Hello and welcome. My name is Fawzi Khawaja, and I'm an associate at J.P. Morgan. It's my pleasure to introduce our speaker for today, Scott Koenig, CEO and President of MacroGenics. With that, I'll hand over to Scott to get us started. Well, thank you very much, Fawzi, and thank you to JP Morgan for the invitation to present today. I'll be making forward-looking statements during the presentation. Please refer to our SEC filings to understand the risks associated with an investment in MacroGenics. Despite the challenges in the marketplace for the industry at large this past year, in 2022, we were able to build upon our significant achievements of our clinical and pre-clinical pipeline, initiate multiple partnerships, advance multiple collaborations, and extend our runway through upfront in-licensing payments, milestones, as well as the internal consolidation of our employees in multiple facilities. In 2023, we see great opportunities for advancing both our pipelines and our platforms. Over the past two decades, we have built MacroGenics to discover, develop, and commercialize innovative immune-based therapeutics using proprietary platforms that we created or we advanced. The examples of these molecules and our platforms are illustrated here and include molecules such as first-in-class molecules targeting B7-H3 in an ADC backbone. Combination checkpoint molecules that are both validated and new, or they're ligands, as bispecific molecules in a DART configuration or in a multi-con configuration, and next generation DART molecules that engage T cells and to mitigate cytokine release associated with T cell activation. This will allow us to apply and extend an integrated approach for inducing T cell killing, either through direct killing mechanisms or through immune-mediated mechanisms. This is our deep and differentiated pipeline of products. Leading off is MGC018, now called vobramitamab duocarmazine, which is in a clinical study in castration-resistant prostate cancer. This molecule is also being used in combination with lorigerlimab, our PD-1 CTLA-4 molecule, in a dose escalation study in multiple tumors. lorigerlimab is also being examined individually in expansion studies in four different tumor types, updates of this clinical study will be presented next month. Tebotelimab, our PD-1 by LAG-3 bispecific molecule, has shown activity in both late stage non-Hodgkin's lymphoma and solid tumors based on clinical data we've presented to date. While Enoblituzumab, our Fc-engineered B7-H3 molecule, which was in a phase two study in front line head and neck cancer in combination with checkpoint molecules, was stopped in 2022 due to increased bleeding associated with the tumor site. We intend to look at future development of this molecule, possibly, for instance, in prostate cancer, where very encouraging data was presented at ASCO last year in a neoadjuvant study in patients with high risk primary prostate cancer. MGD024 for AML is our next generation molecule, which is now in dose escalation and has been recently partnered with Gilead. IMGC936 is in a 50/50 partnership with ImmunoGen and will complete a phase 1 study in the first half of this year and targets a very novel metalloproteinase called ADAM9. In the past year, we have advanced our pre-clinical pipeline as well with a new partnership with Synaffix around three slots for their linker toxin technologies, and we have been advancing new ADC molecules, going forward, of which the first one is likely to enter IND phase later this year. In addition to these pipeline assets, well, our partner programs provide historical and potential future cash flows to the company and validation of our platforms. The top three partners are listed here as, evidence of great opportunities as exhibited with $150 million of funding that we achieved in the second half of 2022. From these three partners. They include the partnership with Gilead around the next generation CD3 123 molecule, a two slots using our next generation DART CD3 technology, in which we receive $60 million upfront and potentials for $1.7 billion in future milestones. We received a next milestone from Incyte for retifanlimab, our anti-PD-1 molecule. This molecule is now in multiple registration studies, so there's high likelihood for future milestones and royalties. I applaud Provention Bio, who late last year achieved the approval of Teplizumab, an anti-CD3 molecule for the treatment of high-risk patients with type 1 diabetes. We played a significant role in the development of this molecule historically, and with this approval in the United States, we achieved a $60 million milestone and expect future milestones and royalties from continued development of this molecule. In addition to these three top partners, we have a continued good relationship with our commercial partner, EVERSANA, who is selling MARGENZA in the U.S. Zai Lab, who have filed for approval of MARGENZA in China, in which we have additional partnerships around preclinical molecules, and with Janssen around a research non-oncology DART project. Let's look up some of these programs in a little more detail. MGC018 is our antibody drug conjugate targeting B7-H3. It contains a cleavable linker and Duocarmycin toxin payload. B7-H3 is highly overexpressed in most solid tumors. This molecule then binds to the surface of B7-H3 expressing cells, gets incorporated, the toxin gets cleaved in the lysosome, travels to the nucleus, alkylates DNA, and promotes immunogenic cell death. B7-H3 is highly overexpressed in dividing cells on the endothelial cells of tumor vasculature, on cancer stem cells, as well as Treg cells, which induce immune suppression. In studies that we presented updates at an ESMO meeting in patients with castration-resistant prostate cancer, we observed approximately 50% of these patients had PSA 50 reductions of 50% or greater. As noted here on this slide, these patients had very high levels of B7-H3 expression by their H scores, and responses were seen both in terms of PSA responses as well as objective responses even in cases of low B7-H3 expression. We saw responses both in populations that were response evaluable based on the tumor in the viscera and lymph nodes, as well as a subset of patients that had tumor limited to their bony areas. We have been working to improve the tolerability of this molecule and have incorporated in the clinical trials the ability to reduce doses, interrupt doses, and also manage the side effect profiles. This has led to improvement in the side effect profiles. The three top side effects include fatigue, neutropenia, and palmar-plantar erythrodysesthesia, of which, with regard to grade three adverse events, neutropenia represents the highest with much lower levels of the others. Based on the results of these expansion studies in prostate and other cancers, we decided to initiate a phase 2, 3 study called TAMARACK, and with advice to the FDA and the EMA designed the study. Patients who are eligible for this study include those with castration-resistant prostate cancer who have progressed on a taxane and androgen receptor axis targeting agent, and in some cases, a PARP inhibitor, and in a smaller subset, those with a second taxane treated with Cabazitaxel. Stratification factors for this study include presence of visceral disease, prior Cabazitaxel use, as well as geographic region. This was designed initially in the phase two to look at two- experimental arms at two different doses compared to a control arm treated with a second ARAT inhibitor. With regard to the ex-experimental doses, we examined the results from our expansion studies with this molecule. We looked at the pharmacokinetics of both the conjugated drug as well as free toxin and arrived at two doses of two mg per kg on a Q 4 weekly basis and 2.7 mg per kg on a Q 4 weekly basis, with a plan to enroll up to 150 patients in this arm of the study. Once we have established activity and safety that meets our criteria, this study would then move over to a phase three, where one of the experimental arms will be compared to a control. Primary endpoints will include radiographic PFS and secondary endpoints of overall response rate and OS. The study is up and going in the US with multiple sites initiated and patients being screened, and additional sites will be initiated in the US this 1st quarter. We will begin initiating sites in Europe in the 2nd quarter. Now, turning to the next molecule, lorigerlimab, a PD-1 x CTLA-4 bispecific DART molecule. This was designed as a tetravalent bispecific molecule with two binding sites for PD-one, two for CTLA-4, built on an IgG4 backbone. The idea around this molecule was to achieve all the activating T-cell properties of an Ipi-Nivo combination, but reduce the side effect profile, which is typically observed when Ipilimumab is used at greater than 1 mg per kg. In preclinical toxicology studies, we observed all the activating properties of that Ipi-Nivo combination, and in fact, even greater based on expansion of T-cells in the various lymphoid compartments, biomarkers of activation, as well as evidence of ICOS upregulation based on the interaction with CTLA with a much greater safety profile. We were able to treat these patients, these monkeys with up to 100 migs per kg without those limiting toxicity as compared to very toxic doses observed historically of Ipi-Nivo in monkeys. This led to a dose escalation study with planned dosing up to 10 migs per kg, where we did not achieve dose-limiting toxicity. Clinical responses were observed in a number of patients, including a patient with castration-resistant prostate cancer and a stable colorectal cancer, a patient with chemotherapeutic resistance containing a thymoma, and then a patient with serous fallopian tube. These responses were seen at 3 migs per kg. As noted on the right-hand side of this slide, is that expression patterns of PD-L1 were very low or absent in these patients. Given the salutary effects here, we then also looked at biomarkers and observed at very low doses at 1 mig or 3 migs per kg and higher, activation both of CD4 and CD8 cells based on KI67 incorporation, as well as ICOS upregulation in CD4 cells, an indicator of engagement of CTLA-4. Given these positive results, we moved forward in expansion cohorts of four different tumor types and the stable colorectal cancer, castration-resistant prostate cancer, melanoma, and frontline lung cancer. The safety profile of this drug was well tolerated up to 10 migs per kg, with side effect profiles mimicking that of a anti-PD-1 molecule. Given that we were seeing the salutary effects in much lower doses and evidence biomarker activity at these lower doses, and since we were seeing the greatest toxicity at 10 migs per kg, we had decided to reduce the dose in these expansion cohorts to 6 migs per kg on a Q3 weekly basis. We expect to present the first results of this study next month, and as reported yesterday at the GU ASCO meeting here in San Francisco. Now, turning our attention to AML and our next generation CD123 by CD3 molecule, MGD024. CD123 is highly overexpressed on AML cells and AML cancer stem cells and CD3, obviously on T cells. The mechanism in which this is inducing killing is done in an MHC unrestricted fashion. This molecule was designed for a monovalent interaction with each one of those components. An Fc domain was added to this molecule. This was a next generation molecule as compared to Flotetuzumab, which had the exact same variable domain for CD123, but a CD3 component which has now a single amino acid within the CD3, so that you can achieve the killing effect that we saw in Flotetuzumab but have dramatically reduced cytokine release. In addition, because of the addition of the Fc domain, this drug can be given intermittently. The studies in Flotetuzumab indicated the activity in patients with refractory disease and primary induction failure. Now the way this is designed with lower cytokine release and the ability to give this drug intermittently, it opens the possibility of expanding the use of this drug. We are looking to develop this molecule in the context of frontline and late-line AML, myelodysplastic syndromes, and a number of other CD123 tumors, including refractory Hodgkin's disease, hairy cell leukemia, BPDCN, ALL, and others. More recently, as I noted before, we have entered into a collaboration with this molecule with Gilead. This molecule is now in dose escalation in patients. At a previous ASH meeting, we've presented the preclinical data of MGD024 as shown here on the left-hand panel in studies done for tolerability in cynomolgus monkeys. What is observed here is that MGD024 has very little cytokine release as evidenced here for IL-6 as compared to the wild type containing CD3 component similar to that of Flotetuzumab, which showed very much higher levels of interleukin and other cytokine production. On the right-hand panel, we looked in animal mouse animal models of AML, combinations of MGD024 and Venetoclax and Cytarabine as observed here. Those combinations give even greater antitumor responses as compared to the individual agents alone, thus opening the opportunity to combining these agents at early line therapy, using orthogonal mechanism for treatment. Once we have established the dose for this drug, combination studies would likely be initiated with advice from our partner, Gilead. Anticipated 2023 milestones include for vobramitamab duocarmazine or MGC018. We hope to enroll a majority of the patients in the TAMARACK study in 2023 and continue into 2024. The potential for the combination study, as noted earlier of Vobramitamab plus lorigerlimab, with possibilities of updates later this year on the combination study. For lorigerlimab, as I said, we will be presenting the first data on the expansion studies at ASCO GU next month. Plan, and we'll discuss the initiation of a phase two study later this year. MGD024 will continue in dose escalation in the various populations I outlined before. With regard to the preclinical ADC programs that we have been working on in the past year, we plan to submit the first IND late this year for first molecule, then advance additional molecules over the course of the following years. Finally, with the approved and late-stage partnered assets, the launch of Tzield in the type one diabetes population is likely to garner us additional capital. Obviously, the advancement of Retifanlimab in the registration studies is ongoing and controlled by Incyte. Finally, with regard to our financials, at the end of the third quarter, we had $124 million in cash equivalents, but this did not include the $60 million payment from Gilead, the $60 million commitment from Provention. On a pro forma basis, we had about $244 million in cash, believe that this cash will last us through 2024 and into very early 2025 at this point. With that, I will end the presentation and open for questions. Thanks very much, Scott. I have one question from my side. I'll open it up to the floor to see if anyone has any other questions. My question is, what expectations do you have for business development activity in 2023? Well, as, you know, we had a very successful year this past year with regard to business development. In even, in the history of the company since our IPO in 2013, we have brought in over $800 million in non-dilutive capital largely through business development activity and prior to our IPO, additional capital as well. We have very active team working and engaged, both large pharmaceutical companies and biotech companies across our portfolio and a lot of interest across all the clinical and pre-clinical programs we've presented today. We're actually opened up for the possibility of a multiple business development execution this year. Given our history annually of being able to do this, I would not be surprised if we're very successful. Great. Thank you. Let's see if there are any further questions from the floor. If none, we can conclude the presentation. Thanks so much for joining us. Thank you very much. Thanks, Scott.