Good morning, everyone, and thank you for joining us at the fourth day of the annual Needham Healthcare Conference. It is my pleasure to have with me this morning Michael Richman, President and CEO of NextCure. Michael will walk us through his presentation, following which there will be a Q&A section. If you have any questions while the presentation is ongoing, feel free to put it through the box on the web link. With that, Michael, you have the floor. Great. Thank you so much, Gil, and thank you for providing NextCure the opportunity to participate in the 24th Annual Needham Healthcare Conference. We greatly appreciate the continued support, especially in these challenging times. It is a pleasure to introduce NextCure to everybody today. This next slide is our forward-looking statement. NextCure is really focused on pretty much a single asset at this point. This is a clinical program, a value-driven ADC, antibody-drug conjugate opportunity. Our asset is currently in phase one clinical development named LNCB74, which is an antibody-drug conjugate targeting B7H4. It is a differentiated antibody-drug conjugate, and I am happy to walk you through some of those differentiating factors today. The nice thing about the program is B7H4 is pretty much a validated target based on its overexpression in many different tumor types, predominantly those cancers impacting women's health, looking at breast cancer, endometrial, and ovarian cancers. The program is working its way through dose escalation, and we hope to report clinical proof of concept in the first half of next year, 2026. We're well funded as an organization. Our balance sheet was $68 million as of the end of fourth quarter last year, and our runway takes us into the second half of 2026. This is our timeline and pipeline slide all in one. LNCB74 is being co-developed with our partner, LigaChemBio. This is a 50/50 co-development arrangement. As I mentioned, the LNCB74 is targeting B7H4 with an MMAE tubulin inhibitor payload coupled with a unique proprietary linker system that we've acquired from LigaChemBio. As I mentioned, we're currently focused on predominantly three tumor types in breast, ovarian, and endometrial cancers. Each of those tumor types expresses B7H4 at a fairly high level, and we'll be reporting safety, efficacy, and biomarker data in the first half of 2026. I'll tell you a little bit of just kind of a brief overview of the program itself. We're currently engaged in a 50/50 co-development partnership with Ligacam Bio. As I mentioned earlier, this is a phase I clinical asset working its way through dose escalation. Our goal is to develop this through four dose cohorts and then advance into either additional cohorts or continue backfilling existing cohorts from a safety and biomarker perspective. The US trial is ongoing. I should add, we also have a unique CLIA-validated IHC immunohistochemistry biomarker assay. This was developed as a tool to take biopsies from patients and to look at their B7H4 expression levels so that we could identify those subjects expressing high levels of B7H4 and that we believe will be most responsive to LNCB74 therapy. As I mentioned, and I'll walk you through shortly, the key differentiating factor independent of the antibody and the payload in our clinical development approach is this unique antibody linker system acquired by Ligacam Bio, which is based on glucuronidase. This next slide shows kind of the clinical path that NextCure is taking in developing LNCB74. As I mentioned, it's working its way through dose escalation. We've just completed the second dose cohort, and once we complete the safety period over the next few weeks, we'll start administering drug to the third cohort. We're currently looking at four dose cohorts. We hope to see some sort of clinical activity in cohorts maybe three and four. We're dosing patients every three weeks, and we hope to enroll about 65 subjects in this dose escalation strategy coupled with safety and biomarker backfills. As mentioned earlier, we hope to demonstrate clinical proof of concept in the first half of next year, and then we'll quickly move into a dose expansion phase of the study where we'll kind of narrow down the dose cohorts to two. We'll kind of select two tumor types, and we'll look at about 80 patients, whereby we'll look at pre- and on-treatment biopsies to identify those patients that express high levels of B7H4. This next slide kind of talks a little bit about the drug itself. LNCB74 is an anti-B7H4 MMAE antibody-drug conjugate. The antibody was selected and modified in the FC to protect it from various immune cell interactions, but more importantly, to give high affinity and tolerability of the antibody itself as it relates to penetration into the tumor. The linker we will talk a little bit about more shortly. This is based on a glucuronidase cleavable linker. We believe this will provide improved safety and efficacy of the candidate. We are currently using an MMAE payload at the door for constructs. This next slide talks a little bit about the differentiation. When one looks at antibody-drug conjugates, there are many different types of variables we look at. We look at high affinity antibodies. We look at various payloads, predominantly looking at tubulin inhibitors, such as in our case. Others are looking at topoisomerase inhibitors. One of the key features that differentiates one ADC from another is the linker system. Many of these linkers have certain limitations based on their stability, or I should say instability. This instability often leads to off-target toxicity. When these various ADCs are trafficking through the human blood, sometimes there's a breakdown of the toxin being released, and you see certain toxicities in various tissue. What we've done here at NextCure, working with Ligacam, is we've overcome that problem by using the glucuronidase linker system. This is a stable linker that avoids any of that breakdown through trafficking through the blood. It reduces any of the untoward or off-target toxicities that leads to certain adverse events. We believe our LNCB74 will be much more safer in not only attacking the tumor and killing it, but also avoiding any toxicity. This next slide continues to talk a little bit about the various linker systems and focusing on glucuronidase. The glucuronidase system, this is a site-specific chemical linkage to the antibody itself. It's highly stable, so that stability helps avoid any of that release of the toxin prematurely that would create off-target toxicity and potential safety concerns. The beauty of the linker is the specificity too. It's not cleaved until the antibody and the payload enters the tumor where you have specific cleavage of the glucuronidase linker and releases the toxin into the tumor to kill it. This gives you much greater efficiency of the release of the payload. I think more importantly, we hope that it will give us the ability to improve the therapeutic index to get a higher concentration of the payload drug itself into the cancer cell. This is some of the in vivo work that we've done with LNCB74, looking among a number of different tumor types. In this case, we've looked at breast cancer and ovarian cancer, looking at CDX and PDX models. In each of these models, you can see quite clearly that LNCB74, in multiple doses, clearly pretty much eradicates the tumor with a very strong, durable response. We've been able to show this in breast cancer, triple-negative breast cancer, and ovarian tumor models. This next slide shows some comparability data with respect to a molecule that uses a val-cit linker, the linker we talked about earlier with respect to the instability. This is, again, looking at LNCB74 in a number of different tumor settings, in particular in looking at breast and ovarian cancer models. What you can see quite nicely in red is that the LNCB74 at an equivalent dose to a comparable molecule using a different linker system gives you much more effective and durable killing in these animal models. This next slide shows kind of the competitive environment we're in. Anyone that follows antibody-drug conjugates, there's a significant amount of focus and somewhat differentiation of different approaches to ADCs looking at various targets. There's a number of different companies as shown in this slide working in the B7H4 space. Each one of these programs uses a different type of linker system. The payloads are also different with respect to tubulin inhibitors like the approach we're taking, and in many cases, topoisomerase approaches others are taking. We think we're going to clearly be differentiatable. As we kind of continue to enroll patients throughout this year and get prepared to report data first half of next year, hopefully we'll be able to demonstrate better safety and efficacy with the goal of having a best-in-class molecule. In summary, we believe we have a significant opportunity in the B7H4 space. This is based on the differentiation of a highly engineered antibody with high affinity and strong penetration. We think the linker system using glucuronidase provides important benefits from a safety and efficacy perspective. Again, our focus is predominantly right now in looking at breast, ovarian, and endometrial cancers, but we may have the opportunity to expand into other cancer types that overexpress B7H4. Independent of our LNCB74 program, which has been prioritized and significant and most of our resources moving in that direction, we also have been very active on the partnering front from a business development perspective. We've got a number of programs that have either been in the clinic or near the clinic that we think will provide important value to a potential partner. In the process of seeking partners for our Layer 2 program, this is our NC410, where we were able to demonstrate significant and important overall ORR in ovarian cancer and CRC patients. Also, our NC525 is an antibody against Layer 1, looking at AML, also seeking a partner. We have two programs outside the oncology space that continue to get some important attention. One is an antibody against SIGLEC15, looking at osteogenesis imperfecta, but also looking at chronic health issues as it relates to the aging population and the impact of osteoarthritis and osteoporosis. Finally, NC1A1 is a humanized monoclonal antibody targeting APOE4. APOE4 is one of the key genetic markers associated with Alzheimer's disease. Both the NC605 and NC1A1 programs are about a year away from the clinic. Hopefully, we'll be able to identify a partner to support the advancement of those programs moving forward. In summary, currently, NextCure is focused on our key value driver, our B7H4 antibody-drug conjugate. We think this is a de-risked approach against a clinically validated target of B7H4. We've got a differentiated linker system for improved safety and efficacy. We're focused on some very important tumor types. We also have a very strong balance sheet to continue to advance this program through clinical proof of concept in the first half of next year with a runway towards the end of 2026. At that point, thank you very much. I thank Needham for, again, providing us the opportunity. Thank you, Michael. At this moment, the floor is open for questions. Maybe I'll start with one. As it relates to your phase one, ongoing phase one study, what do you think the bar is as it relates to results and of efficacy to move forward with the expansion cohorts? That's a great question. I think when it comes to antibody-drug conjugates, most of them are in that 20-25% overall response rate. These are predominantly chemotherapeutic agents that have been linked to antibodies. Our goal is to try to have a go, no-go decision with overall response rates greater than that. I think from our perspective, any response rate over 30% would justify advancing into phase two and more pivotal studies in any of the indications we're pursuing. I think also in the future, there will be the opportunity to combine these with other ADC molecules to further increase efficacy. The goal will be really figuring out ways to manage toxicity and also sequencing on how best to administer one ADC over another. That's another advantage of LNCB74. Since we're taking a tubulin inhibitor approach versus many of the others taking a topoisomerase inhibitor approach, we may be able to really tackle the resistance issue that many of the competitors may see in looking at topo inhibition and resistance. A related question there. What about durability? How important is it in an agent that is a technically targeted chemo? Yeah, durability is always important. That's one of the things we focus on in developing anti-cancer drugs. How long is the effect you see? How frequent do you have to administer the drug when you have toxicity? In In some cases, people have to manage that quite clearly. Durability is really important. It's different for each tumor type. In the various tumor types, one may look for a certain durable response over a certain period of time. Our goal is obviously to look at an improvement over current drugs out there as we look to improve over the standard of care. NextCure has had some experience with a monoclonal antibody for the same target. What lessons have you guys learned from that as you're now moving forward with an ADC? Yeah, so we had a naked antibody approach, NC762 against B7H4 earlier. And we had selected those patients that had high levels of B7H4 expression. We actually learned a lot. We had developed a CLIA-validated test. This was an immunohistochemistry test where most of those samples, we were able to evaluate various levels of B7H4 expression. We think that's going to become really important as it relates to selecting patients that we think will be most responsive to therapy and also looking at maybe even monitoring patients on therapy. In the case of the not too long ago approval of Elahere, which is an ADC for against folate receptor alpha, that approval was predominantly focused on high-level expressors. Our goal is obviously it would be great to be able to treat successfully all patients that express the target. We are going to have the ability and the knowledge to tease out whether or not we are seeing responses in one B7H4 expression level group versus another. Maybe this is a longer-term question, but as it relates to combination studies, what do you think is the strategy there? Is it something you should be looking at during your expansion cohorts, maybe afterwards? Yeah, that is going to be really important. That is one thing oncologists do really well is combining things. The ADC field is kind of evolving in multiple areas. Right now, we are kind of in the midst of looking at existing payloads. I think what we're going to do is people are going to look at combining various ADCs based on expression profiling of different targets because these different targets may be expressed at different periods of time as tumors progress. I think that's going to put a lot more push on killing tumors and to hopefully avoid some of the resistance. The second thing, as I kind of alluded to briefly earlier, is not all ADCs are the same. We're trying to improve safety, but obviously improve overall and durable responses, as you mentioned earlier. I think you're going to start seeing the sequencing of ADCs. Do you start with an ADC with a topo payload, or do you start one with a tubulin payload? Can you go back and forth between those two? There's a lot of work being done preclinically. I think eventually we'll start seeing clinically as various drugs get approved, as people gain more knowledge on how patients are responding to them, and then what resistance, if any, people observe. While people see competition as a negative thing, and I must admit, sometimes I used to see that, in the case of this field, I think it opens up opportunities well beyond what many folks may traditionally think about because there could be multiple drugs approved and used differently depending on the tumor type, depending on the expression level of any particular target, and depending on the payload and the resistance one observes. Okay. It appears that one of the things you guys have optimized for is maintaining the payload on the ADC to improve the therapeutic window. Is there a downside to that as it relates to bystander effect? Yeah, no, we think it's actually going to be helpful by really maintaining the payload and the antibody together as it traffics through the bloodstream into the tumor. I think you're going to see a much greater, more specific delivery of the drug and the cleavage from the linker, and then obviously a bystander effect for those other tumor cells within close proximity. I think we see a benefit of it because what happens is if you're losing drug due to an unstable linker, you're going to have toxicity, and you're going to have to give a patient a much lower dose of the ADC. If you've got a stable system and you're not releasing the toxin until you get to the tumor, you could conceivably, and what we've seen preclinically, actually increase the therapeutic index. Our goal is to actually administer a much greater dose of ADC and get a much greater tumor-killing effect and bystander effect, as you mentioned, and avoid the side effects. Makes sense. I do not currently see any further questions. We are going to end a little early today. Gil, thank you very much for your time. Great seeing you. We hope for positive times ahead. Thank you.