Good afternoon, everyone, and welcome to the IGM Biosciences conference call. Today's call is being recorded. At the end of the prepared remarks, we will open the call for a question-and-answer session, during which time we request that participants limit themselves to one question. At this time, I would like to turn the call over to Misbah Tahir, Chief Financial Officer. Please go ahead. Good afternoon, everyone, and thank you for joining today's call. Before we begin, I would like to remind you that any statements made during this call that are not historical are considered to be forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by statements as a result of various important factors, including those discussed in our Risk Factors section and in IGM's most recent quarterly report on Form 10-Q, as well as other filed reports with the SEC. Any forward-looking statements made today represent our views as of today, September 30, 2024, only. We announced in a press release issued this afternoon a strategic shift for our company, with the decision to pivot exclusively to autoimmunity while minimizing future spend on the development of aplitabart and other oncology candidates. This shift also comes with a change of leadership and our broader team. We are deeply grateful to the contributions of all our employees and thank Fred, Chris, and Bruce for their years of service to the company. I'm joined today by our new Chief Executive Officer, Mary Beth Harler, who, as many of you know, is a trained general surgeon and led the Bristol Myers Squibb Immunology and Fibrosis programs prior to joining us, where she successfully led the late-stage development of innovative therapies such as Sotyktu, Orencia, and Zeposia. Also joining us is Lisa Decker, our Chief Business Officer, and Eric Humke, our Head of Clinical Research and Development, who will be available for Q&A at the end of the call. With that, I'll turn the call over to Mary Beth. We can move to slide four. Thank you, Misbah. I have dedicated decades of my life to helping patients, initially as a surgeon and then as a drug developer. I am truly excited to be with IGM at this watershed moment, when the therapeutic potential of deep B-cell depletion may fundamentally alter the autoimmune treatment landscape. In reflecting back on the many conversations I have had over the years with patients suffering from autoimmune disease and the clinicians caring for these patients, it leaves me more motivated than ever to help deliver medicines that offer significant relief from these chronic, oftentimes devastating diseases. IGM was founded on the belief that we could push beyond current treatment approaches to envision a better way to address diseases with high unmet need by leveraging the highly differentiated characteristics of IGM antibodies. Our focus has now crystallized around what we view as the most transformational opportunity for IGM, the application of our pipeline of T-cell-engaging antibodies to autoimmune disease. Today, IGM has established a leadership position in developing T-cell engagers in multiple autoimmune diseases. We also remain very excited about our collaboration with Sanofi to develop innovative new therapies to support their pipeline. And as we announced earlier today, the changes we have made are expected to extend our cash runway into 2027. On slide five is an overview of our pipeline in autoimmunity. As you can see, we have a broad clinical development effort underway with imvotamab, with ongoing trials in severe lupus, rheumatoid arthritis, and myositis. It is important to note that between imvotamab and our CD38 x CD3 T-cell engager, IGM-2644, our pipeline offers the potential for coverage of all pathogenic B cell drivers in autoimmunity. As previously noted, we also have a very active autoimmune collaboration underway for a series of IGM-based agonist targets with Sanofi. Turning to slide six. Here we share an overview of imvotamab. One of the key advantages, which I will get into in a moment, is our focus on depth of depletion. We define depth of depletion in a couple of different ways: eradication of tissue-resident B cells, but also the elimination of even those low CD20-expressing cells that may be beyond the reach of existing therapies. In addition, imvotamab has also demonstrated a favorable safety profile in a phase 1 clinical trial in non-Hodgkin's lymphoma, and we believe this will be a critical consideration for both patients and physicians in the treatment of autoimmune disease, particularly in the community setting. Slide seven highlights some of the data supporting the potential of imvotamab. These data arise from a cynomolgus monkey GLP tox study, demonstrating that a cyno cross-reactive version of imvotamab not only reaches the key tissues of interest, but it also deeply depletes B cells within those tissues of interest. Turning to Slide eight. Here, we highlight a number of key B cell subsets heavily implicated in driving autoimmune disorders, including switched and activated memory B cells. It is well known in the field that switched and activated memory B cells are key drivers of autoimmune disease. These preclinical data demonstrate a meaningful potency advantage for imvotamab over rituximab. This superior potency is seen despite progressively lower CD20 expression in these particular cell types of interest. We view this as a key differentiator for our platform and for this molecule. These data demonstrate the potential of imvotamab to deliver the depth of depletion necessary to stop the train of B-cell maturation in these diseases. Right cells, right depth. Turning to slide nine. In addition to imvotamab's potency advantage over rituximab, we also show that imvotamab demonstrates superior potency in binding to and killing low CD20-expressing cells as compared to a bispecific IgG CD20 by CD3 molecule in vitro experiments. These data give further confidence that imvotamab can deliver the depth of depletion needed against key B-cell subsets, including those low CD20 expressers. Turning to slide ten. This slide highlights an overview of the broad clinical development program we have implemented for imvotamab. I'll remind you, we've been in this space for the last couple of years, and we led the way in initiating a multi-pronged clinical development program for a T-cell engager in autoimmunity. For severe lupus and RA, we are evaluating three dose cohorts. As previously guided, we have cleared the first and second cohorts in RA and the first cohort in lupus. The RA trial is a placebo-controlled, double-blind study enrolling up to 24 patients, while SLE is a single-arm, open label study in up to 18 patients. Our goal is to announce data from these programs toward the end of this year or early in 2025. We have been extremely pleased with the progress being made on these programs and the level of interest being shown by both investigators and patients, including in the community setting, where more complicated therapeutic approaches can be a challenge. This interest underscores the level of unmet need for more effective therapies in these diseases. On the right, we highlight our ongoing myositis trial. We're very excited to be working with Stanford University on this study. This study will complement our work in SLE and RA through deep translational data, including biopsies of skin and muscle, as well as imaging. Turning to Slide 11 and summarizing. We are very excited about the potential of imvotamab in autoimmune disease. There are multiple reasons we believe in this molecule. CD20 is a clinically validated target with multiple approved therapies in autoimmune disorders, unlike CD19, which has no approved therapies in this space. Our cyno data demonstrates that the molecule reaches and deeply depletes within tissue. Imvotamab is clearly an active molecule. We saw complete responses in all major subtypes of NHL, and we believe the safety profile of imvotamab in NHL is favorable among the current T-cell engagers, as supported by our data in nearly 100 patients with NHL. Unlike other options in autoimmunity, imvotamab offers convenient administration in an off-the-shelf outpatient setting. Turning to slide 12. IGM-2644 is a newer addition to our pipeline. It is a novel CD38 x CD3 T-cell engager, and we are excited about what this molecule could bring to patients suffering from autoantibody-driven diseases. If the therapeutic goal is to deeply deplete autoantibody-producing cells, a CD19 targeting approach will not fully address these populations. Recall that CD19 is not expressed on plasma cells. With our CD38 x CD3 molecule, we are targeting both plasma cells and plasmablasts. Of note, this molecule has been evaluated in a small cohort of patients with multiple myeloma. We ended that multiple myeloma study and announced late last year our intention to move IGM-2644 into autoimmune diseases. We anticipate initiating a phase 1 study in myasthenia gravis with IGM-2644 by the end of this year. Slide 13 shows a sampling of the in vitro data on IGM-2644. These cells demonstrate the potency advantages of IGM-2644 over daratumumab in human myeloma and lymphoma cell lines, representing the depleting potential of IGM-2644 across a range of antigen expression. We are encouraged by these data, given the case reports of daratumumab in patients with autoimmune disorders. We look forward to evaluating the full clinical potential of our molecule in patients suffering from autoantibody-driven disease. Turning now to slide 14. We believe the IGM T cell engager pipeline offers great flexibility to target specific B cell subsets to achieve the breadth and depth of depletion necessary for a given autoimmune disease. This includes monotherapy as well as the potential for sequential approaches such as induction followed by maintenance therapy. And for those patients with very severe disease who may be refractory to available treatment options, there is the possibility to combine these agents, particularly in situations in which CAR-T access is not possible or not available. Turning to slide fifteen. In summary, we believe we have a compelling set of opportunities before us with our T-cell engager pipeline across a range of B-cell mediated autoimmune disorders, and we are leading the way in tackling a broad cross-section of these diseases. The changes in our company direction and leadership will allow us to focus our resources on enabling value creation across these opportunities. And finally, on slide sixteen, we continue to reinforce our leadership position with T-cell engagers in autoimmunity through a variety of ways. I would encourage the audience to read an upcoming paper we wrote in collaboration with Bill Robinson, Chief of the Division of Immunology and Rheumatology at Stanford University and a leading physician scientist in B cell driven disorders. I'll also remind you, we look forward to sharing our initial data disclosure on our clinical program for imvotamab at the end of this year or early in twenty twenty-five. And with that, we'll open up the call to Q&A. Thank you. Ladies and gentlemen, we will now begin the question-and-answer session. Should you have a question, please press star followed by the one on your telephone keypad. You will hear a prompt that your hand has been raised, and should you wish to cancel your request, please press star followed by the two. I would like to advise everyone to have a limit of one question, and if you are using a speakerphone, please lift the handset before pressing any keys. One moment, please, for your first question. Your first question comes from the line of Stephen Willey from Stifel. Please go ahead. Yeah, good afternoon. Thanks for taking the questions. I guess my one question, the cash runway extension into 2027, can you maybe just you contextualize what that assumes just regarding imvotamab dose expansion in any of these autoimmune diseases, and whether that contemplates the pursuit of other opportunities for IGM-2644 beyond myasthenia? Thanks, Stephen. It's a question very much aligned with our current thinking on the immunology strategy front, so I'll pass it over to Misbah to respond. Hi, Stephen. I think in extending our cash runway into 2027, we've certainly been very thoughtful and deliberate in making sure that our resources, our capital, are really prioritized against our autoimmunity objectives and to fully support and enable us to achieve success in this pivot. What you see outlined in our pipeline chart and in the slides we've just walked through, that's what's contemplated in our current cash runway assumption. Okay. I will jump back into the queue. Thanks. Thank you. And your next question comes from the line of Roger Song from Jefferies. Please go ahead. Thanks. Thanks for taking the question. I think maybe my one question relates to the new preclinical data. So since you give us some in vitro- ... data against the IgG form of the CD20/CD3. Just curious, have you done the in vivo similar study? If so, you know, what are the, you know, would you present some data in the near future on what's the observation you have seen? Thank you. Thanks, Roger. You know, as we've discussed, I think, you know, in the past, you know, given where we are at with our clinical program, frankly, we are going to have in-human data with imvotamab very, very soon. We continue to have a very robust translational effort underway for both our CD20 x CD3 program as well as now the CD38 x CD3. But, you know, as far as any additional in vivo work, you know, frankly, we're waiting for the human experiments to complete. Got it! Makes sense. Thank you. Thank you. And your next question comes from the line of Michael Schmidt from Guggenheim Partners. Please go ahead. Hi, this is Paul on for Michael. Thanks for taking our questions. One for Mary Beth. Perhaps if you could comment on any strategic shifts for the company that you're focused on following the deprioritization of oncology, and perhaps any advantages that you'd highlight on your platform in autoimmune that's really a sort of a differentiated aspect versus oncology. Are there any plans to meaningfully adjust or expand development plans for imvotamab or 2644 beyond what was previously planned? Thank you. Thanks. There was a lot packed in there, but great set of questions. Our strategic focus going forward is very clear: maximize the value of our T-cell engager opportunities in autoimmunity. We do believe that this platform, as manifested through imvotamab as the most advanced molecule, plays very well to the needs in an autoimmune setting. Again, you know, CD20 is a clinically validated target. We know we got a solid target. We have an active molecule, as demonstrated by, you know, complete responses in an NHL setting. And we believe that the safety profile of imvotamab in NHL may be particularly well suited among the currently available T-cell engagers to be an appropriate therapy in chronic autoimmune disease settings. With respect to where else we may pivot, you know, at this point in time, we are laser-focused on delivering the current programs, generating the value that we believe resides within those data, and we will reserve those future decisions for a point in time when we have a better understanding of what the opportunities might look like. Great. Thanks so much. Thank you. And your next question comes from the line of Brian Abrahams from RBC Capital Markets. Please go ahead. Hey, good afternoon. Thanks for taking my question. Your press release talked a little bit about some of the emerging information out of aplitabart that, in part, helped to catalyze the strategic shift. Can you maybe talk about, maybe, generally speaking, what you're also seeing out of imvotamab so far from the safety and biomarker side that's helping to catalyze this shift to autoimmunity? Thanks. Thanks, Brian. Excellent question. We have not yet disclosed any data. You know, our intent is to come forward by the end of this year or early in twenty twenty-five with our initial tranche of information for imvotamab in autoimmunity, right? And in addition to the safety, yes, that will be question number one: Can we safely administer a T-cell engager in an autoimmune setting? But we also want to be able to address questions such as, right, you know, are we achieving the depth of B-cell depletion that we are seeking? Are we starting to see an impact on biology that would be suggestive of a meaningful improvement in outcomes for patients? And last but not least, of course, we are keeping an eye on the phenotype of those reconstituting B-cells to understand if we are actually seeing a shift towards a more naive phenotype. So more to come towards the end of this year or early into 2025. I think it's also fair to say we're seeing continued engagement, strong engagement with investigators- Absolutely. - and with patients, based on the enrollment that we've been seeing, especially over the last few months. Excellent point, Misbah. Thanks. Thank you, and your next question comes from the line of Eric Joseph from JP Morgan. Please go ahead. Hi, thanks for taking the question. But maybe just to follow up to that last question about sort of what you're you know looking toward in terms of the initial data readout with imvotamab later this year, early next year. I guess, in addition to sort of the cadence of B cell depletion and recovery, I guess, are there other efficacy measures that you might perhaps just have us focus on? I guess, should we also expect sort of a population reflecting both the RA and SLE opportunity? And maybe just as a follow-up for IGM-2644, can you just talk a little bit about what sort of grounds your confidence in a CD38 T cell engager being you know a potentially differentiated option within IGM? Thanks. Thanks, Eric. With regard to your first couple of questions, we are evaluating as exploratory endpoints in the RA and lupus study and, outcomes on disease activity, so for RA, using the DAS28, you know, measurement, you know, which gives certainly in the context of early clinical development in RA, a fairly good read on changes in disease activity over time. For lupus, we will be evaluating the impact on the SLEDAI-2K score, and to remind you, you know, for both of these diseases, we are focusing on patients with severe disease. In the lupus study, all patients are required to have a SLEDAI-2K baseline of ten and above, which is very severe disease, so again, we'll be evaluating the change in SLEDAI-2K over time following treatment with imvotamab. I do want to caution, however, right, these are phase one B studies. Our objectives, as appropriate, understand the safety, understand the PK, the impact on biology, and of course, we're interested in the impact on clinical disease activity, but these are very appropriately exploratory measures given the small sizes of these studies. With respect to twenty-six forty-four and why we believe, right? It actually, it stems from a couple of elements. Some of the data that we shared with you coming from an in vitro setting where we showed very nice max killing and potency relative to daratumumab. Certainly, the understood safety profile of currently available CD38 molecules gives pause in an autoimmune setting. Because of the architecture of the IGM molecule, we believe that this platform, in and of itself, may confer safety advantages with respect to T-cell engagers, and the rationale behind that is highlighted in one of the opening slides. So all of that information, together with the, you know, the number of recent reports coming forward on other CD38 plays in autoimmunity, leave us very excited about the possibilities for what this molecule could bring to patients suffering from autoantibody-driven diseases. Thank you. And your next question comes from the line of Charlie Yang from Bank of America. Please go ahead. Great. Thanks for taking the question. So I guess my question is just regarding, you know, targeting CD20 versus CD19, right? Just given, I guess my understanding on some of the biology is that some of the autoantibodies are produced by the long-lived plasma cells, and those are tend to be targeted by CD19. So can you just talk about kind of what makes you believe the CD19-20 approach, you know, will be, obviously, kind of effective in this lupus population as well as RA? Perhaps just giving in context of, you know, recent kind of emergence of this data, you know, in MG, that would be great. And maybe I'll do a quick follow-up just on the CD38. If you can just talk about, you know, what kind of specific population you'll be targeting in myasthenia gravis? Thank you. Mm-hmm. Thank you. This is a question we receive on a fairly regular basis with regard to nineteen versus twenty, and there are a number of reasons for why a CD20 makes sense, particularly in the context of a T-cell engager. Before I provide that rationale, however, I think it's very important that we all remember that B-cells drive autoimmune disease through numerous functions, not just the autoantibody production that has gotten so much airtime recently. B-cells are also professional antigen-presenting cells. They can be prolific generators of pro-inflammatory cytokines, and all of these functions together contribute in various ways to different autoimmune diseases. So if we now start drilling down on the question of a CD19 versus a CD20 approach, remember, you know, CD20 is a well-established, clinically validated target in autoimmunity, with numerous approved therapies across multiple autoimmune diseases. CD19 is not a clinically validated target in autoimmunity. There are no approved therapies, right? The two markers are co-expressed on the vast majority of B cells, and where they differ in the region of interest at the far end, as memory cells become activated memory B cells and ultimately progress into short-lived plasmablasts. That's the space that you're talking about. The vast majority of those short-lived plasmablasts die off within five to seven days. Now, if one really wants to go after autoantibody-producing cells, it is not with a CD19. CD19 is not expressed on plasma cells. That's a lot of the reason we are so excited about bringing our CD38 by CD3 into this portfolio, allowing us now to capture a broad range of pathogenic B-cell drivers, with the ability to modulate the depth of depletion that we can deliver through various, you know, monotherapy or combination approaches. So you asked me a lot of questions, I gave you a lot back, but I, I hope that addresses the key questions. Great. Thank you. Thank you. There are no further questions at this time. I will now hand the call back to Ms. Mary Beth Harler for any closing remarks. Thank you so much, operator, and I thank you all for calling in today, and we appreciate your continued support. Thank you. Thank you, and this concludes today's call. Thank you for participating, and we all disconnect.