All right. Good afternoon, everyone. Thank you for joining TD Cowen's 45th Annual Healthcare Conference. I'm Tara Bancroft, one of the senior analysts here. Thank you to TScan for hosting our next session. From TScan, we have the CEO, Gavin MacBeath. Thank you for joining us. Why don't you go ahead and get your presentation started, and we'll follow it by some Q&A afterwards. Great. Thank you, Tara. Thank you to TD Cowen for the invitation to talk today. Obviously, TScan is a publicly traded company, so we will be making forward-looking statements. For those not familiar with TScan, TScan is a fully integrated biotechnology company focused on the development of TCR-engineered T-cell therapies for cancer. We were founded back in 2018 and built all of our own programs at TScan, all of the products that we've put into the clinic, which now come to nine different TCRs that we've successfully cleared INDs on. They all came from our internal discovery efforts. Right now, we have two main clinical programs: a program in heme malignancies, where we're targeting patients that are undergoing allogeneic hematopoietic cell transplant therapy. The goal there is to target residual disease to prevent relapse in those patients. We also have a solid tumor program. With solid tumors, we feel the key challenge in solid tumors is that solid tumors are heterogeneous and so really require a multiplex strategy for treating them. We are putting together a collection of TCRs that address different targets so that we can treat patients with multiple TCRs at the same time. For those not familiar, we released data from our phase I ALLOHA study at ASH in December, showing 26 patients treated on the treatment arm of our study and 13 patients on the control arm. Very promising data from that study. I'll go over some of those data today. Based on that data, we are planning to launch a pivotal trial in the second half of this year with a top-line readout on that trial expected in the second half of 2027. We really feel this is a very attractive market opportunity. In fact, we think that with the current clinical trial, there is an over $1 billion addressable market in the US plus Europe combined. For this year, we have multiple clinical catalysts, including a readout on the ongoing phase I heme study at the end of the year, which will provide now fairly long-term follow-up, including patients that have been on study for two years at that point. In the solid tumor program, we will provide an update on both safety and efficacy in patients treated not just with single TCRs, but with multiplex therapy. Finally, a key part of TScan is that we have brought manufacturing in-house. We do all of our own GMP manufacturing of cell therapy products in-house. We have now engaged a commercial CDMO that will do the clinical manufacturing in our pivotal trial and will handle commercial manufacturing. Just one quick introductory slide on the biology for those not familiar with TCR-engineered T-cell therapies. TCR is the T-cell receptor. It is the natural receptor that T-cells use to recognize their targets. A T-cell receptor recognizes not just the cancer-specific antigen derived from the tumor cell, but also the class I HLA that is presenting that antigen. The TCR has to be matched to that HLA. Of course, that presents a challenge since there are literally hundreds of different HLA types. Your HLA type is actually your class I HLA type, which is six different HLAs, two As, two Bs, and two Cs. The good news is that certain HLA types are much more common than others. The most common HLA type is A0201. 42% of people in the US are positive for A0201. If you look at the top six HLA types, over 90% of people in the US are positive for at least one of those HLAs. We are building a pipeline of TCRs really focused on those six most common HLAs so that we can address the majority of patients with cancer. This is what our pipeline looks like. You see it is a little bit different from other companies in that we specify the HLA type of the TCR that it addresses. In yellow at the top is our heme malignancies program focused on patients undergoing allogeneic transplant therapy. In blue is our solid tumor program. You can see in that program, we now have seven different TCRs all in the same clinical trial working towards treating patients with multiplex therapy. With that, I'm going to dive into the heme program and review some of the data that we updated at the end of last year. In this program, as I said, we're addressing patients undergoing allotransplant therapy. Right now, this is the only curative therapy for patients with AML, MDS, and some forms of ALL. Those patients, obviously, get taken to transplant. The key challenge in transplant is that although it's curative for about 60% of patients, about 40% of patients, particularly those undergoing transplant with reduced intensity conditioning, will eventually relapse. If they relapse, the prognosis is very poor. In fact, about an 80% mortality rate within two years of relapse. This is the key unmet need. Our products are designed to address residual disease to prevent relapse in these patients. The way this program works is that if we identify a patient, and the patient here is shown with pink cells, we match them with a donor shown in blue, where the patient, all of their blood cells are positive for the antigen. I'm using HA-2 as an example. In this example, the patient, all of their blood cells are displaying the antigen HA-2 on the surface, but the donor is HA-2 negative. If that patient undergoes an allogeneic transplant, then post-transplant, all of their new blood cells will come from the donor, and so they are HA-2 negative. Whereas any residual cancer or any residual normal premalignant cells from the patient are still HA-2 positive. The way we surgically remove, I mean, target, remove those residual cancer cells is while the patient's undergoing the transplant, we take T cells from the donor, which are HA-2 negative, and we engineer them with a T-cell receptor that recognizes that antigen. As soon as the patient's recovered from the transplant, which is typically about three weeks post-transplant, we give them their first infusion of engineered T cells. At that point, those engineered T cells will only target the HA-2 positive patient-derived cells, but not target any of the new blood cells that come from the donor. It is a way to really cleanly target residual cells to prevent relapse. When a patient undergoes a transplant, our phase I trial included a control arm. The control arm is transplant alone. First, the subject's identified, then an appropriate donor is identified. The donor undergoes apheresis to get the stem cells, and then the patient gets the transplant. The way our product works, shown in green, is the same process as a transplant, except we have an additional manufacturing apheresis that occurs prior to transplant, which is what we use to manufacture the engineered T cells. You can see post-transplant, typically around day 21, and then again at day 61, the patient receives two separate infusions of engineered T cells. This trial has been running for the last two years or so. To date, back in December, we announced treating 26 patients on the treatment arm, which were either two products, TSC-100 or TSC-101. They are very similar products. They just target different antigens, HA-1 and HA-2 respectively, as well as 13 patients on the control arm. This trial was very well balanced between treatment and control arm. If you focus just on the green and the yellow column on the right, you'll see 26 patients treated with a cell therapy product compared to 13 patients on the control arm. Let me just draw your attention to the very last line. This indicates that these are very high-risk patients. 80% of the patients that we've treated to date were either MRD positive, so positive for minimal residual disease, or they had risk factors like p53 mutations or FLT3 mutations that make them very high risk of relapse. This compares to the control arm, which is also about 80% of patients are high risk. There were three dose levels. This was a dose escalation study. We used an I3 plus 3 design, which means you can treat just a single patient. If there's no DLTs, you can move to the next dose level. We treated very few patients at those early dose levels. We've been treating largely patients at dose level 3, which is two different infusions of engineered T cells. From a safety perspective, this product has been very well tolerated. We've seen almost no adverse events arising from the cell therapy product. There's lots of adverse events, but these are all transplant-related. A very good balance between the AEs that we see on the treatment arm compared to the control arm. We've only seen two instances of CRS arising from the product itself, and one was grade 1, the other was grade 2, and no cases of ICANS. One biomarker or two biomarkers that we've been tracking in these patients to really get an early read on efficacy have been really focused on the residual cells that are left in the patient. Obviously, the goal here is to completely eliminate any residual cells. One biomarker that's very easy to understand is MRD or minimal residual disease. If you can detect any leukemic cells in the patient's bone marrow in a bone marrow biopsy, then that patient is MRD positive. Otherwise, they're MRD negative. The other biomarker that we track is what's called donor chimerism. Donor chimerism is measuring are there any detectable patient cells, whether they're malignant or not malignant, just any patient cells. Again, you're trying to eliminate all patient-derived cells. If the patient has complete donor chimerism, that means you've eliminated all detectable patient cells. They have a very low risk of relapse. Whereas if you have mixed chimerism or detectable patient cells, then they're at higher risk of relapse. It doesn't mean they will relapse. They're just at higher risk of relapse. Let me first share the donor chimerism data. On the left is all the combined data of both TSC-100 and TSC-101 compared to on the right is the control arm. The patient achieved complete donor chimerism. You see a blue check. If they have incomplete chimerism, there's a red X. Just staring at the slide from far away, you can see there's a lot more red Xs on the right than there are on the left. Clearly, all of the patients in this trial achieved complete donor chimerism within three weeks of getting their first infusion of engineered T cells. The yellow diamonds indicate when those patients got infused with engineered T cells. We did see two relapses on this trial in the treatment arm. Two out of 26 on the treatment arm compared to four out of 12 on the control arm. One patient was not yet evaluable on the control arm. On the treatment arm, let me just dive a little bit into those relapses. One patient passed from their relapse. The other showed a relapse. On TSC-101, the one patient that relapsed here was actually the only patient in this clinical trial that did not achieve a response to their induction chemotherapy before getting taken to transplant. Most patients need to achieve a CR before taken to transplant. This patient had active disease when they went into transplant. We would not allow that on our pivotal trial. That's the only patient in the study for which that occurred. The second patient, the TSC-100 patient, this is a patient where, again, one of two exceptions we made in the trial where the patient was getting rushed to transplant. We only started manufacturing the product after the patient had the transplant. Usually, we start manufacturing the product before the patient has the transplant. In this case, that resulted in delayed infusions for those patients. It also resulted in a compromised manufacturing product because the donor gets G-CSF to mobilize their stem cells. That led to a higher granulocyte content in the apheresis product, so compromised the manufacturing. This would not be repeated on the pivotal trial. We focus now on the MRD data. MRD is now assessed in bone marrow biopsies. What you can see on these diagrams is if there's a pink square, it indicates MRD positive. A blue square is MRD negative. These are all in bone marrow biopsies. For a start, if you look pre-transplant, you can see that about 50% of the patients in both the treatment and control arms were MRD positive prior to being taken to transplant. In the upper two-thirds of this diagram are all the patients that received cell therapy. You can see all of those patients achieved MRD negativity as soon as they received the cell therapy product, which is indicated by the green vertical lines. This contrasts to the control arm where you see a lot of MRD positivity, which typically precedes patients relapsing. These are now Kaplan-Meier curves showing, in this case, relapse or event-free survival. Sorry, this is relapse. It's probability of relapse. You can see there's a much higher probability of relapse on the control arm as compared to the treatment arm with a hazard ratio of about 0.3. Similarly, for event-free survival, which in this case indicates an event is either a relapse, a death, or a clinical intervention such as donor lymphocyte infusion, again, a clear difference between the treatment and control arm. Based on this, we've met with the FDA to design a pivotal trial. The key features of the pivotal trial is, one, we're moving forward with one of our products, TSC-101 only, not with both products. The reason is that TSC-101 addresses 98% of patients that have the HLA type A0201. TSC-100 only treats 60% of them. There's overlap between these patient populations. Essentially, we capture the entire addressable market with just a single product, TSC-101. The trial design is a treatment arm focused on transplant plus TSC-101 compared to the control arm. This is not a randomized trial. The FDA actually agreed to our using an external control arm or a synthetic control arm in which for every patient that we treat on the treatment arm, we find three patients in the CIBMTR database, which is every patient that undergoes a transplant in the US goes into that database. We match them on age, gender, disease, risk factors, and they become the control arm for this trial. Based on that, we have a primary endpoint of relapse-free survival that would support full approval. Based on our current rates of enrollment and the planned clinical sites that we're opening, we anticipate a top-line readout within 24 months of first patient in on this study. We will start this study in the second half of this year with a top-line readout in the second half of 2027. Now, just a quick word on the addressable market. Right now in the US, about 7,350 patients a year with AML, MDS, and ALL undergo an allogeneic transplant. We can address 42% of them with our product, TSC-101. That is about 3,000 patients a year. We have also specified that these patients need to undergo transplant with reduced intensity conditioning with a donor that is either a haploidentical donor or a mismatched unrelated donor. If you look at the current clinical practice, that is about 1,000 patients a year in the US plus Europe combined. However, if this trial is successful, if we really reduce relapse rates by over 50%, then patients that currently get matched unrelated donors, we believe, would start to get haploidentical donors instead because that would enable them to get on-label use of our product. Right now, the outcome data for matched unrelated versus haplo donors is about the same. This is a clear, easy decision for a physician to match them with a haplo donor instead of a matched unrelated donor to get our product. In fact, we've already seen that happening in our clinical trials. Similarly, if our trial is successful, the relapse rates with our product will actually be lower than the relapse rates we currently see with myeloablative conditioning. That's an easy choice again. It's much more tolerable to get reduced intensity conditioning. We anticipate a change in clinical practice in which patients that would normally undergo myeloablative conditioning would get reduced intensity conditioning in order to get on-label use of our product. We believe the addressable market is somewhere between 1,000 and 5,000 patients a year based on what degree of clinical practice change actually occurs. Moving quickly to the solid tumor program. The solid tumor program, very different story. Here, we believe the key challenge in solid tumors is that solid tumors are heterogeneous. It is a little bit difficult to see on this slide just based on the lighting. What you can see on the left here is a non-small cell lung cancer tumor that has been stained in red for PRAME and in green for MAGE-A4. What you can see is that some of the cells are red, some of them are green, very few cells are yellow. Yellow would indicate co-expression. It is really distinct populations of cells that are expressing these markers, which means that if you were to give a patient like this just a PRAME TCR, you would kill half their tumor cells, and that patient would have short durability of response. They would rapidly relapse. If you could treat that patient with both a MAGE and a PRAME TCR, you would have a much greater chance at having a deeper response, maybe even a complete response and a long-term remission. That is the strategy that we are taking as a company. Test a patient's tumor, figure out what targets are expressed in their tumor, and then give them a combination of TCR therapies. In addition to that, we're also further enhancing our T cell therapy product. All first-generation TCR therapies only engineered the patient's cytotoxic T cells with the TCR. The reason is the TCR requires the CD8 co-receptor to function, and cytotoxic T cells have CD8. Now second-generation products are being developed, Adaptimmune, Immatics, ourselves, we're all developing second-gen products in which we're not just introducing the TCR gene, we're also co-introducing the CD8 co-receptor. Now the product also includes helper T cells that have been engineered to recognize target. We've gone one step beyond that. In our solid tumor program, we also are dealing with the hostile tumor microenvironment. In particular, TGF-beta is a very immunosuppressive signal. We have introduced a dominant negative form of TGF-beta receptor into our T cells so that they can continue to function even in the presence of TGF-beta. It is an enhanced TCR-T cell product that we have put into the clinic. This is the overall strategy. We are building a collection of TCRs that address different cancer-specific proteins, which are the rows, as well as different HLA types, which are the columns. When a patient comes in, we test their tumor, figure out what targets are expressed in their tumor, then go to that collection and pull out the best two or three TCRs, and that becomes a customized multiplex therapy for that patient. That is the grand vision for the program. Where are we right now? We actually have seven different TCRs that are all cleared INDs. They're all in the same clinical trial. The agreement we reached with the FDA is that we would first test each TCR T on its own to make sure that it's safe before we start combining them. Each TCR T goes through two different dose levels. Dose level one is 500 million T cells. Dose level two is 2 billion T cells. Once a TCR has cleared dose level two, it becomes eligible to be combined with any other TCR that's cleared dose level two. At dose level three is when we introduce multiplexing. We call the product T-Plex. At dose level three, two things happen. One, we treat a patient with two different TCRs at the same time. On the same day, they get two successive infusions. We are also introducing repeat dosing at dose level three. At dose level three, the patient will get a repeat of those two TCRs 28 days later. Dose level four is a further escalated amount of T cells. We are also including single-plex therapy at dose levels three and four for patients that only are expressing a single antigen. That will provide us with the data so that we can compare multiplex treatment with single-plex treatment. The data update that we provided in December, as of December 10th, showed we had treated eight patients at that point with four different TCRs and already had cleared dose level two for two of these TCRs, our HPV16 TCR and our PRAME TCR. This trial is ongoing. We continue to enroll patients. Our goal this year is to treat a substantial number of patients with multiplex therapy at dose levels three and higher so that we can generate an interpretable data set. To that end, we have also decided to focus on specific key indications. Specifically, if patients are HPV positive, we will enroll patients with either head and neck cancer, cervical, anal, and genital cancers. This is where HPV16 is driving oncogenesis. For HPV negative patients, we are focusing entirely on lung, sarcoma, and head and neck. We believe these are all unmet needs. We are targeting second and third-line patients in these settings where clearly the introduction of cell therapy would be transformative in this space. To that end, if we get all seven of these TCRs through dose level two to be eligible for multiplexing, then what our own screening study has shown is that about 25% of patients with lung cancer would qualify for two or more TCRs. About 40% of patients with head and neck cancer or even up to 60% of patients with anal and genital cancer would qualify for two or more TCRs. With those seven TCRs, a fairly substantial fraction of patients would qualify to receive multiplex therapy. I just want to end by sort of reiterating our public guidance around milestones this year. Already, we've opened expansion cohorts at dose level three in our heme study. Our plan is to, in the second half of this year, launch our pivotal trial for TSC-101. I didn't have time to talk about it today, but we've also got other TCRs in our heme program that are addressing other HLA types, in this case, targeting epitopes from CD45. We plan to file an IND on our first such product in the second half of this year. At the end of the year, we will provide updated clinical data on our ongoing phase I study, which will include patients that are out past two years at that point. On the solid tumor program, we already announced that we've dosed our first patients in the study. We're aiming to dose our first multiplex patient in the first half of this year and then provide both safety and efficacy data on the solid tumor program, including patients with multiplex therapy by the end of the year. I will just end on the starting slide. This is the high-level view of TScan. Just want to indicate what we put out this morning in our 10-K. We have $290 million in cash right now, which gives us runway into the Q1 of 2027. With that, I want to thank you for your attention and happy to take Q&A. Yeah, thanks so much for that really detailed presentation, Gavin. It is great to see the progress that you guys are making. I think with the last five minutes or so that we have, I think we could do one question on heme and one on solid tumors. Both regarding expectations for the data updates that are coming. For the heme data, the patients that are out at two months or sorry, two years by the time that you are going to be presenting that, can you just give us some context of where the control arm might be, what you know from historicals, what do you think the benchmark is that it would have to be, and how many relapses could occur without the TSC-101? Yeah, absolutely. Historically, now focusing on patients getting reduced intensity conditioning, we typically see most of the relapses occur fairly early. 22% relapses at six months, 33% relapses at one year, and 42% relapse rate at two years. As we get to two-year data, the expectation on the control arm is about a 42% relapse rate. By the way, the control arm currently is performing according to expectations. We're seeing a 33% relapse rate, and most, the average time is about a year on the control arm, which is in keeping with historical standards. The bar we're looking for is we would like to see about a 50% reduction in relapse rates. If we can drop the two-year relapse rate to 20% rather than 40%, that would be transformative in the area of transplant therapy. Our physicians have told us they'd be happy with a 15% reduction in relapse rates, but we're not happy with that. We are looking for about a 50% reduction. Okay, great. Next, solid tumors. I know you just dosed your first multiplex patient, which is great to see. In thinking about the solid tumor update that's going to happen later in the year, how many patients do you think you can escalate through at that point and up to which dose level? Do you think you'll have any single-plex patients at the dose level three or four? Yeah. Just a quick correction. We have not announced first patient dose with multiplex therapy yet. We are guiding to that in the first half of this year. My bad. No, what we're looking for is, one, we'll obviously have more single-plex patients to treat because we're trying to get through dose level two across all seven TCRs. We had already done that for two TCRs back in December, but the trial's obviously been going since then. We're looking to try to get to about 12 patients with multiplex therapy by the end of the year. They would all have different lengths of follow-up time. How much six-week CT scans and 12-week CT scans and beyond that we'll have at that point is going to be variable depending on patient. That's roughly the numbers that we're targeting. Yes, we will be enrolling patients at dose levels three and higher with single-plex therapy so that you will see some of those data as well. Okay. We do have another minute or two. What do you want to see in that data from both single-plex and multiplex to maybe be able to go straight into a pivotal? Yeah. That really varies depending on indication. Obviously, we'd be looking at what current standard of care is. Right now, in second and third-line lung cancer, the best products on the market are only achieving 22% response rates. We'd love to see double that with our product. Ultimately, what's going to move the needle is durability of response. That's really what's required with cell therapy products, particularly at the price point that they come in at. Obviously, we won't have durability data this year. One way to assess that is not just response rates, but also depth of response. We believe that multiplex therapy should give you deeper responses than you see with single-plex therapy. In the near term, response rates, depth of response, and then as the data mature down the road, start to see durability of response. As I said, the bar is different for every type of cancer. With our HPV program, the NCI ran a study many years ago with HPV positive cancers. It was just 12 patients, but they saw a 50% response rate there. If we saw a 50% response rate in HPV positive cancers with our program, that would clearly be a signal to move into a pivotal. With solid tumors, we believe that pivotal trials, fairly well-presented, could be single-arm studies, response rate-driven studies. Okay, great. I know I and probably everyone in the room here is really looking forward to all of these updates. Congrats on all the progress. Thank you for being here. Thank you for presenting. Thank you all for listening. Thank you.