All right, we're going to go ahead and get started. I am Stephen Willley, one of the senior biotech analysts here at Stifel, and glad to have us here for the last session of the day. Thank you to all who have toughed this out. We have the President and new Chief Executive Officer of MacroGenics, Eric Risser. Maybe before we jump into Q&A, you can maybe tell us a little bit about yourself, how life has changed for you in the CEO seat, and what MacroGenics is looking to execute on here over the next 12 months. I'm happy to do that. Steve, thanks for obviously the invitation to present at the conference. I am new to the CEO role, but not new to the company. Actually, I've been with MacroGenics over 16 years, originally leading the BD function, and then more recently was the Chief Operating Officer, was appointed in August, just a few months ago. I think it was actually the week that I was appointed, we had our first earnings release that I led, and we did define a couple of the real foundational strategic imperatives for the business, and there really were six of those. One, providing additional clarity on our lower durable development strategy. The second was advance our two ADC programs that are in the clinic. One is directed against B7-H3, one against ADAM9, advance another IND against an ADC for an undisclosed target. That's called MGC030. Advance two additional product candidates from our early stage discovery effort, and that team has been phenomenally productive with, on average, one IND every 12 to 18 months. Another feature, which has been again under my remit, is continue to be very active on corporate partnering and continue to forge high-value alliances and partnerships. The last piece was really how do we continue to solidify and strengthen the financial position of the company. Those were the six kind of critical imperatives. We did have our earnings release yesterday, and at least for three of these, we've made some real tangible progress. The team has done a phenomenal job these last couple of months, really rallying behind the key imperatives that I just outlined. There's definitely a heightened sense of urgency and focus across the business, and that's been kind of one of my critical rallying cries for the business. I'll speak a little bit more about some of those specifics. In terms of broader personal background, before MacroGenics, I worked at Johnson & Johnson in a corporate development role, spent about six years with them. I've also been on the buy side, was actually at Bank of America Ventures earlier in my career, and started off as an investment banker at Lehman Brothers. I've been in your shoes as well, working at an investment bank. I've obviously seen a lot of perspectives around biotech and heavily focused on how do we create shareholder value over these coming years. Okay, great. That was a good intro. On the lorigerlimab side, this is the CTLA-4 PD-1 bispecific. I know that there's a couple of other versions of these that are in development. AstraZeneca has one, [Zymeworks] has one. You're looking at this in two indications: prostate cancer in combination with docetaxel, and also in gynecological malignancies. I believe it's a single agent. Is that correct? The GAINS study is a single agent. As you said, the prostate study was a combination study, and that's the one we provide additional commentary. Okay. And so what was the decision, I guess, to stop the LOWERKEY trial, which was the prostate cancer trial, I guess the commentary that I extracted out of the press release would suggest that maybe it was kind of a, it was more of an efficacy issue. I think we know the IO history in prostate cancer has been a fairly checkered one. You're still keeping the LINNET trial active, which is the gynecological malignancy study. Maybe just talk about how you see lorigerlimab now post the discontinuation of LOWERKEY, and maybe why you're still enthusiastic for this asset in terms of the LINNET trial. We have obviously had a lot of development efforts with lorigerlimab across multiple different indications. What really underscored the conviction around this molecule was the early phase I data set, where we did have, again, evidence that with a single recombinant molecule, you can enable co-blockade of these important checkpoint molecules, but also avoid some of the challenges of just conventional combinations of two separate agents. For instance, when you look at some of the early data from IpiNevo, the CTLA-4 blockade induced by Ipi really also leads to not just synergistic activity, but also synergistic toxicity. That is why Ipi is typically only administered for two or three cycles. In that early phase I data set, we did see patients who have been on continuous treatment for over two years. Again, when we look at some of the hallmark toxicities for Ipilimumab, things like colitis, we only had one or two episodes of grade 3 colitis in that study. That is ultimately a function of the way the asset was built, the fact that we have a two by two structure. It is a tetravalent molecule that preferentially binds to TILs that are dual positive for both PD1 and CTLA-4, and enables you to avoid some of that systemic toxicity. That is the design of the molecule, very good evidence of safety. We also had pretty remarkable evidence of single agent activity in a tumor type that historically has been viewed as more of an immunologically inert indication, prostate cancer. We had about a 26% response rate in that early study. That was really what drove the decision to move into a broader study. In this case, with lorigerlimab, we combined it with both docetaxel and prednisone. It was a randomized controlled study, had fully enrolled late last year, and it was really driving towards the primary endpoint, which was radiographic progression-free survival. We were continuing to accrue the events. As we looked at the interim data in October, it was evident that we were not going to meet that primary endpoint. As we thought about overall competitive environment, the broader portfolio, where we really want to shunt our resources to have maximal impact, we decided to not pursue that study anymore. The trial that is enrolling concurrently, and is still actually ramping up nicely with a lot of investigator interest, is the LINNET study. There are two components to that study. One is the platinum-resistant ovarian cancer population, where we are treating with monotherapy lorigerlimab. We know, again, that the single agent PD-1 experience in that population has been more limited, typically single-digit response rates. Again, some of the data from the IpiNevo studies in this same population have signaled meaningful improvement on that ORR, 20%-30%. Again, there is a commensurate increase in some of that safety events. The CTLA-4 blockade is typically limited for only two or three cycles when Ipi is the operative agent. We are excited about this program. We also have another component of this study that is targeting clear cell gynecologic oncology cancers. That is a rare form of ovarian cancer, and we are also not limiting it just to the ovarian subtype, but it is actually an indication that historically is more sensitive to immunotherapy and is also typically more refractory to traditional platinum-based regimens. This could be an opportunity to maybe even get an outside signal. Again, that could potentially afford us some opportunities for some kind of accelerated development path. That is still relatively early on, but again, ramping up nicely. We do have a global footprint for that study, both sites in the U.S., ex-U.S., including some sites in Asia, which will be helpful given that clear cell gynecologic cancer is more prevalent in Asia. Again, a lot of enthusiasm for that study. We do also recognize that, as in many sectors within oncology, there is a lot of competitive activity. Most of the competition with ovarian cancer is probably related to some of the various ADCs that are in development. Mirvetuximab or Elahere is approved, although it is limited to a subset of patients that have higher levels of folate receptor. A lot of investigational agents with some promising activity. Again, the unifying theme with many of those new ADCs is the durability is really a question mark. That is where I think these could actually be ultimately complementary therapies for us, given that a checkpoint molecule and an ADC are really nice orthogonal mechanisms that could support combination therapy. Okay. I definitely want to move to the ADCs here at some point. That is a big part of your story. Just with respect to LINNET, should we expect any kind of update there occurring in 2026? Will you have kind of a similar interim? I know that there is, I think there is a Simon two-stage structure to this trial design. There's a Simon two-stage study, and it's basically 20 patients moving to the second stage of the study. We expect to have a clinical update for the program mid-next year. Okay. And so there's a pre-specified threshold that needs to be achieved in order to trigger enrollment in stage two? Correct. Okay. So let's talk about the ADCs. You guys were kind of in the lead on B7-H3. That program had a little bit of a, I guess, of a reset, I would say. But you still have another candidate behind that. This is now using a topo payload. And would just be curious as to how you think about the opportunity for a topo conjugated B7-H3 in light of, I guess, what you characterized as kind of an expanding competitive heat map, right? It's getting pretty dense around this target. So how are you thinking about developing this drug? There definitely is an intensifying competitive environment for B7-H3 ADCs. I will say, though, that this target has such a fantastic expression profile that covers so many different solid tumors that I think we're still in the early innings in terms of trying to figure out the utility of this program. There are already probably a dozen or so agents, many of them out of China, spanning a number of different solid tumor indications. There's been clear clinical proof of concept across a number of tumor types. Probably small cell lung cancer is the most active area of investigation, but there's also been evidence of activity in esophageal, sarcoma, prostate cancer, and others. I think there's, again, an expanding orbit of opportunity here. We're very excited about the target, but we're also very excited about the antibody. Here we actually have leveraged some of the basic structure of our first-gen molecule. What we have seen is that it is a phenomenal internalizer in terms of an antibody. We've done some comparative testing actually with our antibody versus the antibody in the deruxtecan construct. We think ours is a much more rapid, efficient internalizer. The actual linker that we're employing, this does enable site-specific conjugation. You get a very uniform molecule with DAR4 species, unlike some of the other agents in development. It's also binding to the native glycan in the Fc portion of the molecule, which also renders essentially an inert Fc. We have seen, and there's a lot of growing literature suggesting, that an active Fc can drive engagement of alveolar macrophages based on some of the Fc gamma receptor binding. That may also be a way to temper any of the ILD or pneumonitis that is seen with some of the other agents, including the Daiichi program. The payload itself, not all topo ones are kind of the same flavor. We're relying on exatecan. Again, there's been a lot of data published suggesting that exatecan versus deruxtecan, which is the operative payload with Daiichi and actually many of the other molecules, we think the Hunso molecule is also a deruxtecan derivative. Those are two- to five-fold less potent. Our agent, we believe, is less susceptible to efflux pump and other escape mechanisms. We also see that our payload has better bystander killing activity based on some of the preclinical characterization. We think we have a great antibody. We think we have a great payload, and we think we have a great linker. The final piece is really how do we declare a development strategy that also enables us to navigate around some of the more crowded areas where these agents are being investigated. It is not dissimilar from the early days of PD1 development, where there is obviously a lot of people piling in around this target, a lot of utility across a number of agents. BMS, Merck obviously planted their flag building their initial foothold in melanoma, but then in subsequent years, you saw obviously the utility broaden well beyond that. We think there is still ample room for us to play with this agent. What we also announced as part of our earnings release is we have now selected a dose for initiating dose expansion, and we have two solid tumor cohorts that have now been initiated. A dose or multiple doses? It's a dose that was selected. Do you feel like you've done your dose optimization work, or do you intend to kind of check the project optimist box at a future time point once you have a handle on dose expansion? Yeah. I mean, there's always opportunities for incremental dose optimization. I will say there's also been a lot of experience with this platform, given that we have two molecules in the clinic. Actually, Innovent, which was a Chinese biotech with the same drug linker employed for a Claudin 18-2 construct, they've also had obviously clinical experience. I think we're definitely in the range of what will be a relevant dose, but whether we want to do additional optimization work to follow, that still remains to be determined. I guess with a better internalizing scaffold, and I know the IDXD antibody is, I think that's an old B7-H3 that was developed as a monoclonal along the way, if I remember correctly. It sounds like with a better internalizing antibody scaffold that you have here, there's potentially the opportunity to kind of widen the TI. That's the hope. It also is a function of a site-specific conjugation. Actually, that's been a lot of the data that Synaffix has published, suggesting that it is, in fact, a much wider TI. They have done a lot of comparative analysis across a number of different targets in both primate models as well as mouse models. Do you take advantage of a widened TI by trying to push dose as a single agent, or do you try to take advantage of it for the purposes of combination-based development? It could be both. It could be both. Okay. Maybe another ADC candidate, 028. So this is the ADAM9. I know that you were working on this target previously with ImmunoGen. Again, I think you've taken the same antibody scaffold, if I remember correctly, tagged it with the same Synaffix tech. Where is this program, and I guess what makes ADAM9 an interesting target from an ADC perspective? Yeah. We were an early innovator around this target. You mentioned we did have a first-gen molecule that was partnered with ImmunoGen, ultimately AbbVie. Actually, a lot of learnings from that program that we've been able to leverage and apply to the second-gen molecule. It is the same binding component, but it is a different antibody. We also are relying on the Synaffix platform, whereas the first-gen molecule, we actually had to engineer in our own conjugation handle, and it was a maytansine-based payload, which we knew going into it, maytansines as a class do have the potential for ocular toxicities, and that was a watch-out. It was a predictable tox that we had seen in some of the early cyno models. We were hopeful that that could be managed in the clinic, but ultimately those became a real challenge. Even with supportive care measures and varying dosing models, that was a persistent concern. With the second-gen molecule, we decided to, again, incorporate the Synaffix platform, topo one-based approach. We also like that class of payload, which tends to be better for kind of GI cancers, which tend to be much more prone for MDR and other resistance mechanisms, where maytansines historically have not worked in those kinds of tumors. We do think it is a better overall class of payload. Many of the indications where ADAM9 is overexpressed are GI-related, things like gastric and pancreatic and colorectal. We also see it across a number of thoracic tumors, including lung cancer. This program, we started the dose escalation early this year, moving nicely. We have also seen, again, this is an emerging theme, a lot of copycat molecules. We've seen a number of companies now also signal that, hey, this is a target of rising interest. Duality Bio actually recently initiated their phase one program for this molecule. We're excited that we're obviously leading the pack. We're trying to obviously accelerate the program as much as we can and more to come on this program. Right now, we're still in the dose escalation portion of the phase one. Okay. It sounds like you have one more candidate that's been nominated as a DC. I don't think you will be filing an IND for that this year, correct? Yes. So that's our MGC030 program, again, employing the Synaffix platform with the exatecan-based payload. That's moving nicely with IND enabling studies ongoing. Expectation is IND would be submitted next year. Okay. If I were to scale risk from zero to five, and put B7-H3 at zero, just given the clinical validation that we have, right, just in terms of the target biology, maybe put ADAM9 at like a four or a five because there is still some uncertainty around the target itself, right, when you conjugate the payload. You're a tough grader. Where does this new target fall in that spectrum? This is a target where some of the biology is understood. Just like ADAM9, where there has been some learnings from our early clinical program that we've been able to apply and essentially de-risk the proposition, some of those same features are evident with O30. It is a target that has been studied before, and we've been able to buy down risk based on some of the early preclinical work and some of the toxicology work that we've done. Again, we're excited about this as a target given that it also has a broad expression profile. A number of solid tumors express the target. There is also some evidence that there is association with target expression and disease severity and outcomes in patients. There is literature around the target, but we do think we're well positioned to potentially have a first-in-class program. That is one we're also aggressively moving forward. Okay. Maybe it is more like ADAM9. Maybe I am a tough grader. Maybe just a bigger philosophical question. I think there is a lot of uncertainty right now as to how all these topo ADCs are just going to kind of find a home within the treatment algorithm, right? I think it is different for different tumor types. I think you talked about ovarian before, and yeah, there are a number of actionable targets against which ADCs are being developed now, whether it is CDH6, NaPi2b, folate receptor, etc. How do you think the sequencing thing is going to play out here, right? Is it going to be ultimately, is a physician going to ultimately have to make the decision that I'm going to get one swing with the topo ADC in this patient along their treatment journey, and it's going to be with this antigen in this line of therapy? Yeah. There will be growing issues with topo1-based resistant paradigms where you won't see probably. There has been data also suggesting that retreatment with another topo1. I know with Daiichi and HER2, people have seen that in those later line settings. It is increasingly challenging to induce a response. Now, for some programs, they do rely on patient selection based on density of target expression. Folate receptor, for instance, with the mirvetuximab soravtansine, is still relegated to those 30% of patients that have higher levels of folate receptor. There may be some white space just based on that, but there are also examples of agents that are approved or will likely be approved indiscriminately. I think there will be, and this is an opportunity for topo one, given that the overall tolerability tends to be manageable to kind of go into earlier line patients as well as explore combinations. I think you're already seeing many of the big pharma interest to exploit checkpoint combos. Pfizer has been very vocal around that, and Merck and BioNTech are obviously all mobilizing efforts. In some cases, even combinations with other types of systemic chemo. Even at ESMO, there were a number of sessions highlighting all the combination opportunities across things like DDR and checkpoints and others. I think that will likely be an opportunity given that we do have three modalities within our portfolio, ADCs being one, but also the biospecific checkpoint molecule, T-cell engagers. We've been an early innovator in that space and are continuing to extend our efforts in that arena. These are also potentially opportunities in the future for combination therapy. In fact, you see some groups already taking advantage of that. Merck, for instance, is doing combos with their DLL3 program with B7-H3. Amgen with their tarlatamab is doing some combos with a Chinese company that has a B7-H3 ADC. I think that will be an increasing opportunity to kind of address these potential resistance mechanisms. Yeah. I think those experiments are really interesting. I know small cell is kind of like the proving ground for that now, just given that's where those assets are located, but I would expect to see a lot more of these ADC-TCE combos. Maybe on the TCE front, you do have a program. You are currently running the phase one for this. It's a CD123, CD3. I know Gilead has an option to this program at some point in phase one. I know yesterday you talked about how this Gilead collaboration has even further expanded, right? Maybe you can talk about the update there. I know non-collaborative revenue securitization has been a big part of the MacroGenics story. It continues to be a big part of the story. Maybe you can just talk a little bit about the Gilead collaboration 024 and where you see an opportunity for more of that collaborative revenue. Yep. I'll just echo what you just alluded to. Yeah, we've been very prolific, but very productive on corporate deal-making. I think every year for the past decade, we've announced at least one partnership. The initial collaboration with Gilead started back in 2022. Late 2022, we signed our first deal, which really covered the MGD024 construct that was the CD123, CD3 molecule. That continues to progress in phase one. About a year after that initial partnership, they extended it with the second molecule, which incorporates our proprietary Trident platform to enable trivalent targeting. As you alluded to just recently in the last couple of days, we've now cemented a third program, which is a DART bispecific. It is a T-cell engager approach, but again, we're continuing to integrate learnings from prior generation efforts and trying to improve on the features of our T-cell engager platform. This kind of represents the continued evolution of that. They have an undisclosed molecule that is part of that license agreement. Three assets are moving all under Gilead. Very excited about that relationship. It is also consistent with the themes of partnering in the past. We have had a lot of repeat collaborators that, once they start engaging with our teams, especially the research group, which has been really so adept at both immunology, protein engineering, early development, that big pharma really welcomes the opportunity to work with that team. Are you working closely with Gilead on the phase one development program in terms of what you are trying to interrogate? It's a very integrated effort. We are really leading the charge on the operational side, but there's a joint governance committee that is very much synchronized in terms of the evolving strategy for that program. Okay. And then maybe just lastly, you can touch upon the Sanofi collaboration that's still paying dividends from the TZield deal that you did. Does the designation, does the CNPV designation for that asset somehow accelerate the milestones that you might now be able to collect from that? Yeah. What you alluded to is we did disclose two additional milestones from Sanofi in the last couple of months, triggered $50 million from Sanofi related to TZIELD. That's on top of the $25 million that we just recognized from Gilead. $75 million, that will be all paid out in Q4. It was not reflected in the cash balance. We've had a lot of non-dilutive capital coming into the company. In fact, in the last three years, over $600 million of non-dilutive capital has come into the company. There are significant opportunities in the future for additional money to come in based on some of these existing partnerships and also the commitment that we are to continue to be active on partnering going forward. Okay. Maybe just to finish up, you can talk about where that pro forma cash now stands and what that allows you to execute on. Yeah. As of the end of September, cash and cash equivalents is $146 million. The $75 million, that will be a subsequent event that will ultimately collect in Q4. We did extend our cash runway guidance, so we're really excited to be able to do that. Now it is into late 2027. Okay. Presumably that gives you a number of data reads on a variety of the assets that we talked about. Exactly. All right. If there's no questions in the room. Eric, thank you very much. Really appreciate it. Thank you. Thank you Thank you so much. Take care. Yep. Take care. Yep. Take care.