Afternoon, everyone. Happy to have the Cullinan Therapeutics team here, CEO Nadim Ahmed and Jeff Jones, CMO. Nadim, maybe over to you for a brief intro to the company, and then we'll get into a Q&A. Sure. Happy to do that. First thing I'll tell you, great to be here in Q4 with multiple catalysts coming up in the weeks and months ahead for our company. Super exciting time for us as we head into 2026. Alex, it's probably worth taking a step back and talking about our pipeline strategy. and so, you know, we really try to exclusively focus on those molecules that we think can either be first in class or best in class, so that they can have a really transformative impact on patients with cancer and autoimmune diseases. If you look at our updated pipeline now, as of last week, we have a series of clinical stage programs where every molecule has shown monotherapy efficacy in the clinic. Every molecule is addressing a well-validated clinical target, and each program represents a substantial market opportunity. and then sticking with the theme of the pipeline, three of our four molecules in our updated pipeline are T-cell engagers. Which has really become a core capability for the company, and obviously represent an exciting new treatment modality for both autoimmune diseases and cancer. Just recently, we also announced last week that two of our programs did not meet our internal go-no-go criteria and were discontinued. That was CLN-617, IL-2, IL-12 fusion protein, and CLN619, which is our MYC-A, MYC-B antibody. I think our view is that this sort of disciplined decision-making and being objective with our go-no-go criteria makes sure that we can allocate capital efficiently, and especially to our highest priority program, which is CLN-978, our CD19 by CD3 bispecific T-cell engager, which we're examining in the autoimmune disease setting. Sticking on that molecule, CLN-978, we believe is a highly differentiated off-the-shelf molecule and potential best-in-class disease-modifying treatment to address a range of autoimmune diseases. Yep. We built out an immunology team that's focused exclusively on CLN978, and they're now managing a global development program with three indications and very high market opportunities. With our SLE study or LUPA study, we've guided to initial data in the first half of 2026. Yep. In parallel, we're running a study in rheumatoid arthritis. That study, we're collaborating with the Erlangen Group, who have done much of the seminal work with either CAR-T or T-cell engagers in autoimmune diseases. For that study, we're also looking at initial data in the first half of 2026. Yep. We recently opened up a study in Sjogren's disease, and so that's now actively recruiting. And then as we reflect on the external dataset for T-cell engagers, certainly at EULAR and more recently at ACR, you know, we've seen external validation now of CD19 as a high-impact target and then T-cell engagers as a treatment modality that's gonna be really important in the treatment of autoimmune diseases. Yep. That's kind of the immunology aspect. With respect to oncology, just last week, we released very promising data from our potential first-in-class, another T-cell engager, but this time addressing FLT3 by CD3 in AML, where we saw a 30% composite complete response rate in a broad all-comer population of patients with relapsed refractory AML. Very excited about that dataset. I think we were particularly pleased to see what we would describe as the external validation of that data with the hematology community. We now have an oral presentation at ASH in the coming weeks. Hope to see you all there with an ASH investor event on that Monday, December the 8th. With AML, this is a disease that has a very clear development and regulatory pathway, and that includes accelerated approval with single-arm studies. This program also aligns with our internal very deep expertise in hematology. and then the other program I'll mention is Zipilant, which is our potential best-in-class EGFR exon 20 tyrosine kinase inhibitor. We recently had a very positive meeting with the FDA, and our partners at Taiho are initiating the NDA submission for the end of this year in relapsed disease. For us, that's a very important milestone for the company. I would also add that Zipilant is not only important in terms of addressing patient unmet needs. Strategically, with the deal we have with Taiho, it's also an important source of non-dilutive capital. Yep. We're still over $130 million in regulatory milestone payments for U.S. approvals in frontline and second-line non-small cell lung cancer. We also have a 50/50 profit share in the U.S. with Taiho Oncology. The last thing I'll say to round this out is, you know, from a balance sheet perspective, we're very well resourced. We recently reported in our Q3 earnings a cash balance of $475 million, which combined with the discontinuation of the two programs I mentioned now gives us runway extension into 2029. For us, that's really important because it'll help to advance our programs, allow us to deliver multiple catalysts. Both near-term and long-term, and also means that there's no near-term need for us to raise capital as well. Hopefully that gave you an overview of all the exciting things that are going on at the company right now. Great. Yeah, definitely. I think to start, I wanna jump in and talk about CLN-978 and the T-cell engager space more broadly in autoimmune. I think maybe starting off with the question, you know, something, you know, an investor might ask, which is, this is still really early. Why do I have to care about these datasets now? You know, why should someone feel a sense of urgency in, you know, owning a T-cell engager stock today? Like, what is, what is the evidence to date? That really gives you confidence that this is gonna be the next big autoimmune classes? Sure. Jeff, do you want the clean question first? Yeah, sure. I think it's a great question, Alex. I'd say, when we made our initial strategic pivot to take CLN-978 from oncology into autoimmune development, it was just based on strong conviction that given the efficacy that had been demonstrated by T-cell engagers in oncology, that was in some instances comparable to CAR-T, we could, with a T-cell engager, a convenient medication that can be delivered in many versatile clinical settings, achieve CAR-T-like results in autoimmune disease development. I'd say that the data that has emerged, largely from clinical experiments, academic experiments, in the clinic, as well as more recently sponsored data, that there is clear evidence now that T-cell engagers can effectively treat a broad range of autoimmune disorders, a range of disorders that includes both neurologic disorders, rheumatologic disorders, kidney disorders, hematologic disorders, and that they can do this with a safety profile that is likely to be amenable over time to outpatient administration. If you think about the ability to deliver disease-modifying, clinical outcomes across a broad swath of diseases across disciplines, but in a format that is more amenable to meeting patients where they live in the community as compared to CAR-T. It's really an incredible opportunity. I think the data has continued to support this. It's case reports, case series, but more recently, some sponsored data has really shown that that's the case. Yeah, I would just add to what Jeff said. I mean, the simple way that we see this opportunity is, you know, we review the T-cell engager opportunity in autoimmune diseases. Yep. Specifically CLN-978 as having the opportunity to deliver the potency of T-cell redirecting therapies. Yep. With the convenience and accessibility of antibody treatment. That's ultimately where we wanna position CLN-978. Yep. Yeah, and I think, you know, with that, I wanna talk about the design of CLN-978. I think historically in rheumatology or autoimmune in general, you know, the experience with, you know, B-cell targeted approaches has been with CD20 as the target. You know, why is CD19 maybe a better target here for autoimmune and sort of dovetail that into the design of the molecule itself? CD19 as a target for immunotherapy covers the broadest real estate in the B-cell maturation continuum, extending all the way from pre-B cells, which are the malignant cells in acute leukemia, all the way to subsets of plasma cells, the mature antibody-producing cells. It spares long-lived plasma cells that are responsible for maintaining humoral immunity. If you think that breadth and depth of B-cell depletion is necessary to achieve disease-modifying outcomes through a T-cell redirecting approach, then CD19 gives you the broadest coverage of the B-cell continuum. With respect to CLN-978 itself, we thought that engagement of the target was probably the single most important thing. 978 was designed with very high affinity to CD19, picomolar affinity for CD19 compared to nanomolar affinity for CD3. Pre-clinically, we've demonstrated that this binding ratio, picomolar to nanomolar, achieves a broad cytokine window. That is a broad window between the dose that is deeply B-cell depleting and a dose that would be productive of untoward levels of cytokines associated with cytokine release syndrome. We saw this, in our clinical experiment when we brought CLN-978 into lymphoma patients, where we saw that at starting dose of only 30 micrograms, we could achieve, a complete response in one of three patients treated with no higher than grade one CRS. This was through subcutaneous administration with, weekly administration in that study. The molecule has half-life extension through binding to serum albumin that will ultimately, at higher doses, lead to, half-life estimated to be about 7-10 days. A very small molecule, literally bite-like in its construct, only about 65 kilodalton as compared to larger monoclonal antibodies that could potentially help with tissue penetration and depletion of B cells in places outside of the hematologic compartment. Altogether, a clinical profile that is amenable, we believe, to outpatient administration as the program proceeds. Then you've mentioned you're now in the clinic with SLE, RA, and, and Sjogren's. Maybe if we could touch briefly on, you know, the, the strength of the data to date, you know, for CD19 T-cell engagers in each of those indications. Yeah. I can take, talk about SLE. You know, the most robust data now for SLE is coming from some small companies in China. The most mature is a company, ITAB Med. They've shared data on at least 12 SLE patients. They updated their experience at ACR. That molecule is limited by some liabilities that require either frequent subcutaneous administration or continuous IV infusion, that will always limit its potential in the clinic. The data to date are quite compelling. They have shown the ability of a CD19 T-cell engager to induce DORAS remissions, that is, treatment-free remissions in patients with SLE. Some of these have been durable in excess of six months and in a few cases of 12. The ability to achieve a treatment-modifying remission that's sustainable for many months is very, very good early proof of concept that this is attainable and with a safety profile that thus far has been acceptable and favorable as compared to what's been reported for CAR-T. Again, probably not the molecule that's going to. Yep. Change the treatment dynamics, but clearly showing the potential for one to do that. In RA, the initial data for T-cell engagers, CD19, was generated by our collaborators at the University in Erlangen. They've shown in a set of patients treated with lenalidomide that you can achieve B-cell depletion not only in the peripheral blood but also in affected joint tissue. These responses were in patients who had failed prior treatment with the CD20-directed monoclonal antibody rituximab in many instances. The patients had not only a pharmacodynamic response but also a clinical response despite the fact that they were refractory to multiple disease-modifying agents. I think in recent presentations, the docs there, and we would certainly agree, believe that lenalidomide was systematically underdosed in those patients. This was the first experiment in the world with this modality in an autoimmune disease. I think they conservatively underdosed patients. I think as the data has matured, for lenalidomide and other indications, it's clear that there's a dose-response relationship for therapeutic benefit. In Sjogren's, no T-cell engager data, much to date, certainly not for CD19, but there is clear evidence that B-cell depleting approaches. Are therapeutic. We saw phase III data from Novartis at ACR for Ianilumab. I think it shows the potential, but that there's still a lot of room. That's why we think it's a great indication, proof of concept for B-cell depleting therapy, but lots of room to improve over what's achievable with a monoclonal antibody. Yeah, I would add. I think we have the opportunity to be the first company to share company-sponsored data in each of those autoimmune diseases, which we're obviously looking forward to. Alan, do you have a question? It's just, I'm still confused about exactly what the product profile you're after. I mean, you potentially, the autologous CAR-T is one and done outside of the toxic burden. Is this, you're thinking of this as directly compatible with that. Sure. Type of depletion or. Sure. You're thinking about earlier. Yep. Replacing a lot of the existing therapies? Just help me understand exactly kinda what the clinical objective is of the trials in terms of how you're gonna position. Sure. No, happy to do that. Great question. Look, you know, I started off saying from a positioning perspective, our view is that T-cell engagers can deliver the potency of T-cell redirecting therapies but with the convenience and accessibility of antibody treatment. What does that look like in a future clinical commercial stage? The first thing I would say is, and certainly based on conversations with rheumatologists, we are definitely not saying there is not a role for CAR-T, but it is not likely to be the answer for the masses of autoimmune disease patients. We would see CAR-T's role to be in a post-T-cell engager setting in the real world. We would expect T-cell engagers to be used before CAR-T. That is certainly what we hear from rheumatologists. I think that is our starting point. I think if the data continues to go in the direction that we've seen it, I think you also have the opportunity to go earlier in the treatment sequence. One of the things we find, and certainly I'll use lupus as an example, you know, the biologics that are out there have produced marginal efficacy. In fact, that was one of the reasons why we got a little delay in accrual because many patients didn't have prior biologics. Yeah. They have produced modest efficacy, and they're always added onto background chronic immunosuppressive therapy. I think with CLN978, we have the opportunity for patients to come off their chronic immunosuppressive therapy, be treated as a monotherapy. To your question, Alan, I think we would start in a post-biologic pre-CAR-T setting but look to move earlier and ultimately displace biologics earlier in the disease because ironically, you want to be able to impact the disease earlier rather than later so that patients can benefit from these long treatment-free remissions. Hopefully I addressed your question. Yeah, I think with this setup, you have your proof of concept studies accruing now. You're gonna have data in the first half of next year. Can you set up what a positive outcome looks like for the SLE study the first half of next year? Sure. Jeff, do you wanna talk to that? Yeah, I mean, I think for, remembering that the data that we'll share in the first half of 2026, for both SLE and RA, is focused on the initial single ascending dose, phase of the trial. What I think a good outcome there is showing that there's a strong relationship between dose response, meaning, B-cell depletion in the peripheral blood in the case of all of our program, but in the case of our RA and Sjogren's trials, a dose-response relationship for B-cell depletion in tissue that we will assess systematically in both the RA and Sjogren's trials. We'll also be able to, like a good outcome would show that that is achievable with a retained therapeutic index, that we don't see untoward rates of cytokine release syndrome or immune effector cell, neurologic abnormalities or other neurologic toxicity. That means that this medication has a favorable profile for further development in autoimmune disease. What I didn't talk about there are really strong indicators of clinical response. I think the data that we were talking about that's accumulating, from these academic experiences is that it will take a longer exposure than just administration of a single therapeutic dose in order to achieve the kinds of disease-modifying benefit that Nadim was speaking about. That will likely require a repeat dosing schedule of, you know, several therapeutic doses over a four- to six-week interval, based on the experience we have to date in order to achieve clinical response. For our program, that won't come until the second part of the trial where we explore repeat dosing schedules, as part of further expansion. Yeah, the one thing I would add is in our RA study, we do have the opportunity to have tissue biopsies. Yep. In Germany, you know, that group and Gemelli in Italy, they routinely take biopsies as part of standard of care for patients with RA. We will also be able to look at B-cell depletion in tissue, which of course is critically important to the point that Jeff just made. Yep. Yep. Makes sense. You know, Nadim, you also alluded to, you made some changes to your protocol to accelerate enrollment in SLE. Can you talk a little about why that was and how enrollment has progressed so far? Sure, Jeff. You know, I think when we're speaking about biologics and SLE, the unfortunate circumstance in the U.S. is that many practitioners, and particularly in community-based practice, aren't completely convinced of the therapeutic benefit attributable to drugs like belimumab. Many patients face difficulties in accessing quality care as well. The reality is that the majority of SLE patients in the U.S. never receive a biologic. In putting together our initial protocol concept, we recognized that and thought that it was reasonable to enroll patients who had had immune suppressants, oral immune suppressants like mycophenolate or methotrexate. In some initial regulatory discussions, there was a concern that we enroll an even more refractory population. As we began the trial, as we got more experience, and the kinds of patients who were interested in participating and available at our investigative sites, it became clear that that entry criterion was too restrictive and that in order to enroll the average lupus patient in the United States who was still in need of a better therapy, that we needed to broaden our eligibility. We did that through a protocol amendment this summer and have already seen that the funnel of patients entering screening has dramatically increased. Yep. We've been able to rescreen screen failures from previously who still expressed interest in the study, and it's made a significant impact on our ability to execute the study. Were you able to dose patients before this protocol change? We had treated patients in this study before that, yes. Okay. So, you know, I think we, we've talked about the progression of the space, you know, past the single ascending dose to the multi-dose studies. What, what ultimately does kind of a, a phase II plus development program look like? Are we thinking about active comparator studies? How do you prove out the. You know, this TPP that we're talking about? Yeah. I think, you know, this is obviously there's a changing regulatory landscape here, right? Yeah. If you look at, some of the CAR-T companies. Sure. Right? They've managed to reach agreement with FDA to be able to take a more accelerated approval pathway with single-arm studies. Yeah. You know, Cabaletta, Kyverna, Autolus. I think as we see, within FDA, close alignment between CBER and CDER, I think there's a potential opportunity that opens up for T-cell engagers too. Yeah. I don't think, you know, our firm belief is that T-cell redirecting therapies, whether it's CAR-T or T-cell engagers, are medicines where patients will be able to come off their background chronic immunosuppressive therapy. If that is true, then it would be, you know, it'd be quite unethical to do placebo-controlled studies, right, in that setting. I think as CBIR, CDIR further align, I do think there will be the opportunity in the future for T-cell engagers also to be able to weave into this kind of accelerated approval pathway. Yeah, I guess, like, is that consistent with the idea that you could compete with, like, the Ianilumabs out there clinically if you had accelerated approval versus a large phase III program? Yes, certainly. I mean, to Jeff's point earlier, I mean, we were pleased to see the Novartis data because it's always good for patients when you have more treatment options. For Sjogren's disease, it's important. At the same time, it's clearly a bar that can be beaten. Yeah. I think, you know, the study that Novartis did that was also done in lupus by Roche recently with benetuzumab, you know, monoclonal antibodies don't have the potency of T-cell redirection therapy. Sure. They have to be added on top of standard of care. This is why you have to do those very large randomized phase three studies. This is where I think CAR-T therapy, T-cell engagers have the opportunity for a quicker regulatory pathway. Makes sense. Shifting gears, you announced a deal a few months ago now to acquire the license for Velinotamig. What was the rationale for acquiring a BCMA-targeted T-cell engager? Yeah, sure. Let me say the first thing that I should say is that it was not based on any issue with CLN-978 or any hedging there, right? We have three ongoing studies we just spent a long time talking about. I think our view was with CLN-978, we have a potent B-cell depleter, and we feel that a plasma cell depleter can complement our ongoing efforts with CLN-978. Strategically, it was important for us to obtain our own plasma cell depleter. I think these two approaches will allow us to reach more patients across more diseases than either approach alone. Yep. Look, there are gonna be diseases where it's B-cell dysfunction that's driving the underlying pathophysiology of the disease, and there CLN-978 makes much more sense. Yep. We also know there are diseases where we have these pathogenic autoantibodies that are produced by long-lived plasma cells. There, clearly, BCMA and velinotamig is gonna be a better approach. Yeah. Between the two, you heard Jeff talk about the B-cell compartment. Between the two, we cover the entire breadth. Yeah. Of the B-cell compartment. Again, it allows us to reach the broadest range of autoimmune diseases. It also brings in another T-cell engager into our pipeline and portfolio, which clearly has become a core capability of ours. Strategically, it made a lot of sense, and we're super excited about the opportunity. What are the timelines for, for that one? With velinotamig, we also took the creative approach whereby our partner, Generix Bio, is conducting the first autoimmune disease study in China. That means they can start at the dose they wanna start at, and they can also go into multi-dosing immediately. That means the data from that study. Will help us accelerate our own ex-China plans. What Generix has guided to at the moment is to start that study by the end of this year. Okay. So maybe the last few minutes, you obviously mentioned your ASH presentation for 049. I guess in general, how are you thinking about investment in your sort of legacy oncology business versus autoimmune and balancing that moving forward? Yeah. Look, we've just updated our pipeline. We don't have a legacy pipeline versus a new pipeline. You have oncology versus autoimmune. We have one pipeline, and I think we have core strengths now with building an immunology team in both oncology and immunology. Yep. If you look at our pipeline, it's also de-risked based on the targets and the molecules we mentioned. We have a robust cash runway. Yep. That will allow us to advance, you know, these programs very quickly. I think we feel very good about the opportunity to internally invest in these programs. And then look, from a BD perspective, we're always scanning the landscape for both inbound, outbound opportunities. Zipilant was a clear example where we went and partnered, and we got a great deal for ourselves. Yep. That's kind of how we think about things. You know, and then with that, you, you've mentioned runway now to 2029. I guess what's embedded in that? I guess, is there, are there scenarios in which you would accelerate the autoimmune development that would actually change that? I could imagine just the breadth of what you can do there would increase quite significantly and maybe change your considerations. Sure. Yeah. Look, I would say today, at least, Alex. Our operating plan contemplates moving all four programs forward. Yep. The fact that we discontinued two programs did create that extra space and headroom. Look, as we move forward, as we generate data milestones, the catalyst, if we need to turn things up or turn things down, I think we feel very good about where we are right now. Great. Any, any final thoughts? I guess maybe what, what should we expect with at the ASH presentation for 049? Jeff! Yeah, I think it's really an opportunity to further highlight that this is really the best data that's yet been demonstrated for a T-cell engager in AML, which is the last big heme indication where a T-cell engager has not been successful. Composite complete response rate of 30% in AML patients, including patients with P53 mutations, targetable mutations who have failed kinase inhibitors. That's our data set. And still a 30% composite complete response rate, which compares favorably with anything that's been approved in AML relapse patients in the last six or seven years. I think it's really an opportunity to show that we have a potential drug in CLN-049 for a very hard-to-treat disease, and with a favorable safety profile, I think not just in AML, but for a T-cell engager in general. I would say hematology is a core capability for us. Yep. You know, this is one that we're very excited about. Great. Nadim, Jeff, thank you so much. Appreciate it. Thank you. Thanks everyone.