the improvement in median PFS is less than two months. These two advances led to the approvals of these agents, but leave a lot to be desired. One key feature, we are an 18.2 asset, and zoby being the first asset to be approved in this indication, we do look across the bow and look for comparisons. The first and easiest comparison to make is zoby is very restricted. It's very restricted because its label is highly dependent on strong expression of Claudin 18.2, another 75% of cells expressing two -plus or greater intensity. This is very rigorous levels of expression. Ours is the broadest in the class, 1% of cells, one -plus or greater. If you quantify patients that between 75% and 100%, zoby's indication, and what we develop between 1% and 74%, we double the patients that are eligible for giva that ordinarily would be eligible for zoby. Another differentiating aspect of giva is, in fact, its design, and that's shown on this slide on the left. One can see that the IgG portion that interacts with Claudin 18.2 is highly avid. It's tenfold more avidly bound to Claudin 18.2 than zolbetuximab. This, I think, underlies the ability of giva to have efficacy, both in monotherapy and in combination to really have efficacy in low-expressing tumors. In the middle of the molecule, you'll see the Fc portion that's been mutated. Why does this matter? We want to engineer out ADCC and CDC, two processes that zolbetuximab relies on for efficacy, but the flip side of that is responsible for a high degree of nausea and vomiting. In their phase III studies, they're seeing almost 20% of patients with very severe nausea and vomiting, Grade 3 or greater. We do not observe that due to this mutant Fc portion. Finally, at the bottom, we have a unique way of activating T cells, not via CD3, so-called signal 1. This is via four scFv fragments that interact with 4-1BB, so-called signal 2 on T cells. If you take the components together, the 18.2 interaction and the 4-1BB activation, we get controlled local activation of T cells only in the tumor microenvironment, which is very exciting. To set up the data I'm about to show you, our phase I monotherapy data was very clear. We had efficacy in third-line gastric cancer patients and beyond. We had an ORR of about 20%. We had a PFS of about five months. Importantly, we were very well-tolerated. We didn't have a DLT or MTD, and in fact, this said, "Let's combine giva with frontline standard of care." This is the study that is currently ongoing, but some of you have seen the data. The data on dose escalation shown on the left was presented at ESMO GI less than a year ago in July of last year. In this study, we compared five, eight, and 12 mg /kg added to the usual dose and schedule of nivo/chemo. Importantly, again, our claudin inclusion is very low, the lowest possible. This is a PD-L1 all comers at six sites in the U.S., which is really remarkable, when we talked to the investigators, we knew they were enthused. If you do the cold analysis of looking at recruitment rates, the recruitment for most of this study was eightfold above historic controls into gastric cancer trials in the United States, telling you how enthused these six leading academic GI oncologists were and are about giva. On the right side, you see dose expansion cohorts. We wanted to really confirm and extend the data we saw in escalation. We recruited 21 patients, each at eight and 12 mg/kg. However, as the offset horizontally is indicated in this slide, the 12 mg/kg cohort was recruited after this eight. That affects the follow-up and subsequently the ability to interpret PFS, which I'll get to in a second. This is one of the most important slides in the presentation. This is looking at objective response rates shown by dose level, eight, 12, or both doses together, compared against the two phase IIIs that I mentioned, as well as a study from Astellas with zolbetuximab, the first presentation any of us have ever seen with zoby plus IO plus chemo. Remember, their current label is chemo alone. This was an important comparison, but look at the numbers here. The objective response rate at eight was 77%, at 12 it was 73%, and combined it was 75%. Compare that against the label for nivo in this indication with an ORR 47%, far exceeding that phase III study. If you look across at ILUSTRO, again, coming in at 62%, our ORR is superior. Moreover, look at the cutoff for PD-L1 above and below 1%. This is a label restriction for nivo in the U.S. and two other checkpoint inhibitors. You can see stellar data for ORR above and below that threshold. Moreover, if we look at different cutoffs for Claudin 18.2 in the rows below, you can see that in the Claudin -high, we're coming in at 76%, 67%, and 72%, comparing favorably again with ILUSTRO. Importantly, look at the 1% - 74%, almost an 80% ORR there. Really strong activity across all the thresholds for either PD-L1 or Claudin 18.2. Finally, the disease control rate is virtually 100%. Only one patient didn't have a reduction in volume of their target lesion. Really unprecedented efficacy data assessed here. This is a waterfall plot, again, showing how 51 of 52 patients had a reduction in tumor volume. This slide is color-coded by dose, and for each patient, we have the best response with corresponding PD-L1 and Claudin 18.2 expression. Well, not only do patients respond extraordinarily in terms of almost 80% of patients responding, they respond quickly. This is important. In our study, we re-scan patients at eight weeks, day 56. If you look at the table on the right, the median time to response was two months. The median time to response was at the time of the first restaging scan, and that is reflected in the spider plots, where you look at a cluster of vertically aligned dots there at the time of the first scan. You can see the slopes of all the lines are trending downwards. Important, if you follow those lines out over time, the responses deepen. The slope of the lines continues to go down. Finally, if you look at the X-axis, we have several patients now out over a year, and we have a couple of patients now out over two years. The responses occur in about 80% of patients. They're rapid, they deepen over time, and they are durable. Well, when we presented the data last year at ESMO GI, everyone said, "Do these responses translate into long-term responses?" The answer is a resounding yes. This is a first look at PFS data, showing the data again by cohort, by eight and 12 mg/kg individually, and then the cohorts together, compared again against the other studies to the right. I want to draw your attention first to the second line down, median follow-up. The median follow-up at 8 is about 11 months, and the median follow-up at 12 is seven months. This translates into 12 events at 8 mg/kg and five events at 12 mg/kg. One can only get discerning and meaningful PFS if you have events. In other words, if you took the inverse of that, which is the patients censored, we had 54% of patients censored at 8 mg/kg, but over 80% of patients censored at 12 mg/kg. Once we draw the Kaplan-Meier curves and we look at the median PFS, our median for 8 mg/kg is 16.9 months. At 12 mg/kg, it's 7.7 months, but with only five events, we know this is artificially low, and we know that this is coming up over time. Nonetheless, if you take each cohort, combine them, take the number of events, generate a new Kaplan-Meier curve, the median PFS again is 16.9 months. Look at the comparison with the very large phase III, 7.7 and 10.6 months. We are far exceeding this phase III data by combining a Claudin 18.2 asset with IO, with chemo. Finally, ILUSTRO, we're coming in two months better than zolbetuximab in combination with IO -chemo, even though that's just in the Claudin very high levels of expression. We're very encouraged by this meaningful PFS data. You can see further down below that the duration of response could only be calculated for the 8 mg/kg cohort, where in fact it was 15.2 months. With extraordinary efficacy in mind, let's pivot to safety. The safety can be summarized in a very simple way, which is the safety, even though we're adding giva to an existing immunochemotherapy standard of care, the profile of adverse events looks very similar to CheckMate 649, the IO -chemo standard of care alone. Perhaps what I always go to in this slide is the fourth row down, which is treatment-related adverse events due to any drug, Grade 3 or greater. We're coming in at 56%, and if you look at those other phase III, we compare quite favorably. Think about it. It's almost too good to be true, where we're actually getting improved efficacy without a significant increase in toxicity. This is really, I think, an extraordinary combinatorial approach to gastric cancer. To give a fair shake to actually individual adverse events, this slide summarizes this. The most common giva treatment-related adverse events were nausea, vomiting, fatigue. However, almost all of these were single-digit Grade 3 incidents. The most common any drug-related TRAEs were fatigue, nausea, and neutropenia. Again, the Grade 3 incidence was low at each dose level, with the exception of neutropenia. This happened early on in this phase I study, and we think it's related partially to inconsistent use of G-CSF, which can keep the neutrophil count from dropping so low. Despite the fact we had these Grade 3 events and a couple of Grade 4 events, there was no febrile neutropenia, no sepsis, and there were no deaths due to any treatment in this study. Finally, if we look at immune-related adverse events, the profile looks very similar to CheckMate 649. There was no exacerbation of any other irAE. However, we did observe immune-related gastritis. We now view immune-related gastritis as a pharmacodynamic marker for the combination of giva plus nivo that leads to profound T cell activation in the tumor microenvironment in the stomach. Gastritis was observed in 33% of patients. However, the Grade 3 incidence was low, less than 12%, and in fact, there were no Grade 4 events. The gastritis was clinically manageable. What we did, and what the investigators did, was withheld giva and nivo. They either instituted or maximized the dose of traditional medicines that would address nausea, vomiting, and abdominal pain. Importantly, the onset of gastritis was two to three months after a response. I showed you that the median time to a response was two months. The median time to onset of gastritis was four to five months. These patients have already had a response in their stomach, a response to this drug combination. After that, when the tumor is gone, when the tumor is regressed, that's when the normal tissue becomes involved there. Importantly, if we withdraw and we use appropriate medications, the gastritis typically resolves. We can restart giva in a large number of patients. Because we withheld giva and nivo, sometimes for a few months, what we found is that if we compare outcomes based on those who had gastritis versus those who did not, to our pleasant surprise, we found that patients with gastritis actually had improved outcomes, improved ORR, PFS, and OS. It's a very exciting development. Again, in the interest of time, I'll go through this quickly, where again, we have profound efficacy across a range of claudin and PD-L1 expression, really nice early PFS data. As Sean mentioned, we're actually recruiting patients into cohorts in our phase I study, where in fact, we're looking into BTC and pancreatic cancer, where the prevalence of 18.2 is about as high as 70%. We're very excited about these frontline cohorts and those tumor types, and we will be presenting this data at a major meeting later this year. There's tremendous market opportunity for giva in gastric cancer. It's approximately a $3 billion peak year sales, and this is due to the fact that zolbetuximab currently occupies a very small share of the frontline market that's shown to scale, that gray rectangle, so you can see where giva's potentially first in class or best in class. To the right, you can see the peak year sales rise to approximately $5 billion if we include BTC and pancreatic cancer. Finally, I'll just end with, again, a really resounding sense of satisfaction that the FDA has given us clear guidance about a phase III study. We are in the process of gearing up to execute that phase III study. We have a meeting planned with them this summer to choose between eight and 12 mg/kg, and we have addressed issues such as CMC and the companion diagnostic. We're really well-poised to execute on this. In the last couple of minutes, I'll talk a little bit about Visara and the VIS-101. I'll simply say Sean covered some of the structure on the left shown on this slide. Importantly, we have seasoned expert ophthalmologists with significant industry experience in key leadership positions in Visara. It's a well-read company. In terms of our phase II-A data in wet AMD, we showed this data recently became available. It's safe and well-tolerated. There's a rapid improvement in vision and improvement in the edema as measured by CST. It's robust, it's meaningful. As Sean said, one of the differentiating features of VIS-101 is the durability that's seen over Vabysmo. Again, you can see the mean BCVA is actually more than 10 letters improvement. The mean CST is a reduction in the edema by about up to 150 microns. Again, tremendous durability. This slide simply shows some of the durability issues. The line graphs on the left are two different doses, 3 mg and 6 mg of VIS-101. In the interest of time, I'll focus your attention on the line graph on the right, where you can see that if we compare Vabysmo or faricimab at 24 weeks, you can see that there's a 45% treatment-free population, but we're up to 64%. If you look at nine months, we have 45% of patients that are treatment free. Meaningful treatment-free periods for patients who have to undergo injections in the eye. Again, I'll just focus here on the next steps, the phase II-B study. We expect to initiate later this year, and we have plans for a phase III study to start in early 2027. All right. Thank you, Phillip. Quickly to touch upon our finances, as I mentioned earlier, we've got a $210.8 million on our balance sheet. We don't have complications on the balance sheet, and this amount of cash is sufficient to support us through 2028 in terms of clinical milestone readouts, which we have plenty. Just to walk you through some of the highlights for giva, the bispecific, we spend some time walk you through the data. We shared back in January top line data from the expansion data. We expected another readout of the expansion data at the more advanced data cut second half of this year. We expected to bring this asset into phase III pivotal clinical development as early as end of this year. We have an ongoing phase II study which is recruiting, and this will position us well in terms of quickly launching phase III by starting clinical activities in some of the countries and regions that we plan to utilize for phase III studies. We also have two additional indications that's currently active recruiting BTC and PDAC we mentioned, and I'm happy to report those clinical studies are well underway. We have two additional IO oncology assets. We have a PD-L1 4-1BB ragistomig. This molecule, although we are not spending too much time talking about, but it is well-positioned to be used for patients who suffer from solid tumors that are resistant to prior line of a PD-1, PD-L1 therapies. This asset is expected to read out top line data second half of this year. We have a CD73 monoclonal antibody that's in clinical development in combination with IO or IO and a chemo positioned as an add-on in the frontline non-small cell lung cancer. We expect it to read out second half of this year by our collaborator, TJ Bio. VIS-101, we completed phase II-A study, expected to enter phase II-B second half of this year and expected the phase II-B to read out first half of next year, which will position this molecule ready for phase III studies. I will leave these slides on to talk about our business model while open the floor, maybe for any questions you might have. If no more questions, we're available for additional conversations and discussions always. Thank you very much for your attention. Thank you.