Good afternoon, everyone. Thank you so much for joining us. I'm Salveen Richter, biotechnology analyst at Goldman Sachs, and really pleased to have with us Clay Siegall, who's the President and CEO of Immunome. To start here, Clay, you formed this company. Maybe you could just level set for everyone in the room who isn't as familiar with regard to your strategy, your pipeline, and really the key focus points you want us to look at in the second half of the year and beyond as you look to execute across the overall company. Sure. Most of you know me through Seattle Genetics in 25 years, which I shortened to Seagen. I am very passionate about making therapies for cancer patients. What Immunome is doing is focusing on targeted therapy for cancer patients to do the best that we can for patients suffering from unmet medical needs. We are very focused on certain aspects of targeting. There are things we do not do because it takes a different infrastructure. We do not do cell therapy, and we do not do gene therapy, and we do not do CRISPR therapies, which are all great technologies, but it is just not the infrastructure we have built. We focus on targeted therapies, a couple of modalities, but we specialize, which is not surprising to anybody, in ADCs. My view of ADCs and the strategy, as you asked, is different than it was 28 years ago when I first started CGEN. At that point, ADCs were, there really were not ADCs. They were not called ADCs. I called them ADCs and started publishing it, and everybody caught on. They had lots of different names. There was one molecule out there called Mylotarg, which was a pioneer, and it had some problems with just building it and stability. I did a lot of high science and came up with what is the modern ADC. I would say I am not the discoverer of ADCs, but rather the discoverer of modern ADCs. Now there are a lot of companies doing it and making a difference in patients' lives. Now, years ago, I would go to a conference and I'd put up a slide and show, "Here are my top 10 targets I'm working with." I can't do that now because there's too much duplication of targets. Now what we're doing is we're working on targets, and once they get to clinic, we talk about the target at that point. Before then, it's largely code numbers. They're really exciting targets. Our strategy is to go after novel and first-in-class targets and not be the 28th HER2 or 29th NEXT in four. I think that it doesn't make sense to me from an efficiency standpoint to go after the same targets. 55% of all ADCs, in my assessment, all go after the same 10 targets. We're not going after any of those 10. We are doing all new and novel and exciting targets. On the payload and linker part, the toolbox, if you will, we looked at a lot of different things. When you look at ADCs, they largely fall under two buckets. One is the bucket of ADCs that are antibiotics, and the other bucket is ADCs that are topos. Those are the vast majority of ADCs. Now you want to look and you say, "Okay, what's good? What's wrong? What can I solve?" With the topos, they've had very good activity. If you take a HER2 and you put it in patients that are P-glycoprotein positive, you get a much lower response rate than if you do if they are negative. That is certainly an area that you could do better in, for instance. We've made topo inhibitors that are not sensitive to the most common resistance pathways, like P-glycoprotein and some others. I don't want to say it's not sensitive to any pathway because I don't know all of them, but anything we could test, it's not sensitive to. We think that could be a benefit for patients. We also have one that's more permeable, so it can get better bystander activity. We have what I think is the best payload out there. We've made custom linkers that are, we think, the best linkers. We haven't been as vocal with talking about our linkers. We have a great toolbox, and then we have dozens of novel antibodies, and we've interrogated at least half of them. We want to see ADCs that have great activity at 2.5 and 5 mg/kg and safety in a non-human primate at 40 mg/kg because when you get into a human, it's more narrow. It always gets more narrow than when you test it in non-human or when you test it in rodent setup tumors and non-human primates. If you have a therapeutic window of 2 in there, it's going to be really tight in a human. You want a therapeutic window of 20 so that when it gets more narrow, when you're treating humans, you have a really good chance to have an effective and safe dose. We have more than a dozen very exciting ADCs we're working on. We have one in clinic. We have three that are being manufactured right now for clinical trials within the next 12-14 months. We have three right behind there. There are more, but we can't do them all at the same time. It just takes time and effort. We have a great team. A lot of our team is ex-CGEN people, my Chief Medical Officer, my head of manufacturing, head of antibody sciences, head of regulatory, and a bunch more. I brought in some really good talent, but it's not just—I mean, these are experienced, quality people that really know how to get the job done and make drugs that get on the market. We are very serious with that. I would say the biggest part of what we are at our pipeline is ADCs. We also are opportunistic to bring in other things that are important. For instance, we did a deal to bring in a small molecule gamma secretase inhibitor that is in phase three with data coming out in the second half of this year, which starts next month, by the way. July is the second half of the year, and it comes quick. If you recall, at CGEN, I was opportunistic and mainly an ADC company, but acquired Cascadian for a small molecule pill, just like the gamma secretase is. It was fantastic chemistry from a company called Cascadian, which was BioMira, then Oncothyreon, then Cascadian. Thirty years, no drugs. I do not know how they made it that long, but it was change of management a lot, no CMC to speak of, perpetually underfunded, not good clinical leadership. It just kind of went in circles a little bit. I'm convinced that Tukysa would not be a drug right now if us or someone else took it over that was seriously developing it. I was opportunistic in buying that drug. I've looked at so much technology and so much drug, so I'm really picky. I don't just run after things. When we found what's now called varegacestat, what we found is a great piece of chemistry, really great phase two data, no CMC to speak of, perpetually underfunded company without the right leadership, executive, or clinical to really make it happen. We really like the chemistry and the early data. We brought it in. The phase three is completed with enrollment. It was gangbusters. Enrollment, a lot of same-center enrollment, which is always a good sign. It's an event-driven study, much like Tukysa was an event-driven study. In the Tukysa case, in the last many months, we did not have an event. We went to the FDA and said, "Look, we can't just sit here year after year with no events." We went forward and talked to the FDA, and we got the green light to go ahead and unblind. We did, and the data was great. The FDA approved it fast. In this case, I'm not going to give you information. I know the event numbers. We have to keep up with that and certain things. I don't know which arm the event's in, unblinded to all that, but I have to know some general things to operate the trial. We've given the best guidance that we can. A lot of investors have asked, "Can I make the guidance tighter? Can I this? Can I that?" We'll see. We'll do the best we can to advise. I'm very excited about that. The phase two data was substantially better than nirogacestat, which nirogacestat was very impressive what SpringWorks did. They took a drug that was being developed for neurologic disease, and they brought it into oncology and got approved based on a 41% objective response rate and other aspects to be the very first drug ever approved for desmoid cancer. That's hard. I mean, I know I got the very first drug ever approved for Hodgkin lymphoma. There were other things that were used, but they were never approved. Just like desmoid, they were using radiation and things like that. It's always hard to start a path and get your first approval in a disease. I have a lot of respect for what they did. We ran into this drug. We were evaluating this drug. We heard about the company and the data, and the chemistry in the drug is exceptional. The phase two data looked 20 or 25 percentage points better than what the SpringWorks drug, nirogacestat, looked. We acquired the drug in an asset sale, and we've been developing it since. Our CMC work has been tremendous. The same guy that did the CMC with Tukysa was doing it, and Phil Tsai. We've done a great job clinically. I think the execution of the trial has been great. The sites have been great. We talk to the doctors all the time. Almost every doctor on the trial has used both drugs. They're very savvy to the drugs and everything. I'm excited for our data to come out. I have a great Head of Commercial who launched—he ran Adcetris and Tukysa at Seagen. He is a very talented guy, Rohit Shah. I am excited with that. Lastly, we have a radioligand. To me, it fits because it is still targeted therapy. It comes from the history of the private company Morphimune when it merged with Immunome and the founder of Morphimune, who has a lot of history in radioligand therapy. What we did is we took what his original concept was, and then we made it into a drug. It targets FAP. Fibroblast activation protein is one of the best targets I have ever worked with because it is on 75% of all solid tumors. It is on stroma, not on a tumor. I have tried to make an ADC to it. It is cumbersome. With a radioligand, I mean, the things that we did is, for example, FAP binding proteins. I mean, there's probably 15 different FAP binding proteins. Okay? When you look at Novartis historically, Novartis went ahead and did a FAP radioligand years ago, and it failed. We made it. We see what it is. It was not a good construct. Clovis took one forward, and they had a few responses, but that did not work well. We have done exquisite science on it. My team has done great science, and we have a molecule that has such great properties and such great activity. It is worth testing in the clinic. We submitted an IND for that, and we got cleared. Now it says we are doing contracts, and we are going to make sure that we get it into clinic and give it a great test. I mean, it would be a—if anybody can make a FAP-targeted drug, it'll be a very big drug and an important drug because it's such a broadly expressed target. That is what we're doing. ADCs mainly and RLT and a small molecule. Right. Starting on the ADCs here, when you were at Seagen, you really focused on building a platform, the vedotin platform, for instance, at the end, where you kind of built all your drugs off of that. How are you thinking about that in the context here and where, when you look at now the landscape of modern ADCs, where you can improve upon with the platform technology? I think antibiotics like vedotin are really important still, and topo ones are important. They're the two main approaches to treating with an ADC by far and the most that sell in an ADC. I look back 25 or more years ago, I tested hundreds of small molecules. Most of them, if you put a linker on them, you kill the drug. Antibody is a big glob, 150,000 daltons. These drugs are like 300. They're like a dot. If you take a linker and you attach it, you inactivate the drug in most cases because you're changing the structure. Now it can't interact with, let's say, tubulin or DNA or whatever it binds to. It doesn't work. We looked over and over years ago at CGEN, and we found that an antibiotic called orostatin E, you could manipulate and put a linker on and still keep it active. That was a big finding because most of the drugs we looked at, we would kill. With topos, you could manipulate them and put a linker on. That is why there are not 50 drugs because it is hard. Most do not work. Now what are we doing? I look at the world and they say, "Oh, Clay, you never made bispecific ADCs." No, I did. "You never made dual payload ADCs." "Oh, yeah, I did." "Okay. You never did this. You never did this." I did all the above. The problem I have had, I can make a bispecific ADC work, for sure. To me, I test it versus the cognate ADCs. I have not found one that is better than the Cognate ADCs. I can make one. It does not mean you want to develop it. They are cumbersome to make. You can get a little aggregate. If you get a little aggregation, you get a lot of lung tox. You have to really be careful. The dual payloads are very exciting, and I have worked a lot on there to try to do that, the new ADCs. You asked about this. Once again, I want to see that they are better than the mono ADCs. I think the best way right now going forward is novel targets with the best drug linker you could have and make it with very low aggregation, ease of manufacturing, and solving some of the real problems. Someday there are going to be very clever people that will make novel technology. I don't think we're completely there yet, even though a lot of people are working on it. I haven't seen evidence that it's better than a really good mono ADC yet. We'll see. For us, it was build the best drug linkers that you can, fixing some of the problems that exist with arguably the best mechanism, which right now is probably topo, to get the highest activity, but fixing the problems. Using a great linker, which we're not going to discuss the specifics of the science, and then novel antibodies. When I talk about novel antibodies, some of our antibodies are targets that, honestly, I had never even heard of before. We're interrogating. Some of them are targets that are a little surprising that maybe weren't as prominent as others for different reasons. We will talk about them in the future when we start talking about the targets. A couple of the targets we have are old antibodies that people had developed and were very interested in and then dropped development because they were not working because they did not have the right activity. Like one antibody I am thinking of was developed in the clinic as an ADC and dropped because it had no efficacy. We looked at that antibody, and the half-life of that antibody was tiny, just so short of a half-life. We took the antibody, which is now old and off-patent, and we resurfaced the CDRs. We created a panel of antibodies. We have antibodies in the resurfaced CDRs that have half-lives of weeks, which is what you want. We have all new IP on this old target that was a fantastic target. It's just that it got dropped. With all our novel targets, it's a mixture of brand new ones I've never heard of or we've identified or we've done business development on and old ones that we've resurfaced. We're really good at antibody engineering. I have great antibody jockeys, if you will. The top two ones came from Seagen, where we had good antibody jockeys. You go where you know. My goal is to make drugs to treat cancer patients. I've been part of quite a few drugs that are out there in the world, and I believe that we have a lot more good targeted oncology drugs to make to help patients. You'll be starting here at the most advanced program that you have, so the small molecule, again, the secretase inhibitor. Given maybe your history with work across the cancer landscape, could you discuss the strategy here with this asset and maybe talk about the tumor indication and the unmet need and the opportunity you see with this drug? Yeah. Desmoid cancer is a kind of a strange cancer. It's kind of related to sarcoma-type cancer. It's treated by sarcoma docs, but it's not exactly the same as a standard bone cancer. It's very painful. It's disfiguring. You can lose limbs. Patients don't die quickly like pancreatic cancer. It's a different thing. You live on with it. There's about 1,600-1,700 new patients a year. These are US numbers, about the same if you take Europe. There's about 32,000 is the prevalence number in the US. They come in and out of therapy, and they get things like radiation and other things. About 5,000-6,000 a year come into therapy, and they try to get treated because they're in pain or they're suffering from one thing or another. It's not, well, it doesn't kill you. This is not a pleasant disease. I wouldn't want it on anybody. We've talked to doctors. We've talked to patients. We've interviewed them. We understand this. We understand what's going on, what they want. Like I said, nirogacestat was approved, and it had nice data. When we ran into this drug and we looked at it, the data was pretty special. The thought was to do better for patients and not to take anything away from nirogacestat, but to do the best we could for patients. It reminds me of developing Tukysa, which was a better molecule than was Tykerb or Nerlynx. It was just much better for patients. By the time it comes out there, it dominates the landscape. The question here is, do we have better data? One of the things is we're once a day. Kind of surprising, doctors have told us over and over how important once a day is. They have told us that compliance is an issue for multiple times a day, like their drug. A lot of people just, and we have interviewed patients. A lot of them are like, "Well, yeah, we took it once a day, and it is not really working. We still have a lot of pain, and we are not going to take it anymore." Doctors say to us, "This is not just convenience. This also will help in efficacy because people will take it." That is a good thing, but it is a surprising thing. It was not the reason we developed it. We developed it because the response rate, the factor that we looked at is ORR, overall response rate, was 20 points, 25 points better. When we looked at the reduction of tumor volume, it was almost 30 points better in the median reduction of tumor volume. When we looked at something, the T2 score, which measures cellularity, you could see whether the tumor is a ghost or a real tumor cell, it's much, much better. A lot of docs, we hear from docs that they look at T2, and they could tell whether the drug's working pretty quickly before a response rate. Once you're out in the world, you're not going to be measuring the tumor as much. I mean, that's a clinical trial thing. They could do the T2 score, and they go, "This is working pretty quickly." They could tell by pain and patients and things like that. We're excited to get our data. Our current plan is to launch it in the US and Canada and Europe and then to work through distributors in LATAM in the Middle East and probably a partner in Asia. We have begun some discussions on it. We are not rushing. We want to make sure we have our data first and make sure it is full value. Can you just put the phase three trials fully enrolled? And as you noted, data is coming in the second half. Can you just walk us through what you saw with the data in phase two and any changes that you've made to the trial design here just so we can understand the read-through to success here? Also, you just talked about launching. How are you thinking about building a commercial team? Right. So there was a lot of questions there. Look at the trial. The difference between our trial and the DeFi trial that SpringWorks did, which was fabulous, that got approval. That trial, you could have the endpoints were either doctor assessment or using a BICR, a blinded independent central review of the data. BICR being more of the FDA gold standard. For our phase three, FDA wanted us to use BICR. Now, they want to see the doctor assessment, so we're collecting that. BICR would be what we're doing as primary. I like that. It's clear using radiologic assessment rather than docs saying things. Not that I have offense to the docs, but I like the radiologic assessment. That's the only difference. Most of their patients did use their BICR, so it was less than half used doctor assessment. I do not think it is going to be that different. That was a difference there. Same center enrollment was great. We think that if anybody is really responding to nirogacestat, they should stay on. If you are responding to a drug, you should not switch a drug. If you have relapsed from that or never responded or you are a new patient, certainly it would be a good opportunity for us to jump on. The Head of Commercial, he was in charge of two drugs at Seagen. He went over to Pfizer. They gave him a broader responsibility. He was really excited and actually contacted me about coming back to what we were building and wanted to do that again. He is talented, and I have no worries about launching the product. I have no worries about the CMC, which when we got the product, I was very worried about CMC. Now we're on track, and I think we're ready to launch if we are so fortunate to get the right data. Okay, phase two. What I saw in phase two, and I'm very picky and do a lot of diligence, I saw three different doses and schedules. The drug worked better than nirogacestat did in their phase two in every dose and schedule with better. Sometimes you look at data and you're at a conference or you're hearing people at whether it's a medical conference or like the Goldman conference or banker conference. Companies will talk about their data and they say, "Well, at this dose, nothing really worked. But at this dose, everything worked. Or at this schedule, everything worked. And that one is nothing." I am very skeptical of that. Good drugs work at a lot of doses and schedules. You can maximize them for sure and do better. The best drug, so usually when I see that and then I see they go and do a bigger study, it usually fails. Okay? I think it's because you're cherry-picking. In this case, three doses, three schedules, they all look better. That said something to me. The other thing is that we interviewed all the doctors, and they liked using this drug for a lot of different reasons. Some I don't want to share right here on this stage. Doctors liked using it. It was user-friendly for patients. The data was special, and the enrollment was excellent. The safety, when we looked at the safety in the phase two, the safety to me, there's not enough N to be 100% sure in a phase two versus a phase three. If I look at their phase three, which is a bigger trial, and I look at the phase two with varegacestat, our drug, I don't see that much difference. I don't know that there's anything statistically meaningful in the difference. I think they're very close. Now, varegacestat, our drug, is 250 times the potency. We use it at 1.2 mg per day. And theirs is 300 mg. It's 150 mg twice a day. It is a very different chemical structure. It has very different pharmacokinetic properties. When theirs gets below trough, you have to dose again. We are fine. It stays in the bloodstream, and you don't need it more than once a day. I am very pleased with the chemistry, the data, the trial, the execution of the trial. I am really looking forward to the data. Provided we have the right data, we will quickly assemble it and provide it for regulators to try to approve. We have given guidance out, and we are doing our best to track events and see where we are. You're also investigating Aurora One targeting ADC. Could you walk us through what preclinical data supports your confidence in this asset to move it forward into phase one and when we could see first data here? Yeah. So I've been interested in Aurora One for a long time. I first ran into Aurora One when I was speaking with Velos Bio. And I was running Seagen, and I was looking at Velos Bio. And quite frankly, I wanted to acquire them because I had Adcetris and had a full sales force doing lymphoma. And I thought, "Wow, this could be very efficient. I wouldn't need one more salesperson and put this in the bag, and the same salespeople could sell two drugs." And so I wanted to do that. But before I could execute upon it, Merck paid $2.75 billion, which was about three times more than I thought the value was. So I wasn't in the same ballpark. And so good for Merck and whatever. And Merck came in and studied it in two ways. They put a lot of effort into solid tumors. Aurora One is kind of a unique molecule. It binds liquid and solid tumors, which a lot of targets are either solid tumor or liquid tumor. Aurora One straddles both. It is expressed on liquid tumors in higher density than solid tumors. It is not identical. The antibody that was used, I know where the antibody that Velos Bio used came from because I looked at it. It was from a little company that does not exist anymore. It was not a selected antibody like I like doing. I like doing 10,000-20,000 antibodies in panels and picking for the best internalization and other properties. This was an antibody that was in a freezer, and it was used. It did not have the best properties. When you look at solid tumors with the low expression, if you do not have a rapidly internalizing antibody, it is going to be a tough battle. They went into a lot of trials combining Keytruda, their PD-1, with this molecule, the Aurora One ADC in solid tumors. They did not see anything spectacular. I think they announced that they were not pursuing that anymore. They are still pursuing some aspects of liquid cancer where it certainly had the efficacy data from the Velos Bio DA SE. They are doing it in some combination approach, which is a long study. I cannot speak to the strategy of it. I will let them do that. I think what we have is a rapidly internalizing antibody, which is differentiated, and a much better drug linker system. We know that molecule we created in the laboratory, and you can compare it. Our molecule is much better than it, not only in liquid tumors, but it's pretty special in solid tumors. It has the properties you need with the rapid internalization and the higher DAR. We use a little bit higher DAR to get more drug-antibody ratio, to get more drug in there. It really, I think, will help with solid tumors. We are in a phase one study doing dose escalation. It's going well. We haven't reported any data yet. As soon as we could, we'll report data. We have given no timing on it. You also announced three solid tumor HC74 payload ADC candidates, all in IND studies. I guess that's a lot for this target, potentially. How are you thinking of managing the development process here across the tumor types? Yeah. We have three ADCs that we are manufacturing. They have unique targets. Together with Aurora One, within a year or so, we intend to have four novel ADCs in trials. The next three are all solid tumors. The preclinical data is spectacular. That does not make a real commercial drug. If you look back at my history, I am not batting a thousand. I have a high hit rate between drugs I have developed and drugs that got approved. In my history, I am about one in four. Industry is about one in 10 average. What we are doing is we are putting a lot of drugs in clinical trials. We have great science. I would like to be better than one in four. We will see. I mean, that is the goal, to do better and better science. I think it's important for companies to have big pipelines. I think you get success, and you really help patients by having big pipelines. We are pounding forward with our pipeline. I hope that a year from now, we have six drugs in the pipeline in clinical trials. A year, year and a half afterwards, we have nine. I think that that is a prescription that's very good for the health of a biotech to do great science, meaningful novel agents with good patents, great underlying science, and good clinical development. I think that's a good prescription for adding more commercial products to the targeted therapy field. Maybe a last question, Clay. Where does the company sit with regard to balance sheet, but also the thoughts around a BD and partnership here? BD, clearly, that's what you've been doing, but partnerships. We last reported, I think it was $315 million about in cash. That takes us into 2027. Our market cap is about $825 million, $830 million. We are happy with that. That is not an unlimited amount of money to develop drugs. We think big. We want to build a multi-billion dollar company with real products. You have to think about that. At Seagen, I did a lot of different deals, and I was very careful with them and did some excellent deals bringing in non-dilutive capital. We are talking with a lot of different companies now about our ADCs, about all our programs. We will just have to see. I do not want to make promises on it. There is a lot of interest in our pipeline by big companies. It may make sense to do some aspect of bringing in non-dilutive capital. When you do these deals, you don't get them for free. You give up something. You give up some percent, some ownership of what you're developing. There's good and bad. As long as the deal is constructed right and as long as there's a lot left for us and it doesn't take our whole pipeline but just some drugs, it's probably worth considering something. We're talking to a lot of important companies. Great. With that, thank you so much, Clay. All right. Thank you. Thank you.