All right, good morning, everyone. My pleasure to kick things off this morning. My name is Eric Risser. I'm the Chief Operating Officer at MacroGenics, and I'm joined by my colleague, Jim Karrels, our Chief Financial Officer. Moving to the next slide here, I'm just gonna quickly note that I'll be making some forward-looking statements today. Please refer to our SEC filings for additional details on risk factors that will impact our business. For those of you that don't know MacroGenics, I'm gonna quickly provide some overview of the company that I'm gonna dive into a little bit more detail on five of our specific programs. MacroGenics is a developer of next-generation antibody therapeutics. We're committed to discovering, developing, and delivering to patients what can be life-changing medicines for various cancer indications. We have a promising pipeline that comprises four clinical stage programs, and these four programs actually span three distinct mechanisms of action. We incorporate external, drug linker chemistries that we've licensed to support our ADC pipeline. We also have a homegrown platform for delivering bispecific and trispecific molecules that's referred to as our DART and Trident platforms. These have actually been applied in a couple different modalities, including T-cell engagers, but also enable co-blockade of different immune checkpoint molecules. One thing that I like to reference is that we're not just a technology boutique. We are really committed to developing innovative medicines and taking them all the way through the development process so we can translate these early research insights into very robust product candidates that navigate all the complexities of regulatory CMC issues to get actually drugs on the market. We have had three assets that originated in our early development efforts that are now on the market in the U.S.: MARGENZA for late-line HER2-positive breast cancer, TZIELD for type 1 diabetes, and ZYNYZ, which is an anti-PD-1 antibody that was actually approved last month in frontline anal cancer. These three assets are being commercialized by third-party pharma partners and specialty pharma companies, but we still maintain a residual economic interest in all three of these assets. We're very well-resourced to execute against our plan with a cash runway that now extends through the first half of 2027. That includes the $154 million in cash and cash equivalents that we had as of March 31st. Also includes anticipated and projected milestones from projected partners, additional savings from some ongoing cost reduction initiatives. Notably, this morning we announced the transaction with Sagard Healthcare Partners that brought in an additional $70 million. That transaction is highlighted on this slide. ZYNYZ is an asset that was originally approved in Merkel cell carcinoma in 2023. As I mentioned last month, it also garnered approvals in frontline anal cancer. The asset was originally licensed to Incyte in October 2017. You can see we have had meaningful economics realized through that partnership. Through the Sagard transaction, we now recognize an additional $70 million of consideration that we've already received. We'll be paying royalties to Sagard on future global net sales of the asset. You can see the royalty rates are tiered 15%-24%. Once Sagard realizes a 2x multiple on their investment, so $140 million, any residual royalties would revert back to MacroGenics. In terms of our pipeline, we have a host of proprietary programs where we retain global commercial rights. That includes Lorigerlimab, the PD-1/CTLA-4 bispecific molecule. We're very excited about this molecule. We're actually developing it in two different indications, both prostate cancer in combination with docetaxel, as well as in ovarian cancer and various clear cell gynecologic cancers. We have three ADC programs behind that, and these employ the Synaffix platform. This is a Dutch company that was acquired by Lonza. We were an early adopter of the platform and actually got broad access to support multiple development programs, including the three that are listed here. 026 is a potential best-in-class molecule targeting B7-H3 and again, leverages a TOPO1-based payload and their site-specific linker technology. B7-H3 is a very exciting target. Even the recent ASCO presentation, a number of companies have highlighted its broad potential across many different solid tumors. 028 and 030, these are both potentially first-in-class molecules. 028 is in phase one dose escalation, and again, it targets ADAM9, which is also expressed across a number of solid tumors, including several GI cancers as well as lung cancer. 030 is an undisclosed target. We're looking to take this to IND in 2026, and we'll have additional disclosures as we get closer to that event. A number of partner programs, including the three commercial assets I mentioned. We also have a T-cell engager molecule called MGD-024, which is subject to an exclusive option agreement with Gilead, which was in October of 2022. About a year after that partnership was announced, Gilead expanded the relationship with MacroGenics and added a second bispecific molecule, which is listed here on the bottom. Again, a bispecific that is being developed for multiple solid tumor indications. To drill into a little bit more detail, I'll start with Lorigerlimab programs. This is our bispecific immune checkpoint. It has a 2x2 configuration where there are two binding moieties for PD-1, two binding moieties for CTLA-4. Really excited about the potential of this product to be almost a pipeline within a product where it has very broad utility across many different indications. We've already started exploring utility in prostate cancer, the ovarian cancer study that we've recently initiated. We have some ISTs that are also initiated, including one in cervical cancer. This can be an agent that potentially could be used both as a monotherapy, but also as a backbone therapy to support combination opportunities. Some of the early clinical results that we presented at ASCO GU in 2023 was the monotherapy experience in castrate-resistant prostate cancer. We saw a very provocative signal in this study, both encouraging safety profile that meaningfully differentiates from what ipi/nivo combinations have shown in the past, and also saw very provocative efficacy with a confirmed ORR of 26% and PSA 50 reductions in about 29% of the patients. The LORIKEET Study, which is the name of our randomized phase 2 study in prostate cancer, fully enrolled late last year. I'll talk a little bit more about the design of that study. We did have, through the Independent Data Monitoring Committee, a recommendation to continue to proceed based on an early futility analysis in February of 2025. We expect to provide a clinical update on this program, latter part of this year. We also recently initiated the LINNET Study, which is the name of our monotherapy study in ovarian cancer as well as clear cell gynecologic malignancies. The early phase one experience that I alluded to that we presented at ASCO GU is highlighted here. We had 42 patients that were treated. These were typically a late-line population. Actually, 50% of the patients fell into what was either fourth or fifth-line therapy. The vast majority of these patients had prior exposure to both docetaxel as well as AR inhibitor. You can see they had extensive tumor burden with 95% of the patients actually having bone metastasis. On the right, you can see in the swimmers plot that we had very good durability with some patients having continuous treatment over two years. That is really remarkable, especially when you consider the early experience with ipi/nivo in the CheckMate 650 study. In that case, Ipi was only delivered for two or three cycles. Even with that short duration, they saw profound toxicity with both grade five events and, with colitis and pneumonitis. Again, we have not seen any grade five events and notably only one or two episodes of grade three colitis in our entire safety population, which is over 120 patients. You know, very good that we can see continuous blockade of both PD-1 and CTLA-4, and in some cases that extending for over two years. The efficacy profile is shown here with the left panel showing those patients with measurable disease, so about 35 patients where you saw a confirmed ORR of 26%. On the right panel, you see those patients with PSA reductions. Here we profiled the full cohort of 42 patients. What we saw also interestingly was that all the patients with an objective response had deep PSA declines of over 90% reduction. Next slide is just reiterating some of the safety. This is again in the broader population that includes both prostate cancer, but also some other solid tumors. Overall, you know, typical kind of AE profile that you see with immune checkpoints, there are some immune-mediated events, but the most frequent AEs were more of these constitutional symptoms: fatigue, rash, pruritus. As I mentioned earlier, things like colitis, which tends to be a hallmark of anti-CTLA-4 therapy, we really saw, you know, very low incidence there with only one or two grade 3 events reported in this phase 1 population. What we also had done in this study, we incorporated a number of pharmacodynamic markers again to underscore the utility and the activity of this agent. We saw a very good blockade of PD-1 at our recommended phase 2 dose, which is 6 mg/ kg on an every three-week regimen. We also saw good evidence of Ki67 activation, which is a marker for T-cell proliferation. And we also saw ICOS upregulation, which is a marker for CTLA-4 blockade. We're, you know, excited to see that the mechanism here is really driven by this combinatorial approach and the fact that we can actually localize the activity to these double positive TILs and again, avoid some of that systemic toxicity, which is again reflected here with the very encouraging safety profile. The two trials I alluded to earlier are shown here in a little bit of additional detail. LORIKEET, this was a randomized study with 150 patients. It's a two-to-one randomization schema where we're delivering Lorigerlimab in combination with docetaxel, which is a standard of care, especially in patients that have already progressed on a prior ARAT therapy. The control arm here is docetaxel monotherapy. Study fully enrolled, late last year. The primary endpoint is radiographic progression-free survival. It is a time to event endpoint, and we're continuing to accrue those events and hope to provide an update on the status of this study later this year. The second study that I alluded to is the LINNET Study. The study actually has two arms, one focused on high-grade serous ovarian carcinoma that includes up to 40 patients and will be administering Lorigerlimab as a monotherapy. The second arm is focused in clear cell gynecologic cancer. That's where we're exploring a subset of about 20 patients. That's a rare form of gyne cancer, and it actually is typically a much more aggressive form of disease with worse prognosis for patients. It is also a disease that typically is less susceptible to platinum-based chemo and potentially more susceptible to immune therapy. We're very excited to see if we could see an early and provocative signal in that population that could potentially support an accelerated approval path. Switching gears, I'll talk a little bit about the ADC portfolio. Again, the three molecules that I'll describe are all leveraging the Synaffix drug linker technology. The first asset is MGC-026, and that's directed against B7-H3. As I alluded to earlier, a lot of excitement around this target. There are a number of groups that are also developing ADCs, and actually to date, there's been clinical validation established by some of these competing programs across, you know, six or seven indications, including small cell lung cancer, non-small cell lung cancer, prostate cancer, sarcoma, esophageal, nasopharyngeal cancer. Actually, the list is continuing to grow. We see this market as one where there won't be a winner take all, but there probably will be multiple groups that can establish a beachhead just given the expansive nature of the indications that overexpress B7-H3. We are, we do think there are some differentiating features with our drug linker approach that we license, including the GlycoConnect linker that enables you to bind to the native glycan. By doing that, you essentially have no Fcγ receptor binding. One thing that has been noted in the literature, and there was a study published back in 2020 in Cancer Science, which looked at trastuzumab deruxtecan and noted that some of the lung toxicities that were observed were associated with non-targeted uptake in the alveolar macrophages. That was mediated by Fcγ receptor binding. In this case, because you're binding to that native glycan, you really abrogate any binding to the Fc receptors. We also incorporate this HydraSpace linker that enables us to bind to more hydrophobic payloads, which would include exatecan. And then the payload itself, as I mentioned, is exatecan, which does have some salient points of differentiation when compared with deruxtecan, which is the payload that is incorporated in the Daiichi Sankyo molecule. First, it's more potent. We've seen in some of the in vitro models, two- to five-fold higher potency. It's less susceptible to efflux escape mechanisms as well as multi-drug resistance and also has superior cell permeability that potentially affords better bystander killing. This molecule is in the phase one dose escalation. We'll be kicking off several expansion cohorts in selected solid tumor indications, latter part of this year. This slide just highlights again some of the comparative advantages that I noted. So exatecan relative to SN-38, which is the payload employed by Trodelvy, and then deruxtecan, which is again the workhorse payload that is used in many of the Daiichi Sankyo molecules against a number of different targets, including B7-H3. And as I noted, you know, better potency, the linker, which binds to the native glycan, and the benefits of potentially avoiding multi-drug resistance. There's been a number of preclinical studies showing the comparison of Synaffix E relative to deruxtecan. And what's shown here on the bottom is some data generated by Synaffix that was presented at World ADC in 2023, which shows that we can outperform with the Synaffix E payload a trastuzumab deruxtecan molecule, even one that has a higher DAR. In this case, it was a DAR 8 molecule employing the deruxtecan payload versus a DAR 4 molecule with exatecan. This is some of our own data. Some in vivo models, both a lung model shown on the top panel and a melanoma model. Both of these are relatively high expressor cell lines for B7-H3. You can see with a single dose, you know, very good control over tumor growth and reduction and again, kind of a dose proportional increase in control. What we've also done is actually profiled some of the other antibodies, including the Daiichi Sankyo antibody. I've shown that our binder has better internalization properties versus some of these other molecules. We're very excited about both the antibody, the linker, and the payload. Ultimately, obviously, we're hoping that we'll be able to see encouraging activity in the clinic as we move into these expansion cohorts. The second molecule I'll highlight is called MGC-028. This is a molecule that targets ADAM9, a disintegrin and metalloprotease 9. This is a type I transmembrane protein. There's been a lot of literature suggesting that dysregulation of ADAM9 is associated with tumor progression and metastasis. It's also been shown that there's overexpression of this target across a number of solid tumors and that there's an association of overexpression with both severity of the disease as well as overall outcomes. Same overall drug linker that I just highlighted for 026. Again, a DAR 4 construct with the same linker, the same HydraSpace polar spacer, and the same exatecan payload. This is a molecule that actually follows on the heels of a first-generation molecule that was called IMGC936. Also was taken into the clinic. We did see some early evidence of activity in patients, but there were some dose-limiting toxicities related to ocular tox, which we attributed to the platform. That That first-generation molecule was based on a mertansine-based payload. And then again, that's a well-known class toxicity. We haven't seen any ocular events in any of our preclinical models. And again, that was a toxicity that was in fact predictable based on the early cyno data with our first-generation molecule. So we're very encouraged by this, overall molecule. It's in phase one. We just initiated earlier this year, progressing very nicely. We have a number of very committed investigators in this study, and they're starting to move through those, early dose escalation cohorts. Here I profile some of the, again, salient features of the target, including some IHC data on the left panel. You can see across a number of GI cancers, including pancreatic cancer, gastric, colorectal cancer, very nice expression profile. Also in adeno, non-small cell lung cancer, very nice expression profile. We've done actually some comparative testing as well, looking at ADAM9 versus other targets that are, for instance, overexpressed in GI cancers and see a really encouraging profile here with very uniform staining, less heterogeneity versus some of the other targets that we've looked at, and actually very broad expression profile. You know, one example would be a target like Claudin 18.2, which is also being pursued in a number of GI cancers. We think in some of our comparative analysis, ADAM9 actually stacks up very favorably. That's also been shown in some of the PDX work on the right-hand panel across a number of tumor types, colorectal cancer, panc, lung. You can see very good control over the tumor with two doses administered at 10 mg per kg. What's also interesting in some of these PDX models, we have seen, patients where they have not been responsive to prior irinotecan therapy, but do show, you know, very profound, response in these, animal models when treated with, MGC-028. Next up is our MGC-030 molecule. Again, this one we've not disclosed the target, also based on the Synaffix platform, an exatecan-based molecule. We're making nice progress completing some of the IND enabling studies and hope to submit an IND in 2026. As we get closer to that, we'll provide additional disclosure around this program. Again, switching gears, I'll talk about a third modality. This is really the T-cell engager. We have had a number of molecules that we have exposed. This is a CD3-based bispecific with monovalent engagement of CD3, monovalent engagement of CD123, which is broadly expressed in leukemic stem cells. We actually had an earlier generation molecule, which did not have an FC domain. The advantage of this molecule is it does have an FC domain, which enables intermittent dosing schema of every week or every two weeks. We have also detuned the CD3 binder here, actually changed the whole kinetics of the binding of that CD3 arm that also mitigates some of the cytokine release potential that we saw with some of our earlier, first-generation molecules. This molecule is option-based agreement with Gilead that we entered into in late 2022. It is going through dose escalation. and again, given the potency of this class of molecule, we did employ MABEL dosing. So starting at very low doses and then, you know, slowly graduate in terms of higher doses. That's ongoing. Disclosure here is again subject to Gilead making a decision around this molecule. They have an exclusive opt-in right, which they can exercise at some predefined time points during the course of the phase one study. A lot going on at MacroGenics. and as I mentioned, we'll have a number of inflection points, and data updates over the course of the next year or two. Lorigerlimab will have our clinical update latter part of this year. And then 026, 028, both progressing nicely in their phase one studies. We'll be continuing to advance additional molecules, including 030, which will be our next IND. Our research team continues to be a very prolific group with, on average, every 12 to 18 months, they've advanced one new IND. We will have additional updates around some of our partner programs, including the two commercial assets that are highlighted here. ZYNYZ is, you know, really excited about the fact that they garnered additional approvals in frontline anal cancer. That was actually some data that they highlighted at ESMO last year at the presidential symposium as potentially practice-changing data. Then TZIELD, which is the program that's now partnered with Sanofi. Sanofi has guided that the latter half of this year, there will be multiple regulatory decisions related to additional indications, potentially moving into the early onset type 1 diabetes population and potentially approvals in other geographies outside the U.S. As I mentioned at the beginning, we're very well positioned with a cash runway that now extends through the first half of 2027. That includes the $154 million that was disclosed as of March 31, additional anticipated and projected payments from some of the existing partners, some additional cost savings from some ongoing cost reduction initiatives, and then the Sagard deal that was just announced this year. What I'll also note, which is again a real tribute to our company, is the ability to continually finance the business through non-dilutive sources of capital. Actually, over the last three years, we've raised over $550 million from various partnerships and milestones that we recognized. Really tremendous effort from the organization. What I'll also say is this is actually the 10th consecutive year that we've announced a transaction, at least one transaction, in some cases more than one transaction that's brought in additional non-dilutive capital. Extraordinary consistent effort and track record there. You can see that in terms of the revenue that has been generated, and the ability to kind of manage the burn and continue to extend the cash runway. With that, thank you for your attention. We look forward to providing additional updates on the company over the course of this year. Thank you so much.