Good afternoon. Thank you for stopping by. Welcome to the Cullinan Therapeutics Genrix Bio License Agreement Conference Call. As a reminder, this call is being recorded. If I think that you may find helpful while listening to this call, it is available on the events section of Cullinan's Investor Relations website at investors.cullinantherapeutics.com. It is now my pleasure to turn the call over to Nick Smith, Head of Investor Relations at Cullinan Therapeutics. Please go ahead. Hello everyone, and thank you all for joining us on today's call to discuss our agreement with Genrix Bio for a global ex-Greater China all-indication exclusive license to Velinotamig, a BCMA x CD3 bispecific T-cell engager. My name is Nick Smith, and I am the Head of Investor Relations at Cullinan Therapeutics. Before we begin, I would like to remind you of the safe harbor provisions outlined on slide number two. During today's presentation, management will be making certain forward-looking statements which are based on current information, assumptions, and expectations that are subject to change and involve risks and uncertainties which may cause actual results to differ materially from those contained in such forward-looking statements. These risks are described more fully in the company's filings made with the Securities and Exchange Commission, including our annual report on Form 10-K. You are cautioned not to place any undue reliance on these forward-looking statements. In addition, this call contains time-sensitive information, accurate only as of the date of the live broadcast, June 4th, 2025. Cullinan undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this call. As shown on slide three, joining me on the call today are Nadim Ahmed, Cullinan's Chief Executive Officer, Dr. Jeff Jones, Chief Medical Officer, and Mary Kay Fenton, Chief Financial Officer. It is my pleasure to now turn the call over to Cullinan CEO Nadim Ahmed. Nadim? Thank you, Nick, and welcome everyone to our call today to discuss a very exciting development for our immunology portfolio and our company at large. We're very much looking forward to providing you with an overview of our licensing agreement with Genrix Bio for global rights outside of China to Velinotamig, a clinical stage potential best-in-class BCMA x CD3 bispecific T-cell engager, which we plan to develop in autoimmune diseases. Shortly, I will ask Dr. Jeff Jones, our Chief Medical Officer, to provide an overview of the molecule and the scientific rationale for the transaction. Mary Kay Fenton, our Chief Financial Officer, will review the terms of the deal and its financial context. First, I want to point out the strategic significance of this deal, which provides an important opportunity for Cullinan to solidify our leadership position in T-cell engager development for autoimmune diseases. The addition of Velinotamig to our pipeline also expands our ability to impact more patients across a broader set of autoimmune diseases. We firmly believe T-cell engagers represent the next wave of innovation in autoimmune diseases. We're also excited to leverage our core internal expertise with T-cell engagers, as well as the immunology KOL relationships we've built to develop another potential best-in-class clinical stage program. Under the agreement, Genrix Bio will execute a previously planned phase I study in China in patients with autoimmune diseases, planned to begin later this year. Cullinan expects the data generated will allow us the opportunity to accelerate the global clinical development of Velinotamig as we move the program forward outside of China. Following completion of the study, Cullinan will conduct all further development of Velinotamig in autoimmune diseases. Adding a BCMA x CD3 bispecific T-cell engager to our pipeline complements our global clinical development of CLN-978, our CD19 x CD3 bispecific T-cell engager, creating the opportunity to address the needs of more patients across a broader range of autoimmune diseases than either molecule alone. We continue to rapidly advance CLN-978 in diseases best addressed by broad B-cell depletion. The addition of Velinotamig to our pipeline opens up new opportunities to address autoimmune diseases that are driven by long-lived plasma cells. We're leveraging the strength of our balance sheet to transact this deal for a clinical stage molecule with best-in-class potential and favorable economics for Cullinan that can generate additional value-driving catalysts. Importantly, as a result of refining our oncology pipeline, we can reiterate our existing guidance to have cash resources into 2028. Despite advances in care, the prevalence of autoimmune diseases continues to grow. Patients are in need of treatments that deliver durable disease remissions, especially approaches that allow them to come off chronic background immunosuppressive therapies. With Velinotamig and CLN-978, we now have the opportunity to address a broader range of autoimmune diseases through both B-cell and plasma cell depletion. CLN-978, which targets CD19, is in active clinical development in systemic lupus erythematosus, rheumatoid arthritis, and Sjögren's disease. Velinotamig, which targets BCMA, has the potential to address multiple diseases which are driven by self-reactive long-lived plasma cells, and we're currently reviewing target indications of interest. With a comprehensive and diverse approach to autoimmune diseases, we now have even more opportunities to match the right target with the right patient. Now, to dive deeper into the scientific rationale for BCMA and the clinical profile of Velinotamig, I will turn the call over to Dr. Jeff Jones, our Chief Medical Officer. Jeff? Thanks, Nadim. Beginning with slide six, you will see that BCMA picks up where CD19 drops off. CD19 has broad expression across the B-cell maturation continuum but spares long-lived plasma cells, making CD19 and BCMA complementary development targets to address a wider range of autoimmune diseases than either target alone. B-cell dysfunction is central to the pathogenesis of many autoimmune diseases, and broadly depleting these cells by targeting CD19 can affect an immune system reset. On the other hand, the autoantibodies produced by long-lived plasma cells are more important to the pathophysiology of other autoimmune disorders. In these diseases, targeting BCMA on antibody-producing cells has the potential to offer a disease-modifying outcome. Moving now to slide seven. BCMA-directed agents have revolutionized the care of patients living with malignant plasma cell disorders, most notably multiple myeloma, the indication for which multiple BCMA-targeted therapies are now approved. More recently, academic investigators have shared initial clinical data demonstrating the potential for BCMA-targeted T-cell engagers in autoimmune diseases. Last year, German investigators at FAU Erlangen-Nürnberg and Charité University Berlin characterized the activity of the BCMA x CD3 T-cell engager teclistamab in a small series of patients published in the New England Journal of Medicine. As shown here, an abbreviated schedule of teclistamab treatment resulted in swift and marked reductions in autoantibody titers that correlated with depletion of plasma cells. Clinical manifestations, variously measured by disease-specific assessments, improved in all five of these treatment refractory patients, providing initial proof of concept for the therapeutic potential of targeting BCMA in autoimmune disorders. Velinotamig is introduced on slide eight. Velinotamig is a one-to-one IgG-like molecule. Velinotamig has high affinity for BCMA and lower affinity for CD3, designed so that the bispecific antibody recruits and activates T-cells to deplete BCMA-expressing cells while limiting nonspecific T-cell activation. A rigid hinge region enhances synapse formation between T-cells and BCMA-expressing target cells, and lower risk for immunogenicity is engineered by using common light chain. While initially studied using IV administration, subcutaneous administration is feasible and currently in development. On slide nine, we share more detail about the clinical development plans for Velinotamig. Genrix Bio plans to conduct a previously planned phase I study in China in patients with autoimmune diseases. The trial will collect important data characterizing the safety, pharmacokinetic, and pharmacodynamic profile, and preliminary clinical activity of Velinotamig in autoimmune diseases. Cullinan expects this data to facilitate initiation of subsequent studies in autoimmune diseases outside of China at clinically relevant doses. Following completion of the Genrix Bio phase I study, Cullinan will conduct all further developments of Velinotamig in autoimmune diseases. Genrix Bio continues to execute a comprehensive clinical development plan for the molecule in multiple myeloma, an indication for which Velinotamig has breakthrough therapy designation in China. Genrix Bio is nearing completion of a pivotal registration-enabling study in relapsed and refractory multiple myeloma, potentially making Velinotamig the first approved T-cell engager for this disease in China. As described on slide 10, Genrix Bio has established expertise in developing therapies for not only cancer but also autoimmune diseases. With a strong portfolio of later-stage assets across multiple targets and autoimmune disease indications, including an approved product for plaque psoriasis, Genrix Bio can access an existing network of leading clinical sites and investigators in China. Genrix Bio expects to leverage these capabilities to quickly complete study startup activities and hasten accrual in the planned phase I study in autoimmune diseases. While our focus today is autoimmune disease, slide 11 summarizes key data for the molecule from Genrix phase I study in late-line multiple myeloma. Among the 48 patients who received the recommended phase II target dose of 180 mg per kg, Velinotamig demonstrated a differentiated and potentially best-in-class efficacy profile. While direct comparisons cannot be made, Velinotamig's higher overall response rate and comparable complete response rates in relation to approved BCMA T-cell engagers in multiple myeloma is noteworthy. Velinotamig's minimal residual disease negative rate of approximately 40% in relation to the 27% reported for teclistamab is also very encouraging. Most notable is Velinotamig's much higher overall response rate in extramedullary disease, or EMD. EMD is a poor prognosis subset of multiple myeloma where malignant plasma cells grow outside the bone marrow in various tissues. Together, these features support the promising potential for Velinotamig when redeployed for the treatment of autoimmune diseases. Safety observations from the same study are summarized on slide 12. With IV administration of Velinotamig at the recommended phase II dose in cancer patients, ICANS was not observed, and cytokine release syndrome was mostly low grade. However, the implementation of subcutaneous administration and an optimized step-up dosing scheme is expected to further mitigate the risk for CRS in patients with autoimmune diseases, who generally have a lower risk of CRS based on their normal volume of non-malignant immune system cells. Turning now to slide 13, I'd like to take a moment to highlight Cullinan's immense progress in executing our CLN-978 development program since our expansion into autoimmune diseases. In a short period of time, we have cleared important regulatory hurdles globally, and we remain the only development stage CD19 T-cell engager with an open U.S. IND for autoimmune diseases. CLN-978 is now in active clinical development in three autoimmune indications: systemic lupus erythematosus, rheumatoid arthritis, and Sjögren's disease. Sites are open to accrual around the world. We have worked quickly to establish an extensive global network of clinical investigators, leading key opinion leaders, and patient advocacy groups, and we are encouraged by the enthusiasm of our partners to advance implementation of our clinical development program. Patients and providers are excited for the potential of T-cell engagers to offer disease-modifying clinical activity in autoimmune diseases in their usual setting of care in their communities. Together, we look forward to channeling the shared momentum to bring a new novel BCMA T-cell engager into our portfolio and potentially help even more patients with autoimmune diseases. Mary Kay Fenton, our Chief Financial Officer, will now provide additional information on the transaction and its financial implications. Mary Kay? Thanks, Jeff. This transaction fits our strategic focus as we're opportunistically leveraging the strength of our balance sheet and adding a highly differentiated asset with best-in-class potential in autoimmune diseases. We believe Velinotamig creates additional opportunities for both near-term and long-term value-driving catalysts. We believe the terms of the deal also provide favorable upfront economics for an asset in late-stage clinical development with meaningful efficacy and safety data already generated in multiple myeloma. As you can see on slide 14, under the agreement, Cullinan will pay Genrix Bio an upfront licensing fee of $20 million for exclusive rights to develop and commercialize Velinotamig globally outside of Greater China. Genrix will also be eligible in the future to receive up to $292 million in development and regulatory milestones and up to $400 million in sales-based milestones, along with tiered royalties from the mid-single digits to the mid-teens. Importantly, after evaluating the impact of refining our oncology portfolio, particularly with regard to the scope of further development for CLN-619, our MICA / B antibody, as well as the impact of this transaction, we can reiterate our existing cash runway guidance and have resources into 2028 based on our current operating plan, a position we continue to view as differentiating in this challenging market. With that, I'll now turn the call back over to Nadim to provide some additional strategic perspective on the transaction. Nadim? Thank you, Mary Kay. As we close the transaction, we're quickly shifting our focus to rapid execution, just as we've demonstrated with our development of CLN-978 in autoimmune diseases. A few important and immediate next steps are highlighted on slide 15. As Genrix initiates and executes their phase I study in autoimmune diseases, we plan to utilize the data to accelerate our own global regulatory and clinical development plans. With our development of CLN-978, we've established an extensive network of immunology investigators and KOLs, which we'll utilize and leverage for the parallel clinical development of both Velinotamig and CLN-978. To conclude, on slide 16, I would like to highlight some of the ways this deal provides us with a compelling opportunity to maximize the potential value of Velinotamig and our immunology pipeline for both patients and shareholders. It also further emphasizes how well the program fits within the framework of our company strategy to align the best target with the best modality to help patients. We firmly believe T-cell engagers, a core area of expertise for Cullinan, represent the next wave of innovation in autoimmune diseases. In licensing, Velinotamig provides an important opportunity for Cullinan to solidify our leadership position in T-cell engager development for autoimmune diseases. We will also leverage the extensive network of immunology KOL relationships we've built to develop another potential best-in-class clinical stage program. The addition of a BCMA x CD3 bispecific T-cell engager complements CLN-978 and creates the opportunity to address the needs of more patients across a broader range of autoimmune diseases by providing a comprehensive approach to both B-cell and plasma cell depletion. Velinotamig has demonstrated meaningful efficacy and safety data in relapsed refractory multiple myeloma, including depletion of plasma cells in the tissues of patients with extramedullary disease, a poor prognosis population. We look forward to leveraging the data generated in Genrix Bio's planned phase I study in autoimmune diseases in China to accelerate our global regulatory and clinical development plans for Velinotamig outside of China. Lastly, this transaction significantly expands our immunology portfolio, resulting in high opportunity and high-impact programs while creating additional near-term and long-term value-driving catalysts, and at the same time, maintaining cash runway into 2028. Thank you for your attention, and I will now turn the call over to the operator to take your questions. Thank you. At this time, we'll conduct a question-and-answer session. To ask a question, you will need to press star one one on your telephone and wait for the name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster. One moment for our first question. Our first question will come from the line of Julian Harrison from BTIG. Your line is open. Hi. Congrats on the deal, and thank you for taking my questions. I guess, first off, you now have two T-cell engagers being developed for autoimmune diseases. With that in mind, are you able to comment on the safety you're seeing with CLN-978 to date, and what gives you confidence in both of these constructs having sufficient safety in the setting of autoimmune disease? Thanks for your question, Julian. Jeff, do you want to take that question? First, for CLN-978, we're not yet sharing data from our autoimmune program. That's still on track for the end of this year. I will point you back to the experience in non-Hodgkin's lymphoma, where we saw no ICANS and no higher than grade 1 CRS, even in patients who had bulky tumor. As we've seen for other T-cell engager constructs, the safety profile is usually better in autoimmune disease patients. I'd say something very similar about Velinotamig in the phase I study conducted by Genrix Bio in patients with multiple myeloma. The rate of ICANS was relatively comparable to what's been—pardon me—CRS was relatively comparable to what's been reported for other approved T-cell engagers and was mostly low grade, and no ICANS was reported. Again, the side effect profile has tended to be better in patients with autoimmune disease versus oncologic indications, and we expect something similar here. Thanks for your question, Julian. Excellent. Thank you. A follow-up, if I may—apologies if I missed it—on the phase I trial being run by Genrix in China later this year. Is there an expectation for data disclosure? Anything you can communicate at this point? Yeah. Julian, because the study is being run by Genrix Bio, we're not offering guidance at this point in time other than that the study will begin later this year. It was a previously planned study by them, and I think we see a lot of opportunities to accelerate our own global development plan once we get data from that study. Thanks. Thank you. One moment for our next question. Our next question will come from the line of David Dai from UBS. Your line is open. Yeah. Great. Thanks for taking my questions. Also, my congratulations on this update here. I'm just curious about the safety profile of this drug. When you look at slide 12, we are seeing a little bit of cytokine release syndrome, but not at RPTV. Maybe just help us understand, as you continue to dose-optimize this drug, can we expect a lower dose as well as any kind of progress on subcutaneous formulation? If you can share on that, that would be helpful. Thanks. David, thanks for your question. Let me ask Jeff to offer his opinion. Sure, David. It's a great question. As a reminder, in the phase I study Genrix conducted in multiple myeloma, the drug was administered intravenously, and they have begun development of a subcutaneous formulation. It is our intention to pursue autoimmune development with a subcutaneous formulation since we do expect that to yield lower rates of all-grade CRS. Genrix is continuing as well to optimize the step-up schedule, and those will be important aspects of initial clinical development in autoimmune disease. Thanks, David. Thank you. Once again, that's star one one for questions. Star one one. Our next question will come from the line of Kaveri Pohlman f rom Clear Street. Your line is open. Hi. Good evening. Congrats on the new asset, and thanks for taking my question. I guess, from the data point of view, can you tell us what exactly in the design of the molecule is so attractive that's driving higher efficacy versus approved agents in multiple myeloma? What level of read-through and in what aspect it provides to autoimmune diseases? Because if we look at the low affinity CD3 bispecifics in oncology, they haven't really shown much success in the past. Thank you. Thanks, Kaveri. Jeff, why don't you take that question? Yeah. Kaveri, thanks for your question. First, I would not say that it is low affinity for CD3. The CD3 affinity is lower than BCMA. Not unlike our 978 program, this is a higher affinity for the target antigen versus CD3. I would not say it is absolutely low. I think the clinical data that was so compelling for us was really about the ability of the drug to convey higher overall response rates in patients with extramedullary myeloma. Those are patients that have a distinctly poor outcome with BCMA CAR-T, somewhat better with approved BCMA T-cell engagers, but this nearly doubled the rate of response of the approved agents. I think that is really important when we consider that depleting abnormal immune system cells in tissue is a very important component we expect for activity in autoimmune disease. Thanks, Kaveri. Thank you. One moment for our next question. Our next question will come from the line of Andrew Berens from Leerink Partners. Your line is open. Thanks. Congrats on the deal and keeping the news flow coming out of ASCO. I may have missed it because I did dial in late, but what diseases do you think would be better targeted by BCMA versus CD19 bispecific? It sounds like you guys are going to try to reformulate the drug for subcutaneous. Just wondering how long that can take and what potential challenges could there be reformulating it? Yeah. Thanks for your question, Andy. Jeff? Yeah. Andy, first, the reformulation work is already being undertaken by Genrix Bio, and they've made significant progress in that work. I expect there not to be any significant delay in introducing that into the clinic. With respect to your first question, I think you're really getting at the essence of how a BCMA-directed asset can complement the development of CLN-978. Here, we think that there are clearly some diseases where autoantibodies produced by long-lived plasma cells are very important to the pathophysiology of the disease. One good example would be myasthenia gravis, where anti-acetylcholinase receptor antibodies are known to be produced by long-lived plasma cells. There's already some proof-of-concept work for BCMA in that indication, and you know that Cartesian is advancing Descartes-08, a BCMA CAR-T cell construct into phase III. Clearly, I think there are going to be places, as Nadim said earlier in the call, we want to match the right target to the right patient. I think there are plenty of opportunities to do that with these two agents in our portfolio. Thanks, Andy. It looks like lupus can be targeted by both. There's some literature. Am I correct in that? Yes. Jeff? Yeah. I mean, you may be alluding to a case report that appeared in the New England Journal of Medicine from investigators at the Charité University Berlin, where they treated a patient with refractory SLE with a BCMA T-cell engager, Teclistamab. That patient did experience a significant improvement in their disease-related symptoms as well as pharmacodynamic evidence of complete plasma cell depletion and subtotal B-cell depletion. BCMA is expressed on some mature plasma cells, but CD19 is not expressed on long-lived plasma cells. I think while there may be some overlap, there are clearly places where BCMA is the preferred target. Thank you, Andy. Okay. Thank you. Thank you. At this time, I'm not showing any further questions. I will now turn the call back over to Nadim Ahmed, Cullinan's Chief Executive Officer, for closing remarks. Thanks, Victor. Look, in closing, I would summarize by saying that the addition of Velinotamig to our immunology portfolio will really solidify our leadership position in the development of T-cell engagers for autoimmune diseases, which we firmly believe represents the next wave of innovation for these diseases. This transaction adds another high-impact program to our immunology portfolio, which allows us the opportunity, as you heard from Jeff, to reach more patients across a broader range of autoimmune diseases, and just as importantly, to generate additional near-term and long-term value-driving milestones for patients and our shareholders. Thank you, everyone, for dialing in, and we'll keep you updated with the progress of our program. Thanks, everyone. Thank you for your participation in today's conference. This does conclude the program. You may now disconnect. Everyone, have a great day.