Good morning, and thank you for joining our session of Citi's Virtual Oncology Leadership Summit. I'm Samantha Semenkow, one of the senior biotech analysts here at Citi, and it's my pleasure today to be hosting Cullinan Therapeutics CEO, Nadim Ahmed, and CMO, Jeff Jones. Nadim, Jeff, thank you very much for joining us today. Great to be here, Sam. Thank you. For those listening live, if you have any questions during the session, please feel free to email them to me directly at samantha.semenkow@citi.com, or you can put them into the portal, and they will go to my email as well, and I'd be happy to ask those questions on your behalf. I think we can just get started then. Nadim, maybe you can kick us off a little bit and talk about the evolution of Cullinan's oncology pipeline, a little bit about what assets you've prioritized recently, the company's overall strategy, when it comes to developing assets for oncology in particular. Sure. Happy to do that, Sam. Look, the first thing I'd say is 2026 is a very exciting year for Cullinan Therapeutics. We've got multiple catalysts across our whole program and pipeline, and especially for our two high-priority T-cell engagers, CLN-978 and CLN-049. If I may, divert slightly away from oncology for a second or two, Sam, so- Of course. Starting with CLN-978, which is our CD19 by CD3 T-cell engager we're developing across autoimmune diseases. There we have a best-in-class potential opportunity with a global development program across multiple large market indications in autoimmune diseases. And thinking about the molecule itself, we believe we have a very highly differentiated molecule relative to other CD19 T-cell engagers, especially since we have very high binding affinity for CD19. We have a very small molecular size, and all of that combined with subcutaneous administration, which obviously is convenient for patients. Also, I think our only aim or goal for the program ultimately is to move up early in the treatment sequence so that we can also displace monoclonal antibodies that are often used across these autoimmune diseases, which are very safe, but with marginal efficacy. So I think we have a potent molecule that can do that. I would add, you know, thanks to the work that Jeff and his team are doing, we have great momentum across our global development program for autoimmune diseases. We have three high-value indications, so lupus, RA, and Sjögren's disease, and we plan to present the first company-sponsored data for a CD19 T-cell engager throughout 2026, so very exciting for that program. And then the last thing I'll add is there's still significant strategic interest in the B-cell depletion space. You probably saw last week, Lilly acquired Orna Therapeutics, so it remains an area that's actually very hot. So now let me get back to oncology, to your original question. So I think the first molecule I'd point out is CLN-049, which is our FLT3 x CD3 T-cell engager, which we're developing in AML. So this one, here we have a potential first-in-class opportunity to bring forward an immunotherapeutic approach to address a broad group of AML patients, and unlock significant commercial value. I would say AML is probably one of the last large, heme malignancies where we haven't seen an immunotherapeutic approach be successful, so obviously, this is very exciting for us. We presented dose escalation data at ASH, in December 2025, where we presented compelling monotherapy efficacy data, which we believe is within the regulatory benchmark for success, and we can certainly come back to that. In 2026, we're really focusing on going from dose escalation to dose expansion, dose optimization, and really using the Fast Track designation status we recently got from the FDA to then select a recommended phase II dose so that we can move towards a single-arm pivotal study for relapsed refractory disease. At the same time, in parallel, we're also moving the program in the frontline setting, so we're planning a phase I/II combination study with venetoclax towards the end of this year. And so we're making sure we're working both in relapsed refractory disease and also taking the frontline opportunity in parallel. With zipalertinib, the program that's been here since I joined the company and has come full circle. So that's our EGFR exon 20 tyrosine kinase inhibitor, which addresses non-small cell lung cancer. Here we have, I would say, both a clinically and financially de-risked molecule with best-in-class potential. And I say financially de-risked because of our partnership with Taiho, where we, we managed to, strike a great deal back in 2022. So our partner, Taiho, is planning to complete the rolling NDA, which was started towards the end of last year. That's again for relapsed EGFR exon 20 non-small cell lung cancer, and to complete that rolling NDA submission this quarter, and at the same time, also complete enrollment in the frontline study in the first half of this year. And so I think with zipalertinib, clearly we see this as a molecule that can address important unmet need. But with the deal we have with Taiho, it also represents an opportunity to bring in significant non-dilutive capital through regulatory milestones and a 50/50 profit share with Taiho. So that molecule is on its way to NDA submission and an important milestone for the company to have our first NDA. So that's another exciting opportunity for the company. And then going back to your question, Sam, about how do we approach pipeline and pipeline strategy, you know, we really focus on molecules that we believe have the potential to either be first-in-class or best-in-class before we actually put them in the clinic, and, and molecules that can really have a transformative impact for patients with cancer and also, of course, autoimmune diseases. And so the pipeline that I went through, I didn't mention velenomatum yet, but if you think about oncology, we're addressing both clinically and commercially validated targets with exon 20 and FLT3. On the autoimmune disease side, we're addressing, again, clinically validated targets with both CD19 and BCMA. So I'd say we have a relatively de-risked pipeline also. All of these molecules have demonstrated monotherapy efficacy in the clinic, and all of these programs are addressing substantive market opportunities. So I think both on the autoimmune side, and on the oncology side, we're looking forward to a really exciting 2026. And then the last thing I'd say, which is very important, is we have a very robust balance sheet. As of the end of December last year, we reported over $430 million in cash, giving us runway into 2029, which allows us to execute on all our programs, but especially CLN-978 and CLN-049, so that we can deliver shareholder value quickly. Thank you. I think that that was a wonderful intro. It gives us a lot to work off of. And I would—let me just say, before you go back to oncology, that I'm very excited for the CLN-978 data that's gonna start rolling out in the second quarter, so looking forward to that. But why don't we, going back to oncology, start with CLN-049? Can you just share a little bit about this molecule design, how it binds to FLT3, and what about this molecule is perhaps differentiated from some of the prior attempts we've seen to target FLT3? Yeah. So maybe, Sam, I'd just start by emphasizing that in this case, we're thinking about FLT3 as a target for immunotherapy rather than as a target for kinase inhibition. So FLT3 is a receptor tyrosine kinase that in about 30% of patients has kinase domain mutations that lead to constitutive activation. But it's actually an oncogenic driver and present on the surface of AML blasts in at least 80% of cases, regardless of a kinase domain mutation. So it really does access the broad patient population of AML, and it is... You ask, how are molecules distinct within prior molecules previously developed for FLT3? There's actually been relatively limited development of FLT3-directed immunotherapies. Ours is built on an IgG backbone. It has two arms binding to FLT3, and at the C-terminus, has two single-chain variable fragments that bind to CD3, although only one of them is functionally active. Preclinically, very high affinity for FLT3, with a favorable cytokine window, which has now been demonstrated in the clinic. In terms of prior FLT3, the program that made the furthest was a BiTE- like structure in the Amgen portfolio. That molecule was on a half-life extended BiTE format that has largely been discontinued at Amgen. So I think the failure of that program ultimately, we have heard for intolerable cytokine release syndrome, may be more of a format liability than a target liability. And we think that you know, the data that we've generated to date for FLT3 really validates that the approach we're taking is a good one. Well, so then maybe let's dive into that data that you presented at ASH. You know, or maybe just give an overview of the efficacy and safety data that you've seen so far, and what's really stood out to you as, you know, impactful for this disease? Yeah. So I think there are, there are two ways. This is primarily a safety study, but in this dose escalation phase, we actually saw really compelling efficacy. And once we had reached a dose of 6 micrograms per kilogram, again, emphasizing the potency of the drug, we began to see complete responses emerge, and complete responses in AML are really what matters. You want all of the AML to be eradicated, and you want normal blood-forming elements, normal hematopoiesis, to recover, and that's what we began to see at 6 micrograms. At the time of ASH, we had further dose escalated up to 12 micrograms per kilogram, and in this group, we saw 8 patients achieve a form of CR, either a complete response or a complete response with incomplete hematologic recovery, which also tend to be quite durable. In that group, at least 5 of the patients had responses that were durable in excess of 4 weeks. So a reasonably high rate of complete response, composite complete response, about 30%, and the majority of those patients durable for at least 4 months. So a measure of clinical benefit in terms of durability. But that's only half the equation, of course. If those responses are achieved, you want to know in which kind of patients, and here we saw that the responses appeared to be achievable, no matter the patient's underlying genetic risk, which often is the key prognostic factor in AML, as well as a predictive factor for treatment. There, the most profound observation was in TP53 mutated patients, probably the worst prognostic subtype of AML, where the drug seemed to work equally as well, with or without TP53 abnormalities. Finally, this was achieved with a favorable safety profile. If you compare the overall rate of CRS, which was about a third of patients, that compares favorably to any T-cell engager yet approved in hematology. And we saw only 1 grade 3 CRS case, that in a patient who received only a single step-up prior to the therapeutic dose. Once we instituted a 2-step-up dose regimen, we did not see further grade 3 CRS, and saw a general trend to lower rates overall and sort of a shift to lower grade CRS, on the whole. That step-up, that double step-up that you found, I mean, is that just, you know, less drug a little bit, to get the patient sort of acclimated to the therapy? Is that proving out as you continue to, you know, expand in those double step-up cohorts? Yeah, it's a, it's a great question. You know, there are a lot of theories why it works, it has become the standard approach to mitigating CRS and initiating therapy with T cell engagers, and all of the approved T cell engagers utilize some form of step-up dosing. It appears that by delivering pharmacologically active doses, that is, doses that activate T cells but are still associated with relatively low levels of cytokine production, you preclude the risk. You limit the risk for higher grade CRS when you deliver higher therapeutic doses. This was first established with the first approved T cell engager, blinatumomab, going back to the 2000s, and now has become sort of standard practice. When you look at the safety profile that you've generated t hus far, is this something that you think could be, you know, an outpatient dosing setting for, you know, in the actual community? Yeah. So, you know, for AML docs, the distinction between inpatient and outpatient is a little less important since they are very used to giving therapy inpatient. Because of the inherent risk of treating an AML patient with a T cell redirecting therapy, I tend to think that therapy might always be started in the hospital. But even now, once patients are established on therapy, treatment can be safely given in the outpatient. And Nadim and I both have experience with commercializing, developing and commercializing drugs in AML, where initiation of treatment in hospital is not uncommon. Okay. All right. There's definitely a path for a bit of outpatient dosing down the road, I think. That's correct. We have a few client questions actually that have come in. Okay. So, you know, one of them is asking: Where do you intend to go one dose from here, and for the data later this year, including the higher doses and the 12 micrograms step-up? So I guess, you know, once you have that, I think, final cohort, I think what they're asking, you know, where do you intend to go from there? Yeah. So Nadim? No, no, I was, I was saying, Jeff. Oh, oh, okay. Sure. So, the next phase of the study that we outlined around the time of ASH is to complete the dose escalation, and we stated our intentions to dose escalate up through a target dose of 24. And that is still the plan. And then, after completion of dose escalation and potentially some backfill within the dose escalation phase, to generate additional PK/PD data, we anticipate initiating expansion cohorts in the second quarter of this year, and we're still on track to do that. That's important to not only confirm the clinical observations from the dose escalation phase, but it is also important to support selection of a recommended phase 2 dose for future development. And we have stated, that our current timeline has us on a trajectory to initiate a registration-enabling study in relapse refractory AML by the end of 2027. The other thing that we'll- When will we- Sure. Just an... When will we- Mm-hmm See that next tranche of data? And are you enrolling more patients at the 12 micrograms step-up that we've seen initial data for, and will that be included in the next tranche of data? Okay, good question. So we've stated our intention to provide a data update in the second half of this year, and we'd provide greater specificity as the year goes on. We have continued to enroll some patients in backfill cohorts at doses of interest, including 12 micrograms, again, to support additional PK/PD observations that help us support a dose for further development with regulators. Yeah, Sam, I would add to what Jeff said, the reason we've also said second half of this year is because we wanna make sure, as Jeff said, we enroll all the cohorts, but we also wanna have enough follow-up to assess durability accurately as well, which is very important for the next data release. That makes sense. And Jeff, I think I might have cut you off mid-response. I don't know if you- No, I think we- Okay. Apologies there. ... got the thought out. No worries. And then they're asking one more question, actually. So, and I think this goes into those higher doses that you're enrolling now. You know, what is the goal here relative to the CR and CRh rates that you've already seen that, you know, are quite encouraging as you continue- Mm-hmm - to dose escalate higher? Yeah. You know, another way of asking—sometimes people ask a different question, and they say, aren't you concerned that the response rates will fall off when you move into expansion or phase 2 development? So the short answer is, we wanna make sure that we don't leave any efficacy on the table. At the time of ASH, we showed that we clearly had a therapeutic index to continue dose escalation, and so we wanna make sure, in this very difficult-to-treat disease, that there isn't an opportunity to further improve efficacy with greater exposure. So that was the intention of continuing the dose exploration. But we don't believe, based on our current understanding of the molecule and modeling, that we need to dose escalate much above, you know, the current level. So we do plan to truncate it at 24. But that's the reason. If we could get to a 40% response rate, we'd be overjoyed, right? So long as we feel like there's still a margin of safety, that's a worthy goal. Got it. That makes sense. And then, Jeff, you alluded to this a little bit, but you're seeing responses in patients that have TTP53 mutations. These patients are responding, and they even have some durability as well. Can you just talk about, you know, how these patients are currently managed and what the KO response has been to seeing responses in this population? Yeah. So TP53 mutated patients have a dismal prognosis, so median life expectancy beyond the time of diagnosis is six months. So that's the worst of the worst in cancer diagnoses. And when you lose your TP53, you sort of become insensitive to the effects of cytotoxic chemotherapy, which have always been the cornerstones of treatment for AML. So therapeutic options for that group are not well established. There's no existing standard of care. Many patients receive venetoclax, but the response rates are woefully inadequate, and survival has not significantly improved. Current treatment guidelines state that the first best therapy for a patient with TP53 at any line of therapy is participation in a clinical trial. And so to be able to see that similar rate of 30% composite CR. Actually, it was a bit higher in the TP53 group. It was 50% in that group. If you see that rate, physicians are really impressed because if you can treat the hardest of the lot, it speaks a lot about the potential for the development of your drug. It's also an alternative development pathway. While we still think our first approach will be development in the broad group of relapsed refractory AML patients, this is another area of particular developments and regulatory interest, and there have been companies that have sought development in TP53 mutated AML as their primary development strategy. So that does present a fallback strategy as well, and there, the threshold for success is likely significantly lower than in a broader group of patients. Got it. But, but the planned single-arm trial that could be pivotal for accelerated approval in relapse refractory, that would include TTP53 mutated. It would be an all-comers sort of relapse refractory or no? Yeah. So I think the data from our initial expansion will help us take a final decision there. There, we are pulling those patients out into a separate cohort for two reasons. The first is sometimes the results in that group have been different than in our broader group. And then secondarily, it's also an opportunity to treat patients with previously untreated TP53 mutated AML. As I stated, standard of care is participation in a clinical trial at all lines of therapy, so it also presents this unique opportunity to give the drug to previously untreated patients, where there is some expectation it may work better, potentially in patients who haven't been somewhat beaten up by exposure to prior therapy. Once we see that, if we were to see that those response rates continue to hold up as largely similar, there wouldn't be a whole lot of reason to continue to exclude them. Got it. Okay, so two separate expansion cohorts that you're planning to initiate, I think you said next quarter. That's still on track? Q2. That's on track. Right. Perfect. And so then you'll take one dose into both of those expansion cohorts, and then those will—what you see there will inform that single-arm pivotal design? Actually, Sam, in at least one of those cohorts, the all-comer non-TP53 cohort, we will likely expand it more than one dose. Standard recommendations or direction, I should say, from the FDA, is to expand in more than one dose to support selection of the recommended phase 2 dose for further development. The earlier you dispense with that dose optimization exercise, the fewer patients, the faster it can be settled with the agency and allow you to move more rapidly into real registration-enabling development. We'll try to get that done as well this year. And then, Nadim, you mentioned this in your intro, how you believe you've already sort of met the regulatory bar that you would need for the single-arm study. Can you just talk a little bit more about that and maybe what gives you confidence in pursuing that accelerated approval pathway? Sure. Yeah, yeah, happy to do that, Sam. I think the fact that we've seen this very promising monotherapy efficacy, as Jeff outlined, including in the TP53 patients, I think that got us really excited. It gives you then, in this disease especially, a very, very clear development and regulatory pathway. So you can get relapse refractory approval, potentially with a single-arm phase 2 study, and then use a frontline study to serve as both the confirmatory study as well as the expansion study to get you in the frontline setting. And so sticking with relapse refractory disease, if you look at the recent precedent over the last few years, you see that companies have generally got registered on a single-arm study of about 100 patients, typically accelerated approval, but sometimes full approval. And-... And all of these molecules have been targeting a specific biomarker-driven subset of patients. So the treatment of relapsed refractory disease is highly fragmented. The fact that we have a treatment that could be broadly applicable, it really gives us an opportunity to both disrupt and defragment the current treatment of AML, and that's why we're super excited about it. And so if you look at those approvals, you see a CR/CRh rate of around 20%-30%, with duration of 4-6 months. And I think that's why we feel very good about where our data are. And as Jeff said, obviously, we need to reproduce it, we need to get more patients, but what we've seen so far is extremely encouraging for both the broad all-comer patient population, but also the TP53 patients. The other thing I would add, and Jeff kind of alluded it before, is that within the company, we also have very, very strong hematology expertise, including Jeff, by the way. So I think between the two of us, we've either developed, commercialized, or launched five drugs in MDS AML. We have deep hematology expertise in the company. So clear regulatory pathway, clear development pathway, with very strong expertise in the company in this space. Got it. Yeah, no, that should serve you very well as you continue to push CLN-049 forward. What about the frontline setting? I guess, what do you need to establish from the dose escalation or the dose expansion cohorts that you're planning in order to move into that setting? And when would you consider starting that study? Yeah. So I think we've seen what we need to see from the program to begin planning a phase Ib to combination study in the frontline, and we've stated our intention to commence that study by the end of the year. But what's the backbone there? We are planning a study built around venetoclax and azacitidine, so hypomethylating-based therapy. And while that is currently approved and largely has been thought of as therapy for elderly or infirm patients with comorbid medical illnesses, emerging data is suggesting that it may be as good or even better than traditional 7+3 induction chemotherapy, which has been the mainstay of treatment in younger, fitter patients since the mid-1970s, with very little modification. Mm-hmm. The data to support that comes from a number of places, but probably the most prominent is a study called the Paradigm Study, a randomized phase II study presented at ASH this year, that showed equivalent, or in some cases, better outcomes in patients treated with VenAza over cytotoxic induction, and much favorable safety. So those were in younger, fitter patients, and so it seems that that's, like, the backbone for the future, and that's where we're built. We do need to do some dose finding, as experienced with other drugs being added to VenAza has shown, you sometimes need to think about the way to introduce your drug into combination, and you need to ensure that you are still maximizing the treatment intensity of the backbone regimen. And so we're working through those design considerations, seeking external input, and we'll ultimately share a study design and time, but are on track still to have that started by the end of this year. Got it. So you could have maybe, I guess, a part of the study that does that dose exploration, and then you move into the pivotal cohort with the selected doses for all three assets? At least a phase II cohort. I mean, I think the anticipation is that because this will be powered for survival in the frontline, it would require a randomized study in order to satisfy regulatory expectations. But this study would be a label-expanding study, but also, you know, a future phase III, but also be a confirmatory study for a potential accelerated approval in second line beyond. Got it. Okay, perfect. That makes sense. So then maybe we go back to the upcoming data update in the second half. We're going to see more durability, obviously, that higher cohort, some backfilled patients. Is there a chance we also see some early expansion cohort data or... And, you know, let me just ask another question then. When could we see that expansion cohort data, considering it will be informing the design of both of your studies? Sure. Yeah. So definitely one step at a time, Sam. So I think, as we mentioned, for the current dose escalation study, the next update will be in the second half of this year. That's the plan, and as Jeff alluded to, this is to make sure we can capture all cohorts to assess both response and durability, so that's going to be very important. I think the other aspect of, that study update is, you know, we anticipate that we'll have a follow-up period of at least six months for most patients. So again, it'll allow us to inform, durability as we move forward. We haven't yet guided to the expansion study data readout. I think we're going to take the time to start the study first, and of course, we'll keep everyone updated in the future. Got it. Okay, that makes sense. So then, you know, just a last question on CLN-049 before I spend some time on zipalertinib. Just what does the addressable market look like as you move- Mm-hmm - into the relapsed refractory patient population first, and then, you know, down the road, potentially, expand the label to frontline? You know, how should we think about, the market opportunity there? ... Sure. Yeah, so, in the US, every year, approximately 20,000 patients are diagnosed with AML. And unfortunately, most of those patients relapse, so that does create quite a large relapse/refractory pool of patients. And the fact that we're addressing an all-comer patient population, for example, unlike the menin inhibitors, which address 30%-35% patients. So when you have the whole pool of patients to work with, a large relapse/refractory pool, the way we think about it, yeah, we anticipate that the relapse/refractory segment could be a billion-dollar segment on its own. And then when you move up into the frontline setting where you have more patients, obviously longer treatment duration, you know, that can potentially unlock a multi-billion dollar opportunity. Again, with a very clear regulatory development pathway, one Phase II study for relapse/refractory approval, one Phase III study for frontline approval. So from a capital allocation ROI perspective, it's a very attractive value proposition. Got it. Makes sense. So, I wanna spend a little bit of time on zipalertinib. So, you know, you mentioned that Taiho is completing the rolling NDA submission. Now, you know, if we assume that does gain approval, I'm wondering just, you know, how we should think about, you know, the market opportunity for that drug, and maybe you could take us through a little bit about the profit share agreement and how to think about the cadence of revenue generation there, you know, giving a 50/50 profit share. Yeah. So I think, the first thing I would say is, you know, our estimate and the publication literature varies, but exon 20 non-small cell lung cancer in the U.S. is probably 3,000-5,000+ patients diagnosed annually, and it's, it's one of the largest subsets of the EGFR mutated patient population. So I think for us, we thought it's an attractive opportunity. In terms of the agreement with Taiho, so when we first did the deal, we had an upfront, cash injection into the company of $275 million, which, quite frankly, has really helped to kind of advance the pipeline and talk about some of the other molecules we spoke about today. So for us, that was a great deal. Taiho owns ex-US development commercial rights, so we have a 50/50 profit share in the US. We also are owed $130 million in regulatory milestones for US approvals in both the second-line plus and frontline setting. So that's what I refer to as a near-term source of non-dilutive capital. And I think the way we think about kind of commercialization here, because we do have a co-commercialization option, is that Taiho is. You know, they're very very well equipped to address these kind of precision medicine approaches with the current portfolio they have in the US, where they're addressing, you know, very unique subsets of patients. So they have a strong commercial capability in the space. They run a very lean organization. The way we're seeing this deal evolve, it's going from a cost share arrangement to a revenue profit share arrangement. With that kind of focused commercialization effort that Taiho has, it becomes accretive very, very quickly based on the opportunity that I outlined. So again, it allows us to use those proceeds to continue to advance our programs, built into our cash runway, et cetera. So I think this is a very clear opportunity, but it also allows us to continue to bring non-dilutive capital into the company. Got it. That's helpful. And can we expect maybe like, as if it were to be approved in that initial quarters of launch, you'll provide more guidance over time on when you shift to profitability down the road, once you have a better visibility there? Yes, most definitely. The thing I can say today is that it will become accretive very quickly based on the very tight organization that Taiho runs in the commercialization space. Got it. Okay, that's helpful. Looking forward to that. And then you're also running, or Taiho is running a first-line study as well. I guess just, you know, briefly, what gives you confidence that zipalertinib can be successful in that first-line setting as well? Yeah. So, if we just look at the data that we've generated in relapse/refractory patients, so patients who would have failed frontline therapy with platinum, we see that their duration of response in the 40% of patients who respond in that setting is beyond 9 months, and the PFS similarly. That compares favorably to the PFS achievable in the frontline with platinum-based standards of care, which is roughly 6-7 months, depending on the series. So we already have some good data sort of suggesting the potential for durability of clinical benefit, which is really important in moving things into the, to the frontline. The design of our phase III study with Taiho is a randomized comparison of standard of care platinum versus platinum plus zipalertinib. This is a strategy successfully executed by J&J in getting Rybrevant approved in the frontline. So we think that in part, de-risks this design. Further, we understand that in some cases, TKIs can add toxicity to the chemotherapy backbone, but the favorable toxicity profile of zipalertinib and non-overlapping toxicities with chemotherapy gives us confidence that that won't be a problem. But the additive clinical benefit seems to be significant. And there, despite the ability of TKI to beat chemo, in the case of osimertinib, when osimertinib was added to chemotherapy in the FLAURA II trial, it not only improved progression-free, but overall survival as well, and survival always trumps. So our belief is that chemotherapy, and our KOLs tell us the same thing, is still a backbone of frontline therapy for exon 20, and that we will maximize the clinical benefit, and there, meaning survival, in combination, TKI plus chemo. A number of lines of thought that sort of build confidence there. Got it. Well, looking forward to that data. I think they've guided to completing enrollment this first half. Is that correct in that study? That is correct. Perfect. Okay. Well, looking forward to that. Well, I think we've been pretty efficient with our time, and this has been wonderful. I wanted to give you both an opportunity maybe just to recap what we have to look forward to, 'cause I know there's a lot of catalysts in 2026 across both the oncology and autoimmune pipeline, as well as any other closing remarks you wanted to share. Sure. Yeah, happy to do that, Sam. So, so summarizing where we are with CLN-049, based on what we discussed. So update from the dose escalation study, second half of 2026. Initiating dose expansion cohorts in the second quarter of 2026, and then completing enrollment of that dose expansion by the end of the year, so that we can identify a recommended phase II dose for a single-arm pivotal registrational trial, as we discussed. And then in Q4 2026, obviously, in parallel, we're continuing to develop the frontline opportunity. So as Jeff mentioned, we will plan to initiate a phase I/II combination study on top of the venetoclax backbone, which will then inform a future frontline randomized study, which will serve both as label expansion and confirmatory study. So lots of milestones for CLN-049. For zipalertinib, we want to get this NDA submission in, and so our partners have guided to finishing that this quarter, which is coming up very soon. And as you mentioned, enrollment of the frontline study in the first half of 2026, so we can fully maximize the opportunity with zipalertinib. And so I'd say with these updates from both CLN-049 and zipalertinib, plus the multiple milestones throughout the year for CLN-978, I think 2026 is going to be a real defining year for Cullinan Therapeutics and a great opportunity to value create for shareholders. Absolutely. Looking forward to all of those updates throughout the year. Thank you so much for the time. This has been wonderful. I really appreciate it. Thanks, Sam. Thanks, Sam. With that, operator, we can go ahead and close the call.