Good morning, everyone, and welcome to Morgan Stanley's Global Healthcare Conference. I'm Sean Lahman, Head of US SPEEDcap Biotech Equity Research here at the firm. Before we commence, for important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/research/disclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. For this session, we have Cullinan Therapeutics with CEO Nadim Ahmed and CMO Jeff Jones. Welcome, and thank you for your time, gentlemen. Thanks, Sean. It's great to be here. Nadim, I might start out by inviting you to make some comments about Cullinan Therapeutics, what the company does, and maybe some catalyst potentially coming up. Sure. Yeah, happy to do that. Thanks again for the invite. Welcome. I would say, as a company, we're at an important inflection point, with a series of catalysts ahead in the coming months, which we're very, very excited about. From a pipeline perspective, we focus exclusively on potential first-in-class or best-in-class molecules that can have a transformative impact so that we can deliver on our mission to create new standards of care for patients with autoimmune diseases and cancer. The other thing I would add is, given the very high rate of failure in early-phase clinical development, we've taken a multiple shots on goal strategy. You'll see, following passing important stage gates through discovery, we've put a series of programs in the clinic over the past couple of years. I think the clinical data from these phase one studies will be important for us to make near-term go-no-go decisions. That's really important because making sure you have a high bar for advancing molecules into late-stage development for us is especially important because we want to make sure we continue to prioritize capital allocation to our highest priority program, which is CLN-978, a CD19 x CD3 bispecific T-cell engager, which we're exploring in a range of autoimmune diseases. Our view on the program is, we have a very competitive executional position. We have a highly differentiated molecule. In CLN-978, we feel that we have an off-the-shelf, potential best-in-class, disease-modifying treatment that can be applied across a broad range of unmet needs across autoimmune diseases. Just last year, when we expanded our R&D efforts beyond oncology into autoimmune diseases, we quickly built out an immunology team that's focused exclusively on CLN-978. As a result of that, in the same year, we were the first company to actually get an IND clearance by the FDA in the U.S. for a CD19 T-cell engager in autoimmune diseases. At the same time, the team stood up a global development program. Now we have three ongoing studies in high unmet need indications and large market opportunities, which is very attractive for us. At the same time, we also added additional external immunology expertise to both our Scientific Advisory Board as well as our Board of Directors. Now we have an ongoing study in lupus, or SLE, that's taking place in Europe, U.S., and your home country, Australia, Sean. Excited about that program. We just updated guidance with a small change in timing, with initial data now expected in the first half of 2026, from Q4 2025, originally. We have an ongoing RA study also in parallel and working closely with the University of Erlangen group in Germany, who have really led the way for T-cell engager development in autoimmune diseases. That timing is per our original guidance, the first half of 2026. We also very recently opened up a Sjogren's disease study, which we're very excited about. I think the other thing I'd add is, we were very pleased to see the recent EULAR data, where we see further validation of CD19 as an important high-impact target, as well as T-cell engagers as an important modality for potentially treating autoimmune diseases. That's kind of the autoimmune disease side of things. From the oncology perspective, we have our EGFR exon 20 inhibitor, zipolirenib, which, pending FDA discussions, our partner Taiho Oncology has guided to an NDA submission by the end of this year, an important milestone for us as a company. Yesterday, we had two oral presentations at the World Congress on Lung Cancer, important patient subsets, both patients who received prior Mavencimab and uncommon EGFR mutations. Next month, we're presenting data on the activity of zipolirenib in brain mets at ESMO. A lot to look forward to. Zipolirenib clearly is addressing a range of important unmet needs. At the same time, though, strategically, based on the deal we have with Taiho Oncology, it also can be a source of non-dilutive capital for the company, where we're still over $130 million in terms of regulatory milestones for U.S. approvals of front-line and second-line non-small cell lung cancer, as well as a 50/50 profit share in the U.S. In terms of oncology, we've also guided to initial clinical data in Q4 for CLN-049, another T-cell engager, which targets FLT3 by CD3. Looking forward to presenting those data later this year. Finally, from a balance sheet perspective, in our last Q earnings, we reported over $500 million in cash at the end of June 2025, which gives us the resources to execute against our priority programs, generate both near-term and long-term catalysts without the need for any near-term capital raises, which I think is really important in this marketplace. Hopefully, I gave you a snapshot of all this exciting stuff that's going on in the company at the moment. It's a snapshot of a lot. You know, very high level of activity, a bunch of catalysts, and well-capitalized. Thank you. Sure. Just one macro question that I have, and I know that Cullinan's got skin in the game here, you know, with China's China biotech's rise in innovation. I mean, how's that influencing your R&D and business development strategy? Yeah, great question, Sean. I mean, the amount of innovation that's coming out of China is pretty amazing. Ultimately, we think it's going to be good for patients. Our recent transaction to license in belanotamab, a BCMA x CD3 T-cell engager, is really an example of us kind of trying to capitalize on that opportunity. The very attractive aspect of that deal was that Generex BioHope had already planned a phase one study in autoimmune diseases. Our very first study with that molecule will be in China, which will then allow us to generate data very quickly. We expect this will allow us to accelerate our regulatory and clinical development plans ex-China also, and allow us to start studies at clinically relevant doses. For us, it's a really important source of innovation. We get to not only bring in a molecule from China, but also get to do some studies in China first, both in a cost-effective and accelerated way. We're excited about that opportunity. Wonderful to hear. I might start with CLN-978. That's your lead immunology program. Before we dive into the ongoing studies, can you provide an overview of your rationale for developing the CD19 x CD3 T-cell engager in autoimmune disease? Sure. I think if you look historically, it's often been the case that drugs that were initially developed for the treatment of B-cell malignancies have found great utility when reapplied to the treatment of autoimmune diseases because they're B-cell depleting. The centrality of the B-cell depletion mechanism is important for the therapy of a number of autoimmune diseases. That's typically been carried out through monoclonal antibodies. Just as T-cell engagers and CAR-T as alternative approaches for CD19 or CD20-directed B-cell depletion are an order of magnitude more potent than monoclonal antibodies, the initial data has been emerging that that same relationship holds true in the autoimmune disease context, where a T-cell redirecting approach, either through a T-cell engager or a CAR-T, can achieve a depth of B-cell depletion that not only ameliorates symptoms, but also addresses the underlying pathophysiology of the disease with disease-modifying effect. This allows patients to discontinue chronic immune suppression and really enjoy some patient-free time. This was initially demonstrated through academic experiments with CAR-T, the results of which most of the listeners will be very well aware of, that have been further validated more recently by sponsored studies. We've since seen the same kind of data emerge for T-cell engagers. Both CD19, CD20, BCMA, but various B-cell-directed targets have achieved depths of response that seemed only attainable with CAR-T, but now with the T-cell engager, some of which have clunky administration, narrow therapeutic indices. We think that an even better molecule, like CLN-978 in our portfolio, has an opportunity to achieve similar results with an improved therapeutic index, allowing the drug to be administered with potent effect in routine settings of care, which for most autoimmune disease patients in the U.S. is in the community. Thank you. Thanks, Jeff. I think I somewhat covered the next question already, but I'll ask it anyway. Following the TC datasets presented at EULAR, what learnings do you take away, and how do you view CLN-978's differentiation from other candidates in development for autoimmune disease? I think there are a couple of, before maybe talking about CLN-978 specifically, just what are the key learnings? The key learnings are that T-cell engagers can achieve a depth of B-cell depletion associated with disease-modifying treatment effects. That can be achieved with a therapeutic index that appears acceptable in the autoimmune disease context. This has been shown across now a range of diseases: inflammatory myositis, systemic sclerosis, places where there aren't many effective therapies, as well as in patients where you would think there are plenty of adequate therapies, like rheumatoid arthritis, but there are still patients who cycle through all of them and have need for additional therapy. There is clearly a dose-response effect demonstrated. It does appear that when patients are treated at doses closer to the oncologic-approved doses of these repurposed molecules, the responses are deeper. It's generally requiring application of more than one therapeutic dose, but still a defined duration of a B-cell-depleting dose. If we look now to CLN-978, we've shown preclinically and in our initial first-in-human study in non-Hodgkin's lymphoma that we could achieve depths of B-cell depletion greater than 95% peripheral blood B-cell depletion at doses that were associated with no ICANs and no higher than grade 1 cytokine release syndrome. We believe that in application in autoimmune disease settings, the safety profile will likewise hold up. The molecule is designed to be highly potent through specificity for CD19, exceptionally high binding affinity picomolar concentrations, as compared to nanomolar concentrations for the CD3 binding arm. Preclinically, and again in our initial clinical experiments, this demonstrated a broad therapeutic window between B-cell-depleting doses and the doses where there were high levels of cytokine production that in the clinic would be associated with clinical cytokine release syndrome. The molecule is really small, so in instances where tissue penetration is important, 65 kilodalton versus antibody-sized molecules in the 130-plus range, we think that this drug, through binding to human serum albumin, extends half-life to give it antibody-like kinetics, but with bite-like features. Together, it presents a very compelling molecule for developments in autoimmune disease. Thank you, Jeff. The non-significant data in SLE, you pushed it back slightly from Q4 to 1H 2026. If you could just provide some flavor to why. When we see the data, what data should we expect to see? Sure, yeah. Happy to cover that. As I said, a small change from Q4 2025 originally to first half 2026 now. Two important things about that. The first and most important, the update was not based on any adverse clinical findings. Let me just make that very clear. The update only applies to the lupus study. The RA study is still expected per original guidance of the first half of 2026 for the initial data. If you think about first half 2026, now we'll be able to have a more comprehensive update with data from both studies, lupus and RA. I think the thing that we've found, which I think our industry has found in general, lupus studies are hard to enroll in. That's the first thing I'll say. However, I will say at the same time, we have seen a tremendous amount of enthusiasm from both our study site and investigators. That was manifest in the way that we saw a very high level of activity in patient screening, which is very, very important. Jeff and the team have been really engaged with sites. I'm going to ask him to elaborate on this finding and also talk about an action plan moving forward to make sure we're able to deliver data in the first half of 2026. Yeah, and maybe Nadim, I'll just underscore that initial point that you made, that investigator enthusiasm has been quite high. The majority of our sites that are active have screened one or more patients for the SLE trial. As Nadim alludes, screening has not always led to enrollment. We've been out speaking to our investigators on site, talking to their teams. What we're finding is that the initial eligibility criteria were a bit too restrictive to facilitate enrollment into the study. This is really around two major issues. The first is around an extent of prior therapy, where we previously required patients to be experienced with either a biologic or cyclophosphamide, and then secondarily, the SLEDI score of eight or higher. In a protocol amendment that we have implemented, we have broadened the eligibility to include patients who receive biologics or small molecule inhibitors, which are much more likely to be given, particularly to patients treated in community settings, and lowered the SLEDI score from eight to six, which is still the cutoff for moderate disease by the SLEDI. In reviewing our screening logs, we can see that this would have allowed a significant number of patients to enroll on the study. As importantly, we understand from our sites and their staff that this would allow more patients to actually enter screening because there's this prescreening rate that it's hard to characterize, but we knew that some patients were not being presented the option of the trial because you could just review their record and know they wouldn't be eligible. We're continuing to increase the number of sites. This will increase the number of academic sites in particular since they are a bit slower to come online, and where they are enriched for patients with higher disease activity and more extensive prior treatment. We'll do this in the U.S., Australia, and Europe to have the broadest reach across the patient population. I'd also emphasize that here in the U.S., we have partnered with some important patient advocacy groups who partner with select companies to accelerate the enrollment to their studies by helping sites activate trials and helping us interact with investigators and site staff. The Lupus Research Alliance, the Lupus Therapeutics Arm, runs a Lucent network, and we're very proud to be partnered with them in working to execute this important trial. I think altogether, these things will help compel us to proceed through the dose escalation far more expeditiously. Yeah, one thing I would add, Sean, on this question is, you know, given that this is our highest priority program, we're going to continue to make sure we're, you know, applying the resources needed to continue to expeditiously advance the program. That's important. Going back to your question about expectations around the initial data for lupus, the way we've framed it is it's going to be data from part A of the study, which is the dose escalation phase. The two key areas, first, safety, obviously critically important in a dose escalation phase of the study, as well as B-cell depletion. They're the two areas we're really going to focus on in this initial data cut. Of course, any clinical findings, et cetera, we have, we'll report out. Things like durability, et cetera, will be in subsequent reports of the data. Wonderful. Thank you. What is the B-cell depletion remission in systemic lupus erythematosus, and what can we expect to see that data for CLN-978? Sure. Yeah, I think the first most important thing to point out is that today, investigators are not getting their patients into B-cell depletion remissions. I do think there's still a little bit of a disconnect between investigator expectations and investor expectations. That's the first thing because when we speak to rheumatologists, what they tell us is currently, when they look at their standards of care, including, by the way, the biologics, the antibodies, they're always adding those treatments on top of chronic immunosuppressive background therapy. I think with the T-cell redirecting therapies, CAR-T or T-cell engagers, this is the first time they're having the opportunity to take patients off their background therapy and truly get into B-cell depletion remissions. I think the advantage, and Jeff alluded to earlier with T-cell engagers, is that you have this off-the-shelf potential disease-modifying approach that rheumatologists can give to their patients in the community where those patients are. That's where we see the very strong advantage. When we speak to investigators and KOLs to ask, OK, what are you looking for, which is really at the crux of your question, what they tell us is, since I can't get my patients into B-cell depletion remission today, if you have something that I can give in the community that can give a minimum of 20% to 30% of my patients and get those patients into B-cell depletion remission, you're going to see systemic widespread adoption. Obviously, we're going to push for higher, but the point is the bar for T-cell engagers is much lower because it's a treatment that they can give in the community, and they don't have to go through all the other things with some of these more complex modalities. We're very pleased about the opportunity we have with CLN-978 for those patients. Wonderful. Perhaps moving away from CLN-978 in systemic lupus erythematosus, but CLN-978 in rheumatoid arthritis, first data expected in 1H 2026, perhaps help us characterize what you see as the unmet need there. Yeah, I think if you look, I mean, RA obviously is a very large indication. If you think about the U.S., you're talking about just under 2 million patients, almost 1 million patients that are the moderate to severe patients. When you look at the truly so-called polyrefractory or difficult-to-treat patient populations, the patients that are going to be in our study that have failed multiple DMARDs, that alone is 60,000 patients. That's like all of lymphoma combined. This is like the magnitude of these large autoimmune indications. I think there, there's clearly a significant unmet need. Our starting point will be in those difficult-to-treat patients. If we see good activity there, we have the opportunity to move up in the treatment sequence and much larger opportunities. Right now, the RA study started quite a bit after the lupus study. The team's really focused on execution. In both the lupus study and the RA study, we are actively dosing patients. For the RA study, because it started later, we haven't given exact guidance to that first data set, but we will do over the coming weeks and months. Thank you. Can we expect to see tissue penetration data here or other data that will differ from what you all shared with the SLE study? Yeah, that's a great question. Just to emphasize that while we would have liked to have included some assessment of tissue-level B-cell depletion in the SLE study, we knew that that would be prohibitive for patient recruitment, which is already a somewhat challenging setting to recruit patients. On the other hand, in RA, particularly in Europe where we're conducting the study, synovial biopsies are often obtained as part of standard of care. We can incorporate synovial biopsies into our RA study at the European centers to look at the level of B-cell depletion in disease-affected tissues. We also have the opportunity in a subset of patients on that study to look at B-cell depletion in lymphoid tissue through lymph node biopsies. In the case of Sjogren's, salivary gland biopsies are also often obtained either for diagnosis or as part of monitoring patients. They're minimally invasive, a part of standard of care, and can be integrated into a clinical trial and allow us to obtain this important tissue-level B-cell depletion data. As Nadim said, the silver lining of presenting the more fulsome data in the first half of 2026 is that we'll be able to have observations from multiple clinical studies. Thank you, Jeff. The place one in Sjogren's, thrilling in the US and Europe, what's the overlap of areas of potential or potential synergy with other autoimmune indications that you're chasing? Yeah, I mean, primary Sjogren's is still quite common in the U.S., about 800,000 patients. If you look at the number of patients that are affected with secondary Sjogren's or as an overlap syndrome with another significant autoimmune disease like RA and particularly lupus, the numbers are many, many times that. Sometimes the features of Sjogren's, in either case, primary or secondary, are relatively untreated, except symptomatically with available therapies. Progress in Sjogren's has been relatively limited. I think part of it is an increasing understanding that while less common, 15% to 20% of patients with Sjogren's will ultimately develop a severe systemic disease that is every bit as severe as other autoimmune diseases, not just dry eyes and dry mouth. For that group of patients in particular, disease-modifying therapies are necessary. I think there's an opportunity in Sjogren's itself. To the extent that you demonstrate activity in Sjogren's, there is a halo effect for therapeutic benefit across a broader range of autoimmune diseases that are sometimes, you know, overlapping with Sjogren's disease. Thank you. You touched on this in the intro and the China question, but with belanotamab, can you talk about what drove the decision and how you see the T-cell engager complementing 978? Sure. Yeah, absolutely. With CLN-978, we have a potent B-cell depletor. With belanotamab, we now have a potent plasma cell depletor. Between the two agents, we now have the opportunity to reach a broader range of autoimmune diseases than either molecule or either approach alone. I think secondly, for us, we still view CD19 as the optimal target, given the breadth of the B-cell compartment that it covers. For those diseases where B-cell dysfunction is a primary driver, then clearly CLN-978 is going to be the right treatment for those patients. However, there are some diseases where the pathophysiology is driven by these pathogenic autoantibodies that are produced by long-lived plasma cells. Long-lived plasma cells typically have very low CD19 expression or no CD19 expression. That is where belanotamab can be really useful. I think between belanotamab and CLN-978, we now cover the full range of the B-cell compartment. It will allow us to, again, reach more diseases and have a very complementary approach with CLN-978 being targeted for those diseases where B-cell biology is important and for belanotamab, those diseases where plasma cell biology is much more important. Great. Thank you. Cullinan will be responsible for further development in autoimmune disease following the completion of the phase one data by Generex BioHope. Those are expected to start by the year end, I believe. Can you provide more color on what will drive your decision to prioritize which autoimmune disease? Yeah, sure. Jeff, you go. Yeah, it's a great question. I do think there is evidence already existing that the role of plasma cells, particularly long-lived plasma cells, are central to the pathophysiology of certain disorders. Probably the single best example is myasthenia gravis, where anti-acetylcholinesterase receptor antibodies are clearly produced by long-lived plasma cells. In that situation, directly addressing the pathophysiologic, the pathologic cell, the long-lived plasma cell offers the opportunity for durable benefit in the absence of ongoing therapy, which would really distinguish the T-cell engager mechanism of action from other available therapies like FCRN. There is a broader group of diseases that are clearly antibody-driven. There are already some case studies reported for patients with thyroid eye disease and Graves' disease. We've also seen emergence of the utility of BCMA after CD19 failure in patients with autoimmune cytopenias, which are all antibody-driven. I think there are some places where existing data tells us there are initial good places to go. I think there are a lot of opportunities. We're continuing to explore those for a differentiated development strategy from CD19, as Nadim alludes. Wonderful. Thank you, Jeff. Moving to zipolirenib, you presented the Resilient One results yesterday. Can you provide a recap of the data shared? Jeff? Sure. With our partners at Taiho Oncology, we actually presented two data sets, one Resilient One, which is our Cullinan-sponsored phase two study. The data that we presented was from a cohort of patients, 84 in total, who had received prior therapy with amivantamab, which, as many following this space will know, is a fully approved drug for the treatment of exon 20 patients. In that group of patients, we showed that in patients who had received amivantamab prior therapy in the broad group, a 27% overall response rate with clinically meaningful durability. If we drill down to the subgroup of patients who had only received prior amivantamab and no other exon 20-directed therapy, like a TKI, the response rate rose to just above 30%, durable out to about eight months, which is a clinically meaningful response and a clinically meaningful durability in a very heavily pretreated group. The safety profile so far is very similar after amivantamab, as in patients who had only received prior chemotherapy, with most of the adverse events being typical for EGFR inhibitors, low grade in most cases. Thank you. Taiho Oncology, I believe, is on track for the regulatory submission to be completed by year end. Can you talk more on the strategy and the launch preparations? Sure. Yeah, happy to do that. The first thing I would say, our partners at Taiho Oncology are leading the commercialization efforts. They have a strong track record in the U.S. of being able to commercialize targeted therapies very effectively. We do have a co-promotion option, which would be post-approval of the drug in the front-line setting. We have plenty of time to decide whether or not we want to opt in. The way the deal is set up, we are still owed that $130 million for first-line and second-line approval. We do have that 50/50 profit share in the U.S. The 50/50 profit share, the cost part of that applies whether we have our own field force or Taiho Oncology has 100% field force. We don't have to make that decision yet until the front-line approval. Wonderful. I believe data from Resilient Two cohort and patients with active brain metastases, they're expected at ESMO. How should we think about the additional market opportunity in the two Resilient Two cohorts? Yeah, I would say, if you look at the uncommon EGFR mutations, that's about 12% of all EGFR mutations. It's of a magnitude of size that's similar to the exon 20 population. That's quite an attractive opportunity. With brain mets, if you have a molecule that can solicit intracranial responses, that can apply across both exon 20 and non-exon 20 subsets. That would really be the hallmark of a very differentiated molecule. That, of course, opens up a pool of broader patients because as patients' disease progresses, you see the incidence of brain mets accumulating. It really is a significant problem. Generating data that, again, shows intracranial activity would be important from a differentiation perspective. I think just to add to your point, Nadim, it's also very important for moving the drug up earlier in lines of therapy where the size of the patient pool is larger, since investigators have told us consistently that drugs with intracranial response rates are important as part of front-line therapy, as well as opportunities for adjuvant therapy after surgery, where you're really focused on preventing intracranial metastasis and prolonging overall survival. Okay. Second to last question, just remind us of the balance sheet and the runway position. Yeah, I think so. In our last quarterly earnings, we reported over $500 million in cash end of June 2025. As we think about this catalyst-rich period ahead of us, that does give us the resource to have both near-term and longer-term catalysts. Just as importantly, you know, ensures that we don't have an immediate near-term need for capital raise, which in this market is pretty important. I think, as you alluded to, Sean, we have cash, we have catalysts, and we have the programs in place to kind of continue to drive value for patients, but also our shareholders. Right. One final question. What didn't I ask that I should have? I think one area that we're excited about is in Q4 this year, for the first time, we'll be presenting our initial data for CLN-049, which is our FLT3 x CD3 T-cell engager. It's another T-cell engager. T-cell engagers have become a core expertise for the company. We look forward to presenting those data in Q4. Wonderful. We're coming short on time. Thank you, Jeff, for your time today and attending the conference. Appreciate it. Appreciate it. Thank you, Sean.