Good morning, everyone, thank you to Jefferies for hosting myself and our CFO, Jen Minai, to this wonderful conference. It's my pleasure to introduce Context Therapeutics and our pipeline of T-cell engaging bispecific antibodies for solid tumors. I encourage everyone to review on their own time our forward-looking statements and various disclosures. Context is developing three different T-cell engagers or TCEs for solid tumors. Our most advanced program is CTIM-76. This is a bispecific antibody that is targeting Claudin 6 and CD3. The basic concept, which I'll reiterate in a little bit, is to encourage the interaction between immune cell and a cancer cell. Our immune system is very good at avoiding cancers. I should say, actually, the inverse. Cancers are very good at avoiding our immune system. What TCEs do is force the physical interaction between the two so that the immune system can find the tumors, then release perforins and granzymes to induce the apoptotic machinery to kill the tumors. Our Claudin 6 program is being developed in primarily ovarian cancer. We have disclosed that we'll have a data update in a couple of weeks that will run through our phase I-A preliminary efficacy, safety, pharmacokinetics, as well as correlative biomarkers such as T-cell exhaustion. That program went in the clinic in early last year. We are on the pathway to exploring Q3W dosing and ultimately phase I-B and hopefully product registrational trials in time. Our second program is CT-95. This is a mesothelin-targeting TCE. We are very interested in exploring the utility of this drug in pancreatic cancers, among others. This program also entered the clinic last year and is on track to have preliminary data in September. Our most recent clinical entrant is our Nectin-4 program, which we refer to as CT-202. Nectin-4 is expressed in a very wide range of tumors. The ones that people are most familiar with are urothelial cancer because of the approval of PADCEV and Nectin-4 ADC. There's great interest in addressing PADCEV resistance. We also are interested over time in exploring colorectal cancer, breast cancer, and lung cancer. As you can see on the bottom of the slide, all three of our antibodies have slightly different formats. Context is a search and development company, so we don't have any in-house research. We've acquired all three of these programs. The reason that they have slightly different protein engineering formats is we look essentially for build-to-suit antibodies. Each target that we're going after, whether it's Claudin 6, mesothelin, or Nectin-4, has unique opportunities and challenges. The various protein engineering choices we've made over time reflect the opportunities and challenges of those programs. For example, Claudin 6 is an oncofetal protein, meaning that it is just found in solid tumors. Therefore, you can really hit that target hard with a T-cell engager because of its tumor restriction profile, or that's at least our thesis. We use a high-affinity Claudin 6 binder as well as a high-affinity CD3. That's a very potent immune activator. We use a very simple format in an asymmetric antibody, no bells and whistles. A lot of other targets, such as PSMA or EGFR, will require a lot more conditionality and technology, such as masking, avidity enhancement, et cetera. Claudin 6 is pretty unique in that it doesn't require those technologies in our view. Our thesis over time and how we intend to build the company is to initially develop our drugs as monotherapy to address resistance to standard of care, which we believe over time will be predominantly antibody-drug conjugates in the solid tumor space. We're already seeing this play out in real-time. What we want to do over time and how we really build strategic value with respect to large pharma companies is to develop our drugs in combination with ADCs and PD-1/VEGFs. ADCs debulk tumors. They release neoantigens, create a very warm, permissive immune microenvironment. We've seen really wonderful synergy thus far with T-cell engagers in various chemotherapies and ADCs. We think this is an opportunity to help ADCs build a moat around what they're doing. PD-1/VEGF, the concept here is to deepen and make T-cell responses more durable. PD-1 releases the immune cell brake. VEGF is inherently immunosuppressive, by blocking it, you create a more permissive immune microenvironment. We think there's a lot of opportunities to partner with some of the largest pharmaceutical companies in the world to exploit the combinations of these various drugs to drive the utilization of our products into earlier and earlier treatment settings. With that groundwork, just to remind everyone, a T-cell engager forces the interaction between a T-cell and a cancer cell. T-cell engagers are still a very new modality. The first approval was about 10 years ago. It was a drug called BLINCYTO. That's now a blockbuster. You can see here there's about a 10-year delay between the approval of BLINCYTO and other TCEs. The reason is people didn't really know what to make of BLINCYTO. They didn't know if it'd be a commercial success, if doctors would use it, they'd be scared of cytokine release syndrome. It turns out people got incredibly comfortable with that particular drug, leading to lower barriers for development of TCEs. Ultimately, we've seen globally 12 TCEs registered, the bulk of which are in liquid tumors, but we do have two approvals in solid tumors. You can see at the bottom right the launch trajectories for these various drugs. Over the last couple of years, you've seen multiple, almost I think five or six drugs now build to what looks to be $1 billion or greater than $1 billion run rates. You could be in a situation as early as next year where you have three or four of these T-cell engagers that are blockbuster drugs, which is just a remarkable change in how TCEs are being utilized in the clinical community. One of the questions we get a lot is, will T-cell engagers work in solid tumors? I mentioned that we've had two approvals thus far. What we show here is just a representative data set of what we believe to be encouraging T-cell engager data in solid tumors. You'll notice it's a range of companies, some very large, some very small, different targets. We have, in this slide, broken some orthodoxies in the space, such as T-cell engagers will never work in cold tumors. You can see tumors here like prostate and small cell lung, which are classical cold tumors, where these products are having really exceptional data. Exceptional data, in my view, means that you're not only shrinking tumors, but you're doing it for a prolonged period of time, which we refer to as durability. That's what you're really seeing emerge here. The last part is the primary dose-limiting toxicity that people worry about, cytokine release syndrome. We've seen as a field, that risk decrease dramatically. We think what's happening is doctors have just gotten much better at using these drugs. They employ step dosing and steroid prophylaxis as a mitigation strategy. It's cheap, easy to do. The result is that you really don't run into dose-limiting CRS anymore for the vast majority of these products. You can dose through it, get to therapeutically active dose levels, which increases the probability of success for these products. With this, I'm going to transition into our Claudin 6 program, which will be the focus of our discussion today. Claudin 6 is enriched in a wide range of solid tumors. We are most interested in ovarian cancer. There's two primary reasons for this. The first is, the vast majority of platinum-resistant ovarian patients will express Claudin 6, and they express very high levels of Claudin 6. Having a lot of target on the tumor cell surface increases the probability of a clinical response. The second part is, in my career, ovarian cancer trials have always been very hard to enroll. They've been very competitive. We've seen a dramatic shift in the clinical algorithm for ovarian cancer. The primary experimental therapeutic that patients are getting are antibody drug conjugates, almost all of which are topoisomerase-based drugs. As we saw over the weekend at ASCO, as Eli Lilly so eloquently showed with their Nectin-4 ADC, the probability of using sequential ADC therapy in generating clinical response is incredibly low. Therefore, what clinicians are looking for is something to administer after an ADC, preferably something that has a different mechanism of action, a different adverse event profile, different resistance pathways. Turns out that's exactly what T-cell engagers bring to the table. There's always a catch. If Claudin 6 is such a great idea, why isn't everyone doing it? Well, it's very hard to develop a Claudin 6 antibody. While Claudin 6 is restricted to the tumor, it's part of a broader family of proteins, the claudins, which are tight junction proteins. They are very similar to cadherins or integrins. They help cells attach to one another. Well, in the case of Claudin 6, it's a developmental gene. While we don't have Claudin 6 in our bodies, as cancers grow, one of the classical hallmarks of cancer is the activation of developmental genes. When we were kids, our bodies were growing like crazy. Cancers want to become like kids and grow like crazy, they'll turn on these genes, one of which is Claudin 6. As you look to develop a Claudin 6 antibody, there's only a small portion that's surface exposed that would be amenable to an antibody. The problem is in that binding domain, also referred to as an epitope, there is significant homology of Claudins 3, 4, and 9. Those Claudins are found in normal tissue, including the liver, pancreas, and ear. Various studies, knockdown, knockouts, have shown that there can be very significant phenotypes associated with impacting those other Claudins. Driving selectivity for Claudin 6 is really paramount. To achieve that selectivity, we developed an antibody that is asymmetric in structure. We evaluate a wide range of antibody formats to optimize the interface between a T-cell and a cancer cell, which is referred to as a synapse. Ultimately, this asymmetric format, which has been around for 20-plus years, was the format that worked the best. We have some additional protein engineering in this antibody, including silencing the Fc function through a LALA mutation and then assuring proper base pairing through another technology. We can manufacture a drug at high yield, and we do it with a very well-known multinational partner. The key preclinical data is highlighted here. On the left, all Claudin 6 companies hopefully can show that they are very selective for binding to Claudin 6. That's not particularly physiologically relevant. The middle panel is more relevant. The reason I say that is T-cells are unique, and they run through bystander effect. It's not a pure one-to-one interaction as the binding image shows on the left. What happens is a T-cell, once it binds to a cancer cell and forms a synapse, it can call its buddies and recruit other T-cells. It can also proliferate and split into multiple T-cells over time, and that's referred to as a scaffolding function. You can have multiple T-cells per synapse. What we do is a potency assay in the middle. This is just a standard cell death assay. You overexpress either Claudin 3, 4, 6, or 9, and you introduce immune cells, either PBMCs or activated T-cells, and you do a concentration gradient. Here, from an in vitro standpoint, we think about the therapeutic window for our drug is about 500-fold. That's the window with which we use to determine our first-in-human dosing and then ultimately, the math for how we want to get to therapeutic activity. On the right, we have great in vivo data as you would expect. This is our trial design. We have learned a lot over the course of the trial. As I like to say, hindsight is always 20/20 with your first T-cell engager. When we started the trial, all of our peers were doing basket trials, ovarian, endometrial, and testicular. As I mentioned earlier, ovarian trials were historically very hard to enroll, and so we all wanted to hedge and include endometrial and testicular patients. What we learned is that actually ovarian, given the circumstances of the clinical landscape and the very high target prevalence, is very easy to enroll. There was no facile way with how we constructed this protocol to say one day we want to enroll more ovarian patients than just them. We had to do some maneuvering, which was the two middle cohorts of 210 and 280 to ultimately get to where we want to be with the Q3W. To unpack that a little bit, we started with what's referred to as a MABEL dose, which is your EC20 and your most sensitive assay. We went to a second dose level. Both of these doses were projected to be subtherapeutic, which they were, then we would get very quickly into active dose levels, starting at 140 micrograms. We projected activity as being the dose at which our drug would be above the EC50 for the duration of treatment over that weekly interval. The EC50 is the dose required to kill 50% of the cells in that cytotoxic assay that I mentioned on the previous slide. Then we continued to escalate, ultimately getting to a dose range that we felt comfortable with. Because it was a 3+3 trial design, there was no efficient way if we did not run into toxicity to expand the number of patients, we added the two additional cohorts, the 210, the 280, to increase the number of ovarian patients that we would have in our June dataset. Where we are right now, we've enrolled quite a few patients, about 15 of whom are at target dose levels, and about 10 of those 15 are platinum-resistant ovarian patients. We've previously guided that the vast majority of those patients, almost all are ADC experienced. We think it's a highly relevant clinical dataset that we'll be presenting in the coming weeks. Then ultimately, we were pleasantly surprised by the pharmacokinetic profile of our drug. After a week, there's still a lot of drug present. Ultimately for patients, we think that every three-week dosing referred to as Q3W dosing is really what those patients are looking for from a patient convenience standpoint. Q3W dosing also aligns with the administration schedules for ADCs and PD-1/PD-L1 bispecifics, which strategically is very important. Lastly, some of you may have seen, this is getting very geeky and technical, but at ESMO this year, there was a wonderful dataset from J&J featuring their drug pesritumig. This is a KLK2 TCE. What they showed very elegantly was to optimize T- cell activity, you don't want the T- cell engager fully active for the dosing interval. That constant, what's referred to as tonic signaling through CD3, will lead to exhaustion and a loss of response. J&J took their weekly dose, went to every three weeks, and ultimately every six weeks, and found that if you let the drug be active for a period of time and then wash out and then let the T- cells recover and re-energize, two remarkable things would happen. One, the efficacy got substantially better, deeper responses, more durable responses, but then also there was no reintroduction of CRS. Even though you're letting the T- cells recover, you would not stimulate Cytokine Release Syndrome. We think the profile that we are seeing right now could create a scenario where a full dosing in 21 day intervals, the drug maybe on board for 10-14 days, wash out, let the T-cells recover for a week until ultimately, what we think could happen is better, more durable responses over time. That's not to say we're not happy with what we're potentially seeing right now, but I do think the field's going in a direction that is very positive for patients and sponsors alike with less frequent dosing. The most recent deep update we provided was right around Halloween, where we provide an update on the first four cohorts. This was dosing through the 280 microgram dose from a safety standpoint, then efficacy for the first three cohorts, which was up to 140. As I mentioned earlier, the first two cohorts were subtherapeutic, and we were just getting into therapeutic target ranges at 140 micrograms. Of those 12 patients, about half of them were ovarian, and then the rest were a mix of endometrial and testicular. They were heavily treatment experienced, that continues to be the case. As we look moving around this slide, from a pharmacokinetic standpoint, at this point, we were seeing linear and dose proportional PK, which is great. It's a very well-behaved antibody. As far as correlates, we were seeing very nice T-cell extravasation, meaning that when you give the drug, the T-cell moves out of the bloodstream towards your target and then recovers back, and then dose proportional cytokine elevations. On the efficacy side, we had reported that at that point, we had one patient in the 140 microgram dose level who had a deep and durable response. This is a patient who at week eight had about a 50% decrease in their target lesions. That deepened to 85% at week 16, and they continued on treatment. That patient, I think, is very clinically representative of the ovarian patients that we've been rolling to date. This patient basically got the greatest hits of ovarian cancer treatments. mirvetuximab, which is a folate receptor alpha ADC, olaparib, which is a PARP inhibitor. They got bevacizumab. All of our patients get bevacizumab, sometimes multiple times across their treatment journey, and then they got an experimental therapy as well. I think that just punctuates the stage of disease that the patient was at. That was really encouraging to us. You always want to see good data early and a jumping-off point, so to speak, that you can build off of. As far as safety, the drug at this point has been exceptional. We noted in October that one patient had Grade 1 CRS. At that point, there were no DLTs and no MTDs. We think what's happening is a combination of Claudin 6 being onco-fetal, so purely restricted to the tumor, which lowers the probability of CRS, and then the fact that we're doing steroid prophylaxis on Cycle 1, Day 1, and Cycle 1, Day 8, as well as step dosing. You take the combination of that, we're seeing potentially very low rates of CRS. That opens up a wide range of really interesting development opportunities, particularly as you think about pushing the drug into earlier lines of therapy and the utilization in the clinical community. Obviously, a trial like this, we're running it in large academic centers. But to bring the drug to the masses, it has to be able to be administered in the community. What we think is if this safety profile continues to hold, that is a real probability with this drug, which is incredibly exciting. Competitively, we really see ourselves and Xencor as breaking from the pack. Xencor is about, based on our read of their public disclosures, about six months ahead of us. I think the truth is it's hard to say how we're dramatically different than them at the moment. We need to compare clinical data. There are some nuances between our antibody approaches. They have detuned their CD3, and they're a two-by-one binder. Typically, one detunes their CD3 to mitigate the risk of CRS. I mentioned earlier, I don't think there's a lot of inherent risk of CRS with Claudin 6. If you detune the CD3, the probability that you're going to have really strong efficacy actually decreases because to be equipotent our drug you have to significantly increase the dose administered. The second thing is they're a two-by-one. To be fair, we have two avidity enhanced antibodies, our mesothelin Nectin-4 program. We like that approach. We just think it may be a challenged approach with Claudin 6. The reason being that if you have two arms that can bind to a tumor antigen, yes, they could both bind to Claudin 6, they can also bind to Claudin 3, 4, and 9. Again, direct binding to those off targets can lead to clinical phenotypes. Now you, from a stoichiometric standpoint, have increased the probability of one of those inadvertent binding events. I think these things either may be really important over time, maybe just on the margin, but we'll have to find out. Again, we're reporting our initial data this month. Xencor has guided to preliminary disclosure later this year, we should be able to know more definitively at that time. The other products are more emerging with, in our view, some significant liabilities in their protein engineering choices and approaches that may limit their utility. We think it's, again, a two-horse race as you look at commercial opportunities for Xencor and ourselves. Right now, there are six different TOPO-based ADCs in phase III development for ovarian cancer, as well as an approved folate receptor alpha ADC with a different payload. All seven of those programs are being developed by large pharmaceutical companies. I think there's a lot of opportunity for two entrants to partner with those companies. I don't think a second group is limiting in any fashion. I do very much hope over time that we substantially differentiate from Xencor and take a dominant position, but I'm not sure how much in the short term that particularly matters. Given the amount of time, I really just wanted to focus on Claudin 6 today. We do, in summary, have two other wonderful programs, our mesothelin T-cell engager, which will have preliminary phase I data in September, and our Nectin-4 program, which will have first patient dose shortly. We learned a lot about TC development, particularly around clinical protocol design for that program. We think that should be in a position to have clinical data in 2027, right around the corner. From a financing standpoint, we last raised substantial capital in 2024. We still have cash into the middle of next year, about a year's worth of runway or so. With that, just want to thank my team and Jefferies for hosting us today. I think we have about five minutes for questions if people want. Perfect. We're good. Thanks so much.