Okay, good morning, everyone. I'm Brian Abrahams, one of the senior biotech analysts here at RBC Capital Markets. We're really pleased to have our next presenting company, Corbus Pharmaceuticals, represented by their CEO, Yuval Cohen. Yuval, great to see you. Good morning, Brian. Thanks for having me. Maybe to kick, let's kick things off on your ADC CRB-701. You recently presented some data, not too long ago, from the first Western data set that we've seen for the drug. Can you tell us a little bit more about those data? I'm really interested to hear your perspectives now that you've seen sort of the first kind of cut of the data, the Western data, what you see as the most differentiating features versus marketed Nectin-4 ADC, Padcev, as well as some of the other Nectin-4 ADCs that are in development. At a sort of a very high-level summary, what the data that's emerging in the West, these were U.S. and U.K. sites, is very similar to what we saw in China. That is reassuring. Overall, the safety looks very comparable. The efficacy in bladder and cervical, although we had at the time fewer patients, looks comparable. The sort of surprise that we had were two things. One, which is less of a surprise, is in the West, we are mandated to use ocular prophylaxis. Unsurprisingly, that led to markedly fewer ocular events versus China, which did not at the time use prophylaxis. That was reassuring. That is a differentiation between the data sets. The bigger differentiation is we had a tumor type that had at the time not been explored in China yet, and that is head and neck. A reminder that PADCEV had data as monotherapy in head and neck at ESMO, no, ASCO 2023. I think the ORR was in the low 20s. We had a small number of patients, seven patients. It doesn't look too bad at all. We were delighted with that. The overall feedback was, I think, from Buyside and others, it's encouraging, but we just want to see more patients. I think that's a really fair feedback. We just want to make sure that we just didn't get very, very lucky on a handful of patients. That will be the next data release with a markedly higher number of patients. In terms of differentiation to PADCEV, what we're seeing is very, very much in line with what our partners in China had already seen. There is a marked, marked decrease in skin and peripheral neuropathy adverse events. As a result of that, there is a very meaningful reduction in grade 3 adverse events related to the drug. Last but not least, a very, very meaningful reduction in discontinuation, dropouts, et cetera. It seems to be, at the moment, an ADC that has a markedly safer profile than PADCEV, but at the same time can deliver a clinical efficacy. Certainly in bladder, it seems to be in line with PADCEV. The last thing I'll say as an intro is a reminder that our approach for this ADC is, as a standalone company, not to try and go after bladder cancer as a label. We are not trying to unseat PADCEV ourselves. That is a very ambitious thing for a company like ours to do. Instead, what we're doing is we're taking this asset into what we look at as empty swim lanes, tumor types where PADCEV is not used and, in fact, not even explored often. The same applies to many of our competitors. One last thing, sorry, that was interesting was China enriched for Nectin-4 a priori based on historical biopsies, but nevertheless, there was an enrichment for Nectin-4 in these patients. We did not. Unsurprisingly, and I say unsurprisingly because PADCEV does not enrich either, it really does not matter. Yes, the more Nectin you have, the better, but it actually does not matter. As long as they have some Nectin, the responses are really very, very satisfactory. Great. What should we be expecting from the next data cut here in terms of numbers of patients and the types of indications that you might be starting to steer patients towards? I know there's a balance of trying to maybe get more and more patients with bladder cancer just because you have a clear benchmark there. At the same time, if you're starting to see some of these signals in head and neck and cervical, where do you want to kind of take this and when will we see more mature data? We're in the midst of Project Optimus, initially as monotherapy, then in combination with a checkpoint inhibitor. There are three tumor types that you should expect to see later this year at a very large oncology conference that we're aiming for. They are the three tumor types that we added at ASCO GU early this year. They are bladder. Bladder is there, as you said, Brian, as a benchmark. It's a positive control because bladder is where we can benchmark at arm's length with PADCEV. Probably of a higher priority for us is head and neck and cervical. We had a handful of patients in each at ASCO GU. Expect a very, very, very significant increase in patient numbers for the second half of this year at that big conference. It won't be an incremental increase. It will be a marked increase in patient numbers. We are delighted with our enrollment. That's great. Really, really delighted. I'd love to talk more about the head and neck indication. If you can provide maybe a little bit more context on the initial responses that you're seeing, anything you're continuing to see there. Are you expecting to or seeing responses in both HPV positive and negative patients? Would you stratify or differentiate your program based on one or the other or really kind of go broad? Let's look at the ASCO GU data set because that's out there. What we saw was it was HPV agnostic. In fact, our first and the deepest responder for that data set was HPV negative. It's also PD-1 agnostic. We're stratifying for both. In other words, we will know the status for both of those so we can look at it in the analysis. Our hope is that it continues to not matter. I think that's a sensible outcome. The other thing to think of for head and neck is we need to start steering our audiences away from PADCEV when we talk about head and neck. PADCEV is not being pursued in head and neck. Pfizer, rightly or wrongly, and I think probably rightly, are focusing overwhelmingly on bladder. It's very sensible. It is a very lucrative market for them. In head and neck, it's really not about us versus Padcev. In fact, at the moment, it's not about us versus any other Nectin-4 asset. What it focuses on instead is what are the other modalities that are being explored for head and neck. The two that I think are going to be top of mind will be Merus and Vikera. Very, very, very different modalities, both ahead of us, both vying for primarily first-line therapy. For Merus, we have a really good understanding of what their monotherapy data looked like. For Vikera, a little bit less. That also sets a helpful benchmark for us. Merus' first-line therapy, off the top of my head, I think was 35% ORR or 36%, something like that. That helps us understand sort of what does good look like. The other question is, where do we go? Do we join them in the fight or the race for first line, or do we try and go after an emptier lane in a later line? Honestly, it will all be data-driven. It's that simple. We'll let the data dictate what those decisions look like. I think the last thing about that is it's all about combination with a checkpoint inhibitor. It's highly unlikely this will be a monotherapy unless it's a later line. We're very, very keen to see the data mature with combination with a checkpoint inhibitor and then showcasing that data. Okay. I want to dig into that a little bit more on the checkpoint combination. When you think about combining 701 with checkpoint, are there specific immune-related biomarkers that you're looking at or prioritizing or baseline characteristics that you're kind of aiming for as you select patients? How do you sort of view this in terms of long-term commercial strategy, having data and maybe pursuing a path for combination? Initially, certainly for Project Optimus, what you have to do, because it is obviously the patients you're seeing had prior lines of therapy, is you cannot mandate that they've never had Keytruda, for example. That will be unethical and problematic. Ultimately, what you really want to see are patients who are, for example, Keytruda naive and to see what that combination looks like. That's where that big fight is happening or emerging with Merus and then Vikera. That will be really interesting to see. In terms of the commercialization, it all depends on data. Data will dictate, do we join the race for first line, their advantages and disadvantages? Remember, the biggest advantage is we have a completely different mechanism of action. And/or do we go after a swim lane that is later line? One of the interesting things to think about is, and this is no criticism, is what happened to Bicycle. In retrospect, perhaps prematurely, on a first-line approach in combination with Keytruda for first-line therapy in bladder, ahead of the PADCEV plus Keytruda data maturing. They certainly maneuvered themselves beautifully from a regulatory perspective. I wonder if in retrospect, what they found themselves with is a comparator now that is just spectacularly effective. It will depend on what our data looks like. Honestly, what's happening with these peers of ours, we do not want to replicate what happened with, as an example, Bicycle. Okay. Got Got it. When might we see additional—I know the study in China is much further along. I was sort of hoping we might see some initial data this first half of this year. What's the latest in terms of when we might see the next cut? I know you're well along now on the U.K.-U.S. study, but what will you be looking for out of the updated results from your partner in China to further guide your development path? China is way ahead of us. Certainly in bladder and cervical, they started in June of last year. From the outside, right, I can't tell you what it looks like from the inside. From the outside, I think there's some interesting patterns you see with not only CSPC, but Chinese companies in general. CSPC, for example, have two late breakers at ASCO this year. The pattern that emerges with Chinese, especially big Chinese pharma, is they very much prefer big mature data sets that get them late breaker oral presentations. They just love it. I think it makes sense. They're very, very big companies. They need big data sets to move the needle, very different than us, right? I think it is a question of at what stage do they conclude that they've reached a critical mass. Because they recruit so much faster than in the West, they can afford to do that because they do not have to wait for years and years and years to get to that critical mass. Stay tuned. It will certainly be at a very large oncology conference. Again, that is another pattern we see with Chinese pharma. Do you think we'll see your data or their data first? I know when our data is coming out, so we have control over that. What I will say is, going back again to the feedback we got around, show us more patients, I suspect, or I'm hypothesizing that the number of patients we will have will be sufficient to dispel concerns around, did we just get lucky with a handful of patients? Just last one on 701. It sounds like head and neck is becoming a higher priority indication. Is that kind of the right read? Are there any other indications that are kind of? Cervical. I really like the way that's developing. Head and neck, 80,000 patients or 75,000 patients in the U.S., half of them become metastatic. This is a very big, as big as bladder type of indication. It also means, though, that while the FDA can grant you some shortcuts and Merus, of course, got breakthrough, still, even with a breakthrough, it is definitely not a single-arm study if the FDA even does that anymore for those types of indications, et cetera. Cervical, what we like about it is it's the polar opposite. It's about 15,000 women a year in the U.S., similar number in Europe. About a third of those become metastatic. There's very, very, very little. Tivdak is second-line monotherapy, which is not a particularly attractive option. There, not only is it a rare tumor type, but remember, it affects primarily women of childbearing age. It's really horrific. There you can see some advantages in terms of speed to label that will be a little bit more difficult to do with a large indication like head and neck. Smaller, but potentially a faster regulatory path. Correct. Okay. Maybe we could shift gears to 913. I think following some of the recent data from Novo and for their CB1 inverse agonist, a lot of people have kind of written off the space. Obesity is obviously getting more crowded. There is a lot of potential differentiating features for your drug, 913. Can you talk about how you guys are designing your phase 1B studies to adequately address any potential risk of neuropsych adverse events early on? What is sort of the bar that you would be looking for in this study to say for sure whether all of the features we know about preclinically and on the drug's profile are actually playing out as having a safer, better tolerability profile clinically? I love how, and you're not the only one following the data from Novo. I have no idea what the data from Novo is. They wrote the most cryptic press release, bless them. Nevertheless, what Novo did as a favor to us, I think, is they created a moat. I'm pretty sure no one in China is working on a CB1 inverse agonist. The moat is very, very unattractive to outsiders. The advantage is we're on the inside of the moat. That is an advantage if it works out. A reminder that the differentiation here is, while monlunabant, the Novo drug, is about half the amount in the brain in rodents, right? We can't do this in people, of rimonabant, of a first-generation CB1 inverse agonist, we are 15 times less in the brain than monlunabant. We are super duper peripherally restricted. I think the way we interpret that very confusing press release from Novo was, the good news is for 120 days, no signals of depression or suicidality. Remember, those tend to happen at the beginning. If they're going to happen, they're going to happen at the beginning. There's some sort of a squeaky wheel there, right? They allude to it very nebulously, but there's some sort of a squeaky wheel. Our hypothesis is simple, that if you now excluded 15 times more than the brain, the squeaky wheel will not be there. It's all about safety for this one. No one, I think, doubts that it's going to work. It is such a clinically validated mechanism. The SAD and the MAD could not be more boring and vanilla on purpose. SAD is they're both in healthy volunteers. SAD is literally a single dose. MAD is seven days or longer, depending on the clearance of the drug. It is in a phase one unit in the U.S. All of our studies are going to use sites in the U.S. I have a slight obsession about that. One of the challenges I think monlunabant may have had was using Canadian academic sites. I think in retrospect, that served them less than optimally. I'm not interested in sites in Australia or other places. I want U.S. sites with U.S. patients that are really indicative of the population that will be treated. All patients are screened. That's normal for all obesity studies. All patients will undergo or are undergoing, actually. They're not patients. They're subjects. I apologize. All subjects undergo CSSRS, PHQ-9, et cetera. Those are the standard neuropsych evaluation that all obesity studies have to implement. I think that what I would be very, very happy with is just no difference, no difference in the placebo. I think that's absolutely achievable. The question is, right, let's say the MAD is seven days or 14 days. Is that enough? Obviously, the next study after that will be a 90-day study in obese patients. What I will say is, again, I wouldn't dismiss the fact that if it's clean during the MAD, especially since the doses are very high, that's a really reassuring sign. We have Kaplan-Meier curves for these neuropsychs from other drugs. They tend to happen very, very early on and then disappear. We should have that data, Brian, in the second half, progressing very nicely. That is the only data set we have that we will not be presenting at a clinical conference because it's a SAD and MAD. What we'll do then is, because of the interest from sell side and buy side, we'll press release it. Maybe we'll do a call about it and discuss it. It is really about was it clean? Will you have any overweight subjects? By definition, SAD, MAD. This is classic. Nothing's wrong with these people. So there'll be no efficacy. If there's efficacy, there's something wrong with the drug. How's the conduct been so far? How are you feeling about the study? I feel extremely good. Not surprising, but I feel very good. One of the questions that's always been out there is peripheral versus central, right? And whether or not having a central component is essential for the weight loss activity of CB1. I know you guys have done a lot of work showing the importance of peripheral, but can you maybe kind of walk through that and your latest thinking on that? Yeah. It boils down to can you make fat mice thin? Dial is wonderfully translatable to humans. Despite the fact, for example, that we are one-fiftieth of the brain-to-plasma ratio of rimonabant, they are equipotent in a dial mouse. Remember, we are not zero in the brain. I'm not sure I want a drug that is zero in the brain when it comes to CB1 inverse agonist. Our hypothesis is that you can markedly, dramatically afford to withdraw from the brain and still elicit the same response by still tickling the brain sufficiently and also markedly, markedly affecting the periphery. We do think you need some engagement in the brain. Okay. Maybe just in the last two minutes, we can move to 601. Can you talk a little bit about maybe how this alpha V beta 8 monoclonal antibody is differentiated from others in development, some of the preclinical data you've seen so far, and when we might see those phase one data? Because now this is starting to move along and people are going to start to pay more attention to this, I think. Second half of this year, we're aiming for a large medical oncology conference. Remember, this is an IO story. So there's a bunch of them that it makes sense to go to. It is not differentiated from the Pfizer one, very little. I mean, there's some preclinical stuff, but honestly, it's the same thing. In a sense that it targets alpha V beta 8, preventing it from activating latent TGF-beta. And then remember, us and Pfizer have our step siblings, which are Roche and AbbVie and Scholar Rock, for that matter, who target the latent TGF-beta directly. The idea there is to prevent it from being woken up by the integrin. AbbVie will have data at ASCO. It looks really interesting. One thing to think about is our study has a monotherapy cohort followed by a combination with a checkpoint. We really want to see something happening in monotherapy. If nothing happens in monotherapy, we're not fans. I think that probably will echo how buy side will think about it as well. Stay tuned. Excellent. All three assets, all readouts, second half of this year. Not going to be boring. It'll be very exciting next several months. Excited. Yuval, thanks so much. Thanks everyone for joining us. Thank you, Brian. Thanks, audience.