All right, I think we're ready to get started. Welcome, everyone. I'm Josh Schimmer from the Cantor Biotech Equity Research Team. Very pleased to introduce from Invivyd, Marc Elia, Chairman of the Board. Marc, give us a very quick snapshot of where Invivyd is in prosecuting its portfolio of COVID monoclonal antibodies. Sure, and thanks for having us. So Invivyd is a commercial stage company right now. We have an authorized medicine called PEMGARDA, which is authorized under emergency use authorization for the prevention of COVID-19 in certain immunocompromised persons. That's, I think, to us, an impressive technological accomplishment that is enabled by our unique technology. We can talk more about that. But critically, it's also just a starting point. We have in the pipeline what we think of as a pre-pivotal space of molecule VYD2311, which is the product of directed evolution of pemivibart. Our strategy is to minimally evolve antibodies as required to improve their biophysical properties relative to engaging SARS-CoV-2, COVID-19 as a target. And we are looking very much forward to letting 2311 express more of the medical benefit that we see flowing out of the technology. Meaning, it is well established through multiple studies, including studies outside of Invivyd, that a good monoclonal antibody can very meaningfully disrupt pathogenesis of COVID-19, which is just the fun and fancy way of saying you will have a hard time getting sick on a good monoclonal. That's a bit of a distinction from the current COVID-19 vaccinations. The ability we have to scale that technology and build medical value for the most people possible is really about our joint work with FDA and, of course, our own innovative engine, and gratifyingly, we've had some change on that front that we're very excited about. We are looking forward to the coming year of elaborating VYD2311 as essentially a vaccine alternative that we believe would be more effective, safer, and scalable for the benefit of Americans in need, whether those are high-risk adults, whether those are pediatric. Our feedback and dialogue with the FDA, I think, has been very constructive about articulating a rapid near-term path to getting there. And so our minds are in two places relative to the question you asked. We want to build our base business, but we very much want to look forward to the next year in which we move the field of medicine from a reliance purely on vaccination to prevent COVID to a field that could be maybe even dominated someday by monoclonal antibody. That is the goal, and that's our quick snapshot. Maybe talk to us a little bit about what some of the headwinds PEMGARDA has faced in kind of reaching the target demographic and how your next-generation VYD2311 is going to kind of power through those headwinds. Sure. So PEMGARDA has one of the more unusual regulatory and operational histories of any medicine I've ever been around, which is to say, back in the year 2022, actually, the FDA and EMA had certain meetings in which they decided what should the role of a monoclonal be in COVID. And they conjured this solution that, of course, in their minds, it should be to prevent COVID-19 purely among the moderately to severely immunocompromised, that that work should be done under EUA. And that as a consequence of all of that, they would essentially build the profile to their liking: a target dose, a target effect size. And we sort of thought, well, I don't know that we see the world the same way, but there's an interesting dynamic. In a regulated industry, you salute and say, well, thank you for your kind thoughts. We'll go ahead and do that. The consequence of that is that PEMGARDA is a quarterly high-dose infusion at a relatively high cost sold to the medically complex. Well, all of which sounds nothing like a blockbuster drug to me, right? That is a specialty medicine that is, I think, very well appreciated by its users and some of the sort of online fan bases you'll find for it, because I think the data around PEMGARDA are relatively stunning. It will give you about, depending on the time cut in our pivotal study, an 85%-94% reduction in your ability to get sick at all. So while it is not a light switch, as I was just saying earlier, if it were a dimmer, you're awfully close to the top of the dimmer on it. You will struggle to get sick on this medicine. But a quarterly infusion for the well is something that I understand is done mainly among hangover sufferers in very wealthy Southern California cities and so on and so forth. It's not a common big medicine approach. And so I think we have struggled to actually cut through from Invivyd to the user base that is in clear need, really through HCPs and infusion centers who just present the logistical burden of actioning all of this, right? It is, in my mind, an excellent medicine. It's a great idea. I personally wish I were on it today just because I would rather that than masking. But I think what we need to do is to use our technology to get to a place that is the thing most humans want: easy. PEMGARDA is a wonderful medicine, but it is not easy. VYD2311 is designed to be a low-dose IM, high efficacy, high safety, high durability, attractive medicine that one might find functionally indistinguishable from a vaccine. You go into the Walgreens and ouch, and you walk out. That's a big turn, a big turn when you are considering prophylaxis, right? I mean, I think Americans are only, I don't know, I mean, if we had a race between eating your vegetables and taking your GLP-1 after the fact, I think we know who's winning that race, so getting people to action, self-care is hard enough. If you make it difficult, you're more or less sunk out of the gates, and I think we are very much looking forward to moving towards very easy and into the classical big medicine elements of ACIP, CDC, those sorts of bodies. So you just came out fairly recently with a really important regulatory and development update for 2311. It almost dovetails with kind of a pullback of the COVID vaccine. So I don't know if there's some correlation there that some of the policymakers said, well, you know what, we might have some unmet need that we're creating by pulling some of the indications on the COVID vaccine and then looking to enable 2311 to kind of fill that gap. So maybe talk a little bit about the update, what it means, and am I reading a little too much into this timing for it? I think you might be reading too little in some ways, right, so I think we are all in the midst of a giant sociopolitical yelling past one another festival, and I think in large part that is because we've only really been in possession of sort of problematic tools, right? The COVID-19 vaccines, whatever you think of them, they have some real weaknesses and then they have some perceived weaknesses, and at a certain point, distinguishing between the two becomes a personal political statement more than anything else, but the science that has been well on display is suggestive, if not demonstrative, of the fact that there are biophysical limits to eliciting antibody responses and immune pressures from vaccination. That's the whole point. We deliver a high potency, highly safe antibody because we can fill the gap between that immune pressure you essentially need to stay alive, which is kind of lower down, and I think we're mostly there, and the immune suites you need to stay well, which is where we're not yet, and so when I look at the broader medical political landscape, I think the only thing that has happened is that an election and a restaffing of some of these central authorities has allowed for a little bit more of a constructive, open-minded attitude towards alternatives. I mean, I don't know how many of you follow our president on Twitter or Truth Social, but it was just Labor Day when I read he's irritated, and I think justifiably irritated about this dichotomy he perceives between people who tell him Warp Speed was amazing and people who tell him the vaccines don't work. Well, if you follow Invivyd's brand new account about 15 minutes later on Truth Social, you would find us saying, hey, guess what? You're kind of both right. OK, when we're immunologically naked and none of us have seen a virus before, getting a vaccine against it is frankly lifesaving. I mean, I believe it saved my own life. But as we become seropositive as a population, as a virus becomes evasive, it is also quite reasonable that, you know, gosh, there's not a lot of more water to draw out of that stone immunologically and medically. So do I think it is all coordinated? Maybe, but I think more what is happening is that multiple aligned minds can start to perceive that maybe there are options, maybe there are alternatives that perhaps the last administration was less open toward. OK. Tell us about now the regulatory path for 2311? Sure. So So everything Invivyd has done regulatorily has been brand new, meaning we were the first to have, and I think will be the only immuno-bridged COVID-19 antibody. That was in effect the product of us saying to the FDA, this is an asset. You can action this asset. You can do it rapidly. We had our idea. They had theirs. They were not so different, but we went with theirs because, you know, they're in charge. And that was great, but it was a brand new thing. And if you read our product fact sheet, you will read a whole lot of molecular virology and arithmetic. And if you can understand it, congratulations. You're among the 0.0001%. Well, we then came around again with another asset, VYD2311, and we had no real interest in repeating PEMGARDA, too, a high-volume quarterly specialty medicine. We wanted to do this correctly. And interestingly, the response this time was much more open and constructive, meaning the FDA, I think, acknowledged the totality of our prior work. This is our third almost identical antibody that we intend to trial. And they cited to, hey, we'd like you to go out and generate some clinical events. I think that is highly concordant with today's understanding of generating gold standard RCT level evidence in support of a COVID intervention. But on the flip side, they also said, hey, by the way, guys, your own CANOPY study would seem to suffice for a full BLA, not an EUA, a BLA, not for immunocompromised persons, but for Americans 12 and up, which is an awfully big group of Americans if you're keeping score at home and radically different. Hey, at your three-month CANOPY data set cut, you had nine COVID events with a 94% reduction in overall risk and a confidence interval of 0.5- 0.99, which in statistical terms is, let's call it wide. But it also reflects a confirmation of clinical benefit. What they cited to and what we will then now work out with them is, OK, what study substantiates clinical benefit and safety in your minds and opens up these populations? But their feedback to us very directly was, this may not be such a big deal. You've already sort of done it. And we thought, well, that's true and we're thrilled that you see it. Let's go. So the work in front of Invivyd now is to design that study, action it collaboratively with the agency, and then go execute it lickety split, which is effectively what we did roughly this time a year and a half ago with PEMGARDA. It's really interesting because as you get through this clinical trial program, you're going to have a product profile that is going to go head to head with vaccines. In many ways that might not necessarily be intuitive on first think, you have tremendous advantages over the vaccines. Maybe kind of like frame what you think your product profile is likely to be relative to what a COVID vaccine is going to be. Sure. So So the advantage gets expressed really at the molecular level for the people that like this stuff out there in terms of our engagement with target, meaning if we make a good antibody and we put it on target, that is a major step change between the immune power any of us are capable of generating as humans in response to a vaccine versus what we can give you from a laboratory, right? So what would the clinical profile of such a thing be? Well, we would look at PEMGARDA. And that would generate an extremely high rate of protection from getting sick at all, call it 70%, 80%, 90%, somewhere in that range, which is, I think, a major, major turn above what a vaccine could ever hope to demonstrate in a modern context. We would, of course, believe that as an IM antibody, you would experience, yeah, the ouch of an administration IM, but no inflammatory reactogenicity, which is, of course, the requirement of generating response to a vaccine. So we would see a major efficacy advantage. We would believe we would see a major safety and tolerability advantage. We believe also that because 2311 has a very long in vivo half-life, we would see a durability advantage. So I don't know the best way to put it, but we would think your experience with a mAb should be the same as your experience with a vaccine. You go somewhere, it hurts a little, you walk away. The difference being a mAb should work better, work longer, and be safer. That's a good running start in a head-to-head comparison. I like our odds, so to speak, because this will be our third time through the clinic with a highly, highly similar mAb. You've alluded to the idea of going head to head in a clinical trial versus a vaccine. Is that part of the planning that you're working through now, or do you expect that would be more of a supplement study? I think, right, I think there's a couple of ways we can handle that. I would say we would imagine a sub-study that is relatively compact because reactogenicity following vaccination is pretty apparent, right? It's a pretty high percentage of vaccine subjects that experience fever, chills, rigor, et cetera. I don't think we need to do a hugely powered head-to-head demonstration to make the point. I do think it's a pretty important point to make. OK, those statements actually, even though they're only a few weeks old, were written before we saw just recently the homework assignment with a due date that the FDA have given to the vaccine manufacturers to deliver an interim efficacy readout by, I think it's May of 2026, and then a longer-term efficacy readout. Forgive me, I've forgotten the longer date. It might be November. But when we think about head-to-head work, I guess where I'm driving at is if we see a VE out of COVID-19 vaccination that sits somewhere around where we might anticipate, which, for example, is estimated by the CDC regularly, and you can go find it in the ACIP documents and so on and so forth, we might actually, in service of changing the practice of medicine, be very tempted to consider a straight head-to-head. Now, blinding such a thing would be a little challenging because it's going to be pretty easy to know if you've been given a COVID-19 vaccination. But the point is we are looking to make the maximum possible medical value we can. And in this very odd circumstance, right, meaning today again is somebody's last or worst day on earth. Again, because of this virus, it may be less than it was. It is still far too many. What I think we are conscious of is that this medical domain has been a minefield of mis- and disinformation and lack of clarity and lack of certainty. And so I think to the extent that we can actually use our research and our development engine to drive to clarity and drive to profile, we'd like to do that because last year in America, 35 million-40 million Americans got a COVID-19 booster that didn't work all that well. I don't think next year Invivyd is going to sell 35 million doses of antibody. But I think we'd like to set the stage whereby such a concept is not unthinkable, that there are millions of Americans who would benefit from highly robust protection. And I think part of sort of winning big prizes is being brave enough to aim at them in the biggest way. And so, yeah, I think we are looking forward to using our tools to demonstrate clearly the medical value we see is available from a technology that can help you just not get sick. If you hit that target profile you're aiming for, you may not even need a head-to-head study because the difference will be so obvious just from your own data across. I would have no doubt that we could aim at something that would be obvious to me and obvious to you. And I would suggest that you and I are poor surrogates for the behavioral whimsy of modern American infectious disease. But I would look forward to us going, well, that's pretty clear, isn't it? And then something will go horribly awry because a tweet will emerge from an influencer that, you know, whatever. I won't even speculate. But you've seen the chaos intellectually in this field. What goes horribly non-awry or what goes incredibly right for you now, we can introduce this new ACIP composition, right? Because if you can bring that profile to ACIP, how do you think about them doing a lot of the work for you? I think what we have to do is begin now with further reinforcement and education of a group that I believe is slated to expand. I think I read that the other day. They're going to add some more members to ACIP. This is a group that unanimously voted in favor of nirsevimab, Beyfortus, which is a Sanofi product that protects neonates from RSV. I think there were some very clear and strong statements made about the merits of monoclonal antibodies. I think when we use mAbs, and again, all of us are used to pharmaceutical mAbs against self-targets, which is sort of the common biotech approach, these are microbial targets, right? Our antibodies, nirsevimab, they hit viruses. I think what we have to remind ACIP of is that if you are worried about such a thing, you need to drop everything, get to the hospital, and undergo emergency apheresis because you are chock full of monoclonal antibodies against viral pathogens right now, all of us, so what are we really doing? We're supplementing a native, natural immune capability in a targeted, directed way that helps a human being navigate the gap they would otherwise have, so I think I appreciate the question because a lot of people, I think, are going to spend a lot of time wondering about our clinical design and the statistical powering and all these things, and they're great questions and important, but our minds are already well on the other side of that, trying to make sure that we drive practice-changing results. So whatever the study is, we would also like the broader medical context to immediately appreciate, well, if we had such a tool in the arsenal, it would be very reasonable, if not logical, if not obvious, to devote more protective capacity to, again, either children or the elderly or high risk. Those are decisions that will have to get made down the road. But yeah, we are going to be focused on continuing to try to build a perception of our work that any political or medical perspective can appreciate. So, I guess Beyfortus went through ACIP, and I think we kind of think of ACIP more vaccine-oriented, but they will flex into some protective antibodies. Maybe help us appreciate the relevance of the decision around Beyfortus. And if you do walk away with a similar positive ACIP recommendation, how does that simplify your commercialization strategy? Sure. So Beyfortus nirsevimab is a fascinating medicine because it is really the replacement to palivizumab or Synagis, which for those of you who are unfortunately as old as I am or older may remember from MedImmune, round one before it was AstraZeneca. Palivizumab was approved, I think, in 1998, and for many, many years was the only monoclonal for infectious disease, which is kind of wild. It is a perfectly lovely antibody. Nirsevimab is simply better. It's more potent. It's got a bunch of nice features embedded into it. And parenthetically, Invivyd is also working on an RSV program, which we hope will in turn better nirsevimab. But nirsevimab came to the fore, I want to say, in 2022 or 2023. And ACIP and CDC have formal boundary conditions they avail themselves of to recommend classically vaccination. You will find in the slides from that year a very clear statement that, well, passive prophylaxis via monoclonal antibody is really no different. I can't cite to the date in the slides, although I think they're open on a browser window at home somewhere. The point is, when you read them, you will observe this is about ongoing evolution and the underlying technology. There is a broad appreciation in those organizations that these molecules are incredibly effective. In fact, ACIP member Cody Meissner, who is a pediatrician at Dartmouth, I think during the June ACIP of this year, the first with a new crew, pointed out to his colleagues, I cannot emphasize enough how effective and safe these medicines are. So I think as this political pendulum swings around, there's a longer arc of a technological change in which we might just find that certain viruses in certain populations are incredibly well suited to this form of protection. In our minds, COVID very much happens to be one of them. It's not the only one. But ACIP, in the end, has now voted multiply in favor of Beyfortus nirsevimab. The consequences, thanks to the Affordable Care Act, the Inflation Reduction Act, and I believe parts of it were recapitulated in the One Big Beautiful Bill Act, if you have an intervention like this with a positive ACIP recommendation, that medicine is free with no out-of-pocket to anyone with commercial or federal insurance, which embraces a huge swath of America. So when we go back to making something easy, certainly arriving at a pharmacy and being told, oh, there's no charge, sir, here you go, is a nice way to lower yet another barrier, which is not available to most medicines. So when I say our minds are forward in that space, we are going to look to put in front of ACIP the most compelling package we possibly can to substantiate monoclonal protection from COVID-19 for certain risk populations. And if we were to achieve such a recommendation, I think that is rarefied territory indeed. I mean, Beyfortus is now a blockbuster on its way to being, I don't know what we call a mega blockbuster now, but it's going to hit $3 billion-$4 billion at some point between U.S. and Europe. That is, frankly, useful only in children under 2, of whom there are relatively few in America and Europe compared to everybody. I know it sounds almost an incredible jump to go from a very specialty IV medicine and make a few molecular tweaks and try to drive in that direction. That's what the science tells us is well possible. That is what we will be working on at high speed. But what is the commercial effort you need to make if you do come away with an ACIP-favorable recommendation? Because this is going to be a retail pharmacy kind of selling point. So what do you need to do to get into the pharmacies? What do you need to do to get people into the pharmacies to get the vaccines? OK, so a huge amount of the work is starting right now, right? So a lot of it is actually about education in advance, meaning the good news is before you have a medicine, you can go out and educate people. And it's not about reps banging on doctors' doors. It is about dealing with KOLs and decision makers and influencers at the level of plans, at the level of guidance writing groups, so on and so forth. That is where we are today. We need to set the stage. Now, you are alluding to the inevitable consequence of some success here, which would be, oh boy, there are now some way bigger problems. One traditionally associates with television ads and all sorts of big pharma stuff. The good news is the digitalization of America, with all of its many faults and problems, comes with some certain leverage in those areas, and so I'm not in a position right now looking a year uphill to give you exactly what we're thinking about yet, but our minds are indeed past ACIP is the actioning of this, and it is traditionally the domain of larger companies, and so our first goal, of course, will be to rapidly become a much larger company so that we can simply execute. Let's just be clear. The commercial effort around 2311 starts now because we may not actually have all that much time. Hopefully, to us, it's a year, two years. That's not a whole lot of time to introduce a brand new field of medicine. I don't also think it is required that we fully action the conversion of a vaccine backbone to a monoclonal antibody backbone in year one. That would be, I think, extraordinary and unanticipated. How do we think about scaling up for what could be tremendous demand? And then with that, how do we think about your margin structure, your product margin structure? Yeah, the good news is these antibodies, certainly in our hands and indeed in many others, have been very high expressors. They're relatively low cost as antibodies go. I remember well what was meant to be the first sort of population antibody, the PCSK9 inhibitors that arose from Regeneron and Amgen back in the day. Those had a price point that were at the time shockingly low for an antibody, call it $10,000-$12,000 a year, I've forgotten. We're going to look to do a fair turn below that. So our expectation, given the dose ranges we're contemplating, is that our COGS would be well below $100 in the, let's call it, many tens of dollars with a corresponding price point that would be inspired somewhere around the nirsevimab experience, hundreds of dollars. OK, so today, a retail COVID-19 vaccine, I don't think I've seen the fall price schedule, but it's around $150-$225, depending on where you go and what you get is my most recent understanding. We would expect a turn above that, perhaps. Again, Nirsevimab Beyfortus is about $500 for the season. The question is, how much value is there in something that works better, is safer, lasts longer, and is not a vaccine? I think there's some value in there. We will be sharpening this case as we drive forward, as we see clinical data, and as we move toward action. Our hope is not to make a specialty medicine. Our hope is to make a broad population medicine and benefit the most people we can. One last consideration is the potential for emergence of resistance to the antibody. I think Stratus is the latest variant. I think you've indicated you've got coverage of Stratus. But if resistance does emerge, how do you kind of layer on a next-gen product? Yes. Well, I mean, look, Stratus is obviously data we're thrilled with and is unsurprising, right? We've long maintained the posture that if our epitope doesn't change, the potency of the molecule will drift around with a methodological sort of variability in the space. But we wouldn't expect our pharmaceutical activity to change. That's kind of normal. And indeed, it hasn't changed. Our epitope has been rock solid since pemivibart was born. OK. So on the one hand, I would say there is no reasonable anticipation that such an event would occur. I would also say, on the other hand, I think we've demonstrated a pretty impressive and still not full-speed replacement cycle. So we're not developing 2311 because we're worried about pemivibart, just as pemivibart arose very quickly from adintrevimab. I can't give you an exact number, but I think it is very unlikely we would need more than very low single-digit quarters if we were to push on all fronts simultaneously to execute a changeover. It is much more likely, based on our lived experience to date, that we will be changing over on our own terms, as is essentially happening from pemivibart on the way to 2311. Excellent. Mark, thanks so much for joining to share the Invivyd update. A lot of great things to come. So looking forward to having you back. Thank you. It's a pleasure.