Good morning, and welcome to the Thursday morning session of the 42nd annual J.P. Morgan Healthcare Conference. My name is Alex Kramer, and I am an associate on the healthcare investment banking team at J.P. Morgan. Today, it is my pleasure to introduce our next presenting company, MacroGenics, and our presenter today, Scott Koenig, CEO of the company. The format today will be a 20-minute corporate presentation, followed by Q&A. With that, Scott, the floor is yours. Thank you, Alex, and thank you very much for the invitation to present at the J.P. Morgan conference. I'll be making forward-looking statements during the course of this presentation, so please refer to our SEC filings to understand the risks associated with an investment in MacroGenics. 2024 looks to be a very exciting year in MacroGenics. In 2023, we built on the successes of our preclinical and clinical portfolio and significantly advanced our cash runway. Since the inception of the company, we've been committed to the development of innovative immune-based therapeutics and their commercialization, derived from molecules from our core platform technologies. Building on our track record of three approved products that came from our pipeline, our current lineup of differentiated antibody-drug conjugate molecules, our bispecific DART molecules and multispecific DART molecules, two clinical assets moving towards completion of phase II studies in metastatic castration-resistant prostate cancer, and a third study in prostate cancer, which will begin this year as an IST, plus two new pipeline molecules moving into the clinic, which are ADCs, positions us quite well for inflection of value for the company. Now, we have been focused on expansion of our efforts within antibody-drug conjugates, and this is derived from the fact that we've had over 20 years of experience in antibody engineering, plus lots of experience in selection and identification of promising targets. Coupled with this is our development capabilities and our in-house commercial-scale monoclonal manufacturing capabilities, complemented by a very experienced external supply chain, and with this, a number of partnerships around ADC technology, which provides us with leading-edge linker toxin technologies that we can choose from. Now, this is our deep and differentiated pipeline of proprietary products. Leading off is vobramitamab duocarmazine, which is an ADC molecule targeted at B7-H3. We recently completed enrollment in a study called TAMARACK in metastatic castration-resistant prostate cancer and are using the same molecule in combination with lorigerlimab, our DART bispecific PD-1 CTLA-4 molecule. Independent of that, lorigerlimab is being tested in a study called LORIKEET, also in metastatic castration-resistant prostate cancer in combination with docetaxel. Enoblituzumab, our Fc-engineered anti-B7-H3 molecule, will start a new phase II study in the treatment of neoadjuvant prostate cancer. IMGC936 is an ADC molecule that is completing phase I development in partnership with ImmunoGen. Tebotelimab, our second, combination checkpoint molecule targeting PD-1 and LAG-3, shows promise both in DLBCL and solid tumors, and a recent publication of this work has been published in Nature Medicine. MGC026 will be the first of potentially seven new ADC molecules coming from our relationship with Synaffix, and we expect to begin dosing patients this quarter. We have additional ADC molecules being developed with the Synaffix technology. Now, our partner programs have provided both historical and potential future cash flow to continue to support our programs. Most notably, since 2022, we have brought in $335 million of non-dilutive funding, and we have up to, actually greater than $1 billion of potential further milestones remaining from Incyte and Sanofi, from the ZYNYZ molecule and TZIELD molecule, respectively. We have a strong collaboration with Gilead around MGD024, our CD123 by CD3 bispecific molecule, that's in dose escalation in hematological malignancies. And recently, a second molecule, a DART molecule, has been nominated, it for development in our research group. On top of this, we continue our relationship with Eversana on the commercialization of Margenza. Now, we had last year a greater commitment and expansion of our efforts within prostate cancer. As I noted, the vobramitamab duocarmazine molecule just completed in 2023 enrollment in a study called TAMARACK in metastatic castration-resistant prostate cancer, and we hope to have results by mid-year, which will then form the basis for selection of a dose to move forward into phase three. Lorigerlimab, the bispecific molecule, is enrolling in a chemo-naive metastatic castration-resistant prostate population in a study called LORIKEET, and we expect to completely enroll this study this year, and if enrollment goes as expected, hopefully to provide the first data cuts later this year. Enoblituzumab, the Fc-engineered molecule, is in a study called HEAT. This will be a phase two study. It's expected to begin enrolling this quarter in patients with Gleason 8-10 and will be given as 6 doses prior to prostatectomy in these patients. This is a controlled study, and these patients will be observed for metastatic disease in a very intense fashion, including measurements of PSA, PSMA PET, and circulating DNA. Now, let's look at some of these molecules in a little more depth. The vobramitamab duocarmazine molecule, as illustrated in the cartoon in the left, target is B7-H3 and has a cleavable linker payload called duocarmycin. B7-H3 is overexpressed on most solid tumors and is expressed both on dividing and non-dividing cells. The antibody will bind to the surface of the B7-H3 on the cells, will be taken up, the toxin will be cleaved, and will migrate to the nucleus, where it will alkylate DNA and promote immunogenic cell death. Release of that toxin will allow for bystander killing. Expression of B7-H3 is seen on the dividing tumor cells, on the endothelial cells in the vasculature, on so-called stem cells, and as well as on T-regulatory cells, which induce suppression to the tumor. Now, at the ESMO 2021 meeting, we presented expansion studies for our prostate cohort of approximately 39 patients, where about half those patients had a PSA 50 reduction from their baseline values. These included patients with RECIST-evaluable lesions, as well as those with only bony disease. As illustrated here on the bottom, as you see, B7-H3 expression is quite high, with H- scores in the majority of these, of these individuals greater than 200, but responses were even seen with those with lower H- score values. Now, in an attempt to improve the safety profile of this drug, after the dose escalation study, we included the ability to include dose reductions, dose interruptions, and obviously medical management of side effect profiles. The three major side effects observed were fatigue, neutropenia, and palmar-plantar erythrodysesthesia, with grade threes greatest in neutropenia, although this was mostly a laboratory value with no evidence of increased infections or febrile neutropenia. However, we decided that it was important to continue to improve the safety profile of this drug, so we have moved forward into the so-called TAMARACK study, where we're enrolling patients with metastatic castration-resistant prostate cancer who have progressed on at least one androgen receptor targeting agent and up to one docetaxel-containing regimen. Stratification for this study include those with visceral disease, prior taxane use, and their geography. The original intent of the study was a 1:1 randomization of vobramitamab duocarmazine at two mg per kg every four weeks, compared to the original start of three mg q three weeks in the expansion study, which I just described. The other experimental arm is vobramitamab duocarmazine at 2.7 mg per kg every 4 weeks. Enrollment of the study was very robust, where we enrolled the entire study in less than six months, and in fact, far exceeded the enrollment targets, having allowed in patients who had been in the screening process, where now we have more than 150 patients that have been enrolled in this study. Primary endpoints for the study are rPFS, with secondary endpoints listed here, including PSA, duration of response, overall response, and various other values as listed here. Obviously, we are going to monitor these things for AEs and looking for improvement beyond the original dosing strategy. We hope that this will provide the dose to move forward for phase three. We would plan to design that in mid-year, and then move forward, hopefully for a start of a phase three study in 2025. Now, lorigerlimab, the PD-1 CTLA-4 molecule, was designed to improve upon the historical side effect profile of combinations of ipilimumab and nivolumab, which had shown improvement of responsiveness, but particularly very severe side effects, often manifested by GI toxicities. As you see on this cartoon on the left-hand side, this is a tetravalent bispecific molecule with two binding sites for PD-1 and two binding sites for CTLA-4 on an IgG4 backbone. This was designed in this manner so that binding would be enhanced to cells that were co-expressing PD-1 and CTLA-4, which are typically enriched and exhausted in the tumor microenvironment, but to improve upon the safety profile, because IgG4s do not mediate ADCCs, this would mitigate against the destruction of T-regulatory cells, which control much of the autoimmune disease. And sure enough, when we initially gave this drug into our toxicology studies in cynomolgus monkeys, we were able to dose up to 100 mg per kg, saw all the T-cell activating properties that one was seen in an Ipi-Nivo combination, but did not see the side effect profiles which were observed, particularly GI toxicity in the monkeys in their toxicology studies. We then went forward in a dose escalation study, where we did not reach dose-limiting toxicity up to 10 mg per kg on a Q3 weekly basis. We had full saturation of PD-1 positive cells at 1 mg per kg and higher. We saw evidence of objective responses in a number of tumor types at three mg per kg. In addition, we saw biomarker evidence of T-cell activation in both CD4s and CD8s, including ICOS upregulation, which is a marker of CTL, CTLA-4 engagement in CD4 positive cells. As shown here on the right side, responses occurred even in individuals that had very low PD-L1 expression on their tumors. Given the good responses and good safety profile of this drug, we moved forward into four expansion cohorts at 6 mgs per kg on a Q3 weekly basis. We presented the cohort of patients with metastatic castration-resistant prostate cancer at the ASCO GU meeting last year, where we observed an objective response rate confirmed of about 26% and a PSA 50 response rate of about 29%, which you should note here on the right-hand side, all the patients who achieved objective responses had PSA reductions of 90% or greater. At this point, many of these patients continued on therapy, and two of them, to this date, are still on study two years later, receiving the lorigerlimab on a Q3 weekly basis. This compares, as you know, that ipilimumab is only given as four doses, where nivolumab is given on a Q3 weekly basis. The side effect profile was that similar to that of other anti-PD-1 molecules, with the foremost common adverse events being fatigue, rash, pruritus, and hypothyroidism. In 127 patients treated at 6 mg/kg or greater, we saw only one grade three colitis in the study. With this, at the same time, at the same meeting that we presented this data, again, here listed on the left-hand side, the final results of CheckMate 650 from the Bristol group was presented for a combination of nivolumab and ipilimumab in a similar population. And as noted here, with the typical dosing of Nivo three, Ipi one, with four doses of Ipi, they saw only a PSA50 response of 13.8% and an overall response of 9.3%. And as shown here on the right-hand side, and consistent with many of the other studies conducted with pembrolizumab, there has been no effective dose found in the treatment of castration-resistant prostate cancer. So given our favorable results here, both in terms of activity, the ability to give this drug on a continuous basis, and an acceptable safety profile, and the fact that there is no approved checkpoint molecule for prostate cancer, we decided to move forward with the LORIKEET study, moving one line up in chemotherapy-naive, castration-resistant prostate patients who have progressed on an androgen receptor-targeted agent. This study began enrollment in the fourth quarter of last year, and we expect to complete enrollment this year. Stratification factors, again, is a visceral versus bony-only disease and geographic region. This is a 150-patient study, 2:1 randomized, where patients will receive standard-of-care docetaxel plus lorigerlimab for 100 patients, and docetaxel in a control group, with primary endpoints of rPFS. Secondary endpoints: overall response rate, PSA 50s and 90s, duration of response, and time to progression. Again, we hope to enroll this study this year, and in fact, if we enroll the entire study in the first part of the year, we may be in a position to begin to discuss the results later this year. In addition, we are also moving forward with our combination study of vobramitamab duocarmazine and lorigerlimab, where the goal here is to identify lower doses of each one of those molecules, when used in combination, would produce fewer adverse side effects and greater effectiveness. We expect to move forward in an expansion cohort in the first half of 2024, and that would include a cohort of castration-resistant prostate patients, as well as other solid tumors. And finally, MGD024 is our next generation CD3 redirected bispecific DART molecule. This was designed with a CD123 variable domain, which targets the alpha chain of the IL-3 receptor, which is highly upregulated on leukemic cells and leukemic stem cells, and a CD3-targeted molecule. The differences of this molecule compared to our first generation DART molecule, flotetuzumab, is there a single amino acid substitution within CD3 that allows for the induction of cytotoxicity, similar to that observed with flotetuzumab, but a dramatically reduced cytokine release profile. Incorporated in this is also an Fc region with an extended half-life. Currently, the study's in dose escalation. This study was, there's an option-based deal with Gilead, which we are in the middle of dose escalation, and they need to make a decision with regard to opt-in by the end of phase one. The opportunity here is quite large, with the ability to treat patients with acute myeloid leukemia, both early and late-stage disease, and other CD123 malignancies, including refractory Hodgkin's disease, ALL patients, patients with hairy cell leukemia, as well as BPDCN. So finally, our financial overview. At the end of the third quarter, we had 256 million in cash. Pro forma, we had 272 million in cash, with $15 million, a little more than $15 million coming after the close of the quarter. We expect our runway to last into 2026. So finally, the anticipated milestones for 2024 include the top-line data in the first half of 2024 for the TAMARACK study with vobramitamab duocarmazine, and the commencement of the expansion studies of the combination with lorigerlimab. Depending on the rate of completion of enrollment of lorigerlimab in the LORIKEET study, we hope to provide some clinical updates in the second half of this year. And then we're very excited, as I started out with, with our emerging antibody-drug conjugate portfolio, with initiation of dosing this first quarter for the first one of these molecules from the Synaffix technology, using a topoisomerase inhibitor called MGC026. Our second IND for MGC028 is expected later this year, and we plan to present preclinical data on both these molecules in the first half of this year. And then, I should note that our partner assets, there may be additional updates this year, with ongoing two phase III studies for ZYNYZ in frontline lung cancer and anal cancer, and plans by Sanofi for TZIELD, based on a successful phase III study in new-onset type 1 diabetes, to apply for regulatory approval of that molecule. And then, our ongoing relationships, particularly with Gilead, regarding MGD024 and the dose escalation study. And with that, I'm open to questions, and thank you for your attention. Thank you very much, Scott. One question from me to start things off. How would you define success for the top-line data readout that you're expecting later this year for vobramitamab duocarmazine in the TAMARACK study? Well, thank you very much, Alex, for that question. And so, as I presented today, for example, we had shown in the 3 mg per kg q3 week initial dosing in the expansion, a prostate study, approximately half those patients had a PSA50 reductions, and approximately a quarter of the patients, as we presented at that time, having a objective responses at that time, both confirmed and unconfirmed. What we have right now is a very good metric based on Daiichi's 7300 data, which was recently presented at ESMO, where they've treated approximately 50 patients with a similar castration-resistant prostate cohort post taxane and ARAT treatments. And there, historically, they had shown a PSA50 in the low 20s, 20%-23%. They saw an objective response rate of 25%, an rPFS of 5.3 months, and overall survival at that time of about 13 months. So if I put this in context, what I feel that is potential for us to achieve through the TAMARACK study is, number one, a PSA50 response likely to be in the 40%-60% range. Acceptable, as we have heard, based on other treatment paradigms, is a PSA50 rate greater than 30%. But as I said, we're trying to hit higher values there. We'd like to have, obviously, at least a 25% ORR response in response-evaluable patients. rPFS, we'd like to beat what Daiichi had reported, of at least six months or greater. Then finally, we have not defined the overall OS, because at this time, we won't be able to do that, given the short follow-up on those patients. Now, one of the most important things and why we're doing this study, and we have discussed this at length, is one of the side effect profiles, which we described today, was a palmar-plantar erythrodysesthesia. While we saw very few patients with grade threes, when a patient develops a grade two response, they get swelling and redness in their extremities in addition to pain, and it's the pain that makes it grade two as opposed to a grade one. Grade one is not a big deal because it, you have red hands and a little swelling, but when they develop pain in their fingers, particularly in their feet, it becomes difficult. So many of the patients who experienced this came off our original study. Our goal would be to see a reduction in grade two to grade one, or also complete the drop in incidence of that side effect profile. In addition, we'd like to obviously improve on the other safety profiles of the drug as well. The bottom line is we'd like to see even further effectiveness of what we've reported from the original study and a better safety profile than we have reported to date. Great. Thank you. And then what expectations do you have for business development in 2024? Well, as you know, Eric Risser, our Chief Operating Officer here, who is been instrumental in our deals in business development and his team. We have, as you know, and what we showed here with all the non-dilutive capital we brought into the company, if you actually go back since our IPO, we've brought in about $1.4 billion of non-dilutive capital from various business development partnerships and other sources. We have constant interaction with both the large pharmaceutical companies, biotech companies, and smaller companies as well, trying to take advantage of our vast pipeline, both of early and late-stage disease. We have said that we've had very strong interest, obviously, around the vobramitamab duocarmazine molecule and B7-H3 program, and it's been particularly heightened, as many of you know, that Daiichi and Merck entered into a collaboration late in 2023, in which Merck paid Daiichi $2 billion upfront for a 50% share of the development of that molecule, and subsequently, there's been a number of other B7-H3 targeted deals. We have been engaged with many of the pharmaceutical companies who expressed strong interest in that. We have not shown them any data. We've wanted to see the maturation of the data before we had some discussions. Given the competitive landscape here, I could envision if, obviously, we achieve what we want from the profile of the drug, and we want to not only develop this for prostate cancer, but for a whole range of other tumors. And in that context, I should say, which I didn't comment earlier, is that we are planning to move forward into multiple other tumors later this year, as we have defined the optimal dose going forward in the prostate TAMARACK study. So I would imagine we'll have engagement on that. In addition, given that we're having a large portfolio of ADC molecules, and given, again, the increased enthusiasm for new ADC molecules and interest even at earlier stages of disease, I would not be surprised that some business development may occur in targeted some of those molecules as well. Great. And then with so many expected readouts, I mean, if you just even look at this page right here, with so many expected readouts in the next 18-24 months, what do you think will be the key to meeting all those objectives that you and the company are setting out to do? Well, as you know, in running this business now for 23 years, obviously, having adequate quick cash to execute on our plan, we have a very experienced team. What we have the luxury of, it's a fully integrated team, and as I demonstrated in one of the slides, it goes everything from early discovery of platforms and targets, all the way to commercialization, including our own manufacturing facility that's at commercial scale, as well as very experienced clinical and preclinical development groups. So we feel that we have enough capital right now to get the readouts on these programs, and obviously, this is not a one shot on goal situation. With multiple shots on goal, we think we're in a very good position, obviously, to get additional sources of capital to continue the growth of the company. And then one more question from me, and you touched on it a little bit there. Just in terms of the preclinical portfolio and the progress you've made there, I guess, what additional light can you shed on that piece of the business in terms of what you're most excited about coming out of that? From the preclinical side, what we've been public about is mostly, as I described today, the ADC opportunity here. Just to put it in context, we feel, based on what Synaffix has presented, as a comparator of their ADC technology versus, for instance, deruxtecan from Daiichi and other Topo I inhibitors, it could be a much superior platform. So by having initial dosing this first quarter of this year of the first one of these molecules, with that technology, the opportunity later in this year to validate that, and as I said, we'll have a second molecule with the Topo I, and we're now planning targets three, four, etc. Validation of that in the clinic, as you can imagine, could spur lots more interest, given that, as I pointed out, our company has a strong history of identifying very good targets to move forward. So we have the variable domains for many of these molecules. We have the technology to develop that. As I said, both the manufacturing and the supply chain is all set up. So this could be a really very active opportunity to put one or more INDs on new molecules through, which could become both the opportunity for organic growth of our own pipeline, but also for business development opportunities. Thank you very much for that. Thank you very much for the presentation. I think if no further questions, I think we can conclude the presentation there. Thank you again, Scott. Thank you!