Dose range for the pivotal study. During 2025, we introduced a fourth dose level into the phase one study so that we could implement fixed dosing rather than weight-based dosing, which is preferable in the commercial setting. At this fixed dose level, patients will receive about 800 million cells in their first infusion and about 1.6 billion cells in their second infusion. In agreement with the FDA, we plan to dose and obtain PK/PD data in approximately five additional patients at this dose level to support the upper end of our proposed recommended dose range prior to initiating the pivotal trial. We anticipate enrolling these patients by the end of this year to support starting the pivotal trial in the second quarter of 2026. In preparation for the pivotal trial, we have also finalized a commercial-ready manufacturing process and completed initial transfer of this process to our external CDMO. Notably, this process has decreased cost of goods and is five days shorter than our phase one process. It is also operationally more straightforward. We have already successfully completed manufacturing for our first patient that we will use. This manufacturing process. As you will see in the ASH abstract that comes out this morning, we are encouraged to see that the initial patients treated with TSC-101 had durable responses, with three patients treated with TSC-101 that are now out past two years. We have also seen prolonged persistence of the engineered T cells. TSC-101 was detectable in all of the treated subjects at last follow-up, including the three subjects that are past two years and four additional subjects that are past one year. As you will see in the abstract, relapse-free survival remains improved in patients that received TSC-101 relative to patients in the control arm, with a hazard ratio of 0.48 as of the July 8 data cut—sorry, the July 18 data cut. As noted by the change in hazard ratio from what we presented at ASH in December of 2024, we have seen additional instances of relapse this year. We have also seen delays in achieving complete donor chimerism using the high-sensitivity chimerism assay in a few patients enrolled in 2025. As we are compiling more clinical data and trying to better understand our product, we have looked for features in the product that might inform efficacy. One feature we have recently noted is that. In the cases of either relapse or incomplete chimerism using the high-sensitivity assay. These cases appear to be associated with high levels of ex vivo T cell expansion during the manufacturing process. Our initial phase one process that we have been using up until recently involves a magnetic bead-based purification step that required substantial expansion of the engineered T cells prior to completing the process. As I mentioned earlier, we have now implemented an improved commercial-ready process that does not require a magnetic bead-based step to purify the engineered T cells. This process is shorter than the phase I process by five days and requires less T cell expansion to achieve a target dose. We believe that this process will enable the cells to expand better and should improve anti-tumor activity in patients, consistent with what others in the field of engineered T cell therapy have previously reported. We will be using this process to dose the additional patients requested by the FDA at the high end of our recommended dose range prior to launching the pivotal study, and we plan to share safety and early chimerism data on those patients when they become available next year. Shifting at this point to solid tumors, we have recently dosed our first two patients with multiplex therapy, as well as seven additional patients with single-plex therapy at dose level three or higher. Despite this recent progress, we have made the strategic decision to pause further enrollment in the solid tumor trial and focus our clinical development efforts on the HEME program. We have encountered the same challenges that others have reported in developing autologous T cell therapies for solid tumors, including challenges for the patient, such as disease progression during the washout time prior to lymphodepletion, and the challenges on the manufacturing end associated with engineering T cells from patients that have undergone multiple rounds of therapies, including therapies that are toxic to T cells. At the same time, we have been impressed with the early efficacy signals seen with in vivo engineered products in the CAR-T field. In vivo engineering could address two of the largest hurdles seen with ex vivo manufacturing: the extended time from patient identification to time of infusion and the need for lymphodepleting chemotherapy. We believe in vivo engineering represents a promising and cost-efficient way to deliver off-the-shelf multiplex TCR-T cell therapy for solid tumors and therefore feel that now is the best time to transition our efforts and resources to accomplish this. We have recently partnered with a third party specializing in the development of a lentiviral-based platform for in vivo engineering of T cells and have initiated preclinical development efforts with this platform. TScan is uniquely positioned to leverage our target and TCR discovery platform, as well as clinical experience with our ImmunoBank of TCRs for solid tumors, to be one of the first companies to develop in vivo engineered TCR-T for solid tumors. With this strategic realignment, we are restructuring the company to prioritize clinical development of the HEME program. Unfortunately, these strategic measures impact a number of our very talented employees, and we are implementing a reduction in force today of approximately 30% of the company. This restructuring enables us to launch the pivotal trial for TSC-101 in the second quarter of next year and extends our runway into the second half of 2027. I just want to take a moment to express my sincere gratitude to all of our employees, especially those affected by this reduction in force, for their commitment to our mission and their dedication to the patients with serious diseases that we are aiming to treat and ultimately cure. I want to end by talking a bit about the opportunity in HEME and why we are so excited about the path forward. This program addresses a key unmet need for patients with HEME malignancies. Right now, allogeneic transplant is the only potentially curative therapy for patients with AML and MDS. Unfortunately, up to 40% of patients undergoing transplant with reduced intensity conditioning relapse within two years of their transplant, and once they do, the prognosis is very poor, with almost all dying of their disease shortly after relapse. TSC-101 and the additional products that we are planning to develop are designed to prevent relapse in these patients. Currently, about 9,000 patients a year undergo allogeneic transplants in the United States, most with AML and MDS, and that market continues to grow. It is a very concentrated market, as there are only about 120 centers in the U.S. that conduct allotransplants. Right now, about 60% of the allotransplants that occur each year in the United States are conducted in one of the 21 clinical sites that are currently participating in our clinical trial. We have also conducted a lot of market access work with physicians and payers this year and believe that we would see rapid market penetration with pricing in the range of recent cell therapy approvals. This program also does not face many of the challenges associated with autologous cell therapy. We are manufacturing product using the T cells of healthy donors, not patients with cancer, and so do not see the same variability in the starting material. Also, we are not racing the clock with our manufacturing. We start the manufacturing process before the patient undergoes the transplant, and their product is ready to be administered before the patient is ready to receive it. Finally, the patient does not have to undergo additional lymphodepletion outside of what they are already receiving as part of their transplant procedure. Our product is very well tolerated and could be administered in the outpatient setting. Overall, these features make this an ideal setting for cell therapy, and we are committed to building our HEME program with two additional IND filings this year. As we have previously disclosed, we are planning to file INDs for TCRs targeting epitopes derived from CD45. One for the HLA type A*01:01 and a second for the HLA type A*03:01. By expanding to one additional HLA type, likely A*24:02, we anticipate doubling the addressable market, making this program a potentially multibillion-dollar opportunity. The strategic realignment that we are announcing today enables us to continue the momentum within our HEME program and brings us one step closer to our goal of providing novel therapeutics to patients with cancers and serious diseases. Thank you for listening, and I'm happy to answer any questions at this time. Thank you. At this time, we ask if you would like to ask a question, please click on the raise hand button, which can be found on the black bar at the bottom of your screen. When it is your turn, you will receive a message on your screen from the host allowing you to talk, and then you will hear your name called. Please accept, unmute your audio, and ask your question. We will wait one moment to allow the queue to form. Our first question will come from Sam Slutsky with LifeSci Capital. You may now unmute your audio and ask your question. Hey, good morning, everyone. Thanks for taking the question. Just a couple. Could you just refresh us on the top line epidemiology as you think about AML and MDS versus ALL? And then kind of on the CD45 program, you mentioned obviously that expands the patient population. Just kind of walk through that and then how far behind that program is versus the initial pivotal. Yes, happy to take that question. As we look at sort of the breakdown between AML, MDS, and ALL, right now, it's about 15% of the patients that would participate in our trial are ALL. Eighty-five percent of the patients are AML or MDS. By not including ALL, we're not including about 15% of the addressable market that was previously being included. However, as I noted earlier, we are adding mismatched unrelated donors as a donor choice in this trial, and that actually increases our ability to find A2- donors for these patients, which actually increases the number of addressable patients in the AML and MDS area. In terms of the CD45 program, right now, TSC-101 addresses about 42% of patients undergoing transplant because the HLA type A*02:01 has about 42% prevalence in the United States. As we add TCRs from the CD45 program, if we look at A*01:01, A*03:01, and A*24:02, obviously there's overlap as people can be positive for more than one, but taking that into account, we estimate that there would be an additional 40% of patients if we include those three TCRs. The plan right now is to move TSC-101 forward, which would address 42% of patients. When we add those three TCRs introduced initially into a phase one study and then ultimately into a pivotal study, that would add another 40%. That's why I mentioned potentially doubling the market with those three additional TCRs. Got it. How far behind do you think the CD45 program is in terms of when you might be able to get that into a pivotal study? I would say at this point, we plan to file two INDs this year for A*01:01 and A*03:01. That puts us in position to potentially start a phase I in the second half of next year, pending funding for that program. We would be in position to initiate a pivotal trial within one to two years after that point. Okay, thanks. Our next question comes from Maxwell Skor, Morgan Stanley. Please go ahead with your question. Great, thank you. Thank you for taking my question. Are you able to hear me? Yes, we are. Okay, great. Was there a specific threshold of T cell expansion associated with relapse or prolonged incomplete chimerism? Also, how did you settle on a lentiviral-based platform for your in vivo engineering of T cells? Any consideration or additional color just around vetting other approaches? Why do you think lenti is the best path forward? Thank you. Yes, thank you for the questions, Max. Let me start with the first question about the threshold for T cell expansion. What we see as we look at these products is obviously there's noise in clinical data, particularly where small numbers are involved. In the patients that did experience delayed chimerism or relapse, we did notice an overall increase in the levels of T cell expansion that those products underwent. That doesn't mean that all of the patients that relapsed had that increased expansion, but on average, it was clearly higher than the patients that didn't experience reduced chimerism or relapse. I think what's most encouraging to us is that the commercial-ready process requires less T cell expansion than even the phase one process in which patients achieved and maintained complete donor chimerism. We're very optimistic about the commercial process as we start treating patients with that. In terms of the in vivo engineering platform, we did review the literature fairly extensively. There are two main platforms that people are using right now for in vivo engineering. One is using lentivirus or various modified forms of lentivirus, and the other is using lipid nanoparticles to deliver nucleic acid. I would say that most of the lipid nanoparticle platforms are delivering mRNA or single-stranded DNA, so basically platforms that are providing transient expression in the T cells in patients. Whereas the lentiviral platforms, just by the nature of lentivirus, enable integration of the DNA, so genetic modification of the engineered T cells, which is ultimately a more permanent solution for the patients. Those T cells could go on to form memory cells and give those patients long-term immune surveillance. Based on that, as well as the fact that there's actually more clinical data available with the lentiviral platforms, we felt that that was the route to go at this time. As I said, we have partnered with an external company to develop this platform and have initiated preclinical work on that now. Great, thank you very much. Our next question comes from David Nierengarten, Wedbush. Please go ahead with your question. Hey, thanks for taking the questions. First, I don't have the slide up in front of me right now. Is there an interim look planned for the pivotal study in AML and MDS for 101 as you start enrolling that? The second one, back to the T cell question. Is there any other quality control, or is that the right word, for making sure the product in the pivotal study is the appropriate product for those patients? Thanks. Yeah, so happy to take those questions. What was the first question again? Sorry. Sorry, is there an interim look planned? Oh, interim. Oh, yeah. All right. Yeah, you're good. Yeah, Crystal, can you take that? Yes. From this particular point in time, we are revisiting all of our associated assumptions with regards to this particular trial design. Once everything is finalized, we're happy to meet to discuss. At this time, we are not planning to do an associated interim. With regards to this being the best product moving forward to the registrational study, this is one where ultimately it's a bit of a nice situation to be in that we'll be able to utilize the commercial-ready process right now while we're getting the additional data that will need to support the higher end of the pivotal dose range. We'll be able to look at the associated early safety, translational, and clinical data to make sure that it's in line with what we're used to seeing with our early TSC-101 product. Just one follow-up on that. This is a characterization of our process that we've done looking at the level of T cell expansion ex vivo. This is not a release criteria for the product. The release criteria are really based on the critical quality attributes of purity, cell viability, vector copy number, and obviously sterility. This is a characterization assay or parameter that we've been tracking. As Crystal said, we'll continue to track that over the patients treated with this process in the phase one prior to launching the pivotal. Thank you. Our next question comes from Tara Bancroft, TD Cowen. Please go ahead with your question. Tara, if you asked a question, we were unable to hear your audio. Can you hear me now? This is Nick on for Tara. Can you guys hear me? There we go, yes. Thank you. Yeah. All right, great. Sorry about that. I just have two. The first one is, what was your findings from the phase one ALLOHA trial? Or I guess more so, what's the hypothesis that you guys have for why the increased or the high levels of expansion led to this relapse in some patients? The second one is, how has the powering changed in the pivotal trial given the requirement for the internal control arm? Thank you. Yeah, you take the first question. It's well known in the field that the longer you expand T cells ex vivo, the more differentiated they get and the more exhausted their phenotype. The hypothesis is simply that if the T cells undergo too many rounds of replication, ex vivo expansion, then that renders them less able to engraft, to expand in vivo in the patient, and continue to function effectively. It's really a matter of ultimately T cell exhaustion that you're trying to avoid by having a shorter process. I'm sure you're familiar with Novartis's T-Charge program in which they took the commercial product KYMRIAH and developed a way to manufacture it in a much reduced time, I believe now a two-day process. That product is clearly more effective even at much lower doses. We're really building on observations like this in the field that a shorter process renders T cells more able to expand in vivo, more able to function appropriately. In terms of the powering for the pivotal trial, we will continue to monitor patients that we now treat with this commercial process. We found that the high-sensitivity chimerism assay is very informative for us to understand our product in a relatively short period of time. We will be using that along with all the data that we've accumulated in the phase one study to ultimately determine how we power the study and at what hazard ratio. Thank you very much. Thank you. Our next question will come from Gil Blum with Needham. Please go ahead and ask your question. Good morning, everyone. Can you hear me? Yes, hi Gil. Hi. Just one question from us. Do you guys have any concern of going after an in vivo CAR-T strategy? One of the ideas of doing ex vivo is the T cells that you get from your patient that are sometimes not the best given how many lines of therapy they got. By expanding them ex vivo, you can boost them, at least that is some way that people view it. Is that a potential risk as it associates to in vivo? Maybe just help us understand why you think in vivo is better. Thank you. Yes, thanks for the question, Gil. You're right in noting that you are dealing with compromised T cells sometimes in patients that have had multiple rounds of therapy, as I noted earlier. However, we are encouraged by the fact that we've seen quite remarkable data from CAR-T companies that are taking this approach. Those patients are also similarly compromised in that fashion. We submit that there must be a sufficient population of T cells that are still functional and able to be engineered and function appropriately in the patient. We also note that the whole field of T cell engagers is based on the endogenous T cells in the patient. I feel like we'd be building on that work as well. Thank you. We have no further questions at this time. If you would like to ask a question, please do so now. Great, thank you. Oh, go ahead. Sorry. That concludes the call. I will now hand the call back to Mr. MacBeath for closing remarks. Thank you. Yes, I just want to take the time to thank everyone for tuning in. What I know is a busy morning for everyone. I am happy to follow up with conversations later as well. Thank you. Thank you.