Good morning, everyone. My name is Gil Blum, and I am a Senior Biotech Analyst here at Needham & Company, covering the immuno-oncology and gene therapy subsectors. Thank you all for joining us on the first day of the Needham Conference. It is my pleasure to have with me today TScan CEO Gavin MacBeath. As a reminder, any viewers who are watching through the conference portal are able to submit questions via the Ask a Question box below the video feed window. With that, Gavin, maybe start with a bit of an introduction on TScan. Thank you, and thank you, Gil, for inviting me. Yeah, TScan was founded back in 2018, and we were founded based on a breakthrough technology that enables us to discover the target of any T cell receptor. In the early years of TScan, we used that technology to study the T cells of patients with cancer to figure out what targets T cells are naturally recognizing. We also used our platform to start building a pipeline of therapeutic TCRs that recognize these antigens and mediate an anti-cancer response. Over the last six years, we've built two main clinical programs, one program in heme malignancies, where we're treating patients with AML, MDS, and ALL that are undergoing allogeneic transplant therapy. The goal here is to address any residual disease following transplant to completely eliminate the cancer and prevent relapse in those patients. I'm sure we'll talk more about our phase I trial and our plans to start a pivotal trial this year with that program. The other program is in solid tumors, where we've, again, built a pipeline of TCRs. We now have seven different TCRs in the clinic. Here we have a slightly different goal. We really feel the core problem in solid tumors is heterogeneity. What we're doing is building a collection of TCRs so that we can give patients more than one TCR-engineered T cell at a time, what we call multiplex therapy, to address that core heterogeneity. Overall, the company is a clinical stage company with now nine different products in the clinic, all TCR-engineered T cell therapies addressing both heme and solid tumor malignancies. Okay, before we jump into the individual programs, it's a little hard to ignore what's going on in the markets these days. Any exposures to tariffs, anything you can add there, and maybe an add-on as it relates to regulatory engagement and cuts in the FDA? Sure, yeah, absolutely. We take a very close look at this. We have a large supply chain team. Our products do involve products that come from multiple different countries and multiple different sources. I would say to date, we have not been grossly affected by these tariffs. We are obviously keeping a close eye on them, but one, it has not interrupted our supply chain, and two, we do not anticipate any major cost increases in our raw materials that we use for our manufacturing. On the regulatory front, obviously, we are deeply concerned with the cuts that are occurring at the FDA. Losing Peter Marks is clearly a really big blow to the FDA. I mean, he has done amazing work over the years. I would say the way it is directing us, again, we do not anticipate any direct effect on us. We are very encouraged that Nicole Verdun is the new head of CBER. I think she's an amazing person that's going to be able to move that organization forward effectively. It's possible that we'll see delays in actions when we submit briefing books, but so far, we haven't seen any delays, and we remain closely in touch with the team that's been handling our regulatory submissions. At the moment, we feel we're relatively unaffected by this. Thank you for that, Gavin. As it relates to your core technology, just to help people maybe not know too much about it, what would you say is the main differences, let's say, compared to a CAR-T or maybe other TCR-T programs that are out there? Yeah, so what we're doing is basically taking a patient, or in our case of our heme program, a donor's T cells and reprogramming them using naturally occurring T cell receptors. In many senses, it is similar to CAR-T in that we're genetically engineering T cells. CAR-T, the primary antigen receptor, is an artificial receptor that's coupling an external antibody to an intracellular signaling domain, whereas a T cell receptor is the natural mechanism that T cells use to recognize targets on foreign cells. We are really taking advantage of 500 million years of evolution. The T cell receptor has been evolved to be perfectly tuned in its signaling response to activate a T cell, to not over-activate it, to not lead to premature exhaustion, but to really be effective in recognizing the cancer and then forming memory T cells that can lead to long-term immune surveillance. We feel that using the naturally occurring T cell receptor just provides the right level of signaling, the right level of T cell expansion, the right level of memory cell generation to lead to ultimately long-term responses or even cures in patients. I think that's the key difference between CAR-T and TCR-T. In terms of how we differ from other TCR-T companies, we have a very core belief that naturally occurring T cell receptors, they've been sufficient in curing many patients' cancer, and they should be sufficient to also address patients who need engineered T cells. We're not affinity-enhancing our TCRs. We're taking naturally occurring TCRs that are both safe and effective. We are enhancing our TCR-T cell products in two ways. One, we're introducing the CD8 co-receptor along with the TCR. This enables us to engineer not just cytotoxic T cells, but also helper T cells. This is a strategy that other companies like Immatics and Adaptimmune are also employing now in their second-generation products. The other thing that we're doing is we're introducing a dominant negative form of TGF-β receptor into our solid tumor TCR-T cell products. What this does is it renders the T cells resistant to TGF-β, which is a very immunosuppressive signal in solid tumors. We've all heard about the hostile tumor microenvironment. How do you overcome that? One of the core ways to do that is to make T cells resistant to TGF-β. Again, it's a fairly benign way of doing it. We're basically knocking out a naturally occurring response rather than trying to put in something that is artificial. Overall, I would say trying as much as possible to take advantage of natural processes in how we engineer our T cells. Focusing a bit on the heme programs, you guys have demonstrated pretty impressive results to date. Maybe walk us through some of the data that's been generated. Yeah, thank you. There are basically two products that we introduced in our heme program. Both of them target antigens that are present in the patient's heme cells, but not present in their donor's heme cells. The way this product works is patients that qualify for an allogeneic hematopoietic cell transplant go into our study, and we pair them with a donor that, as I said, is negative for the antigen that we're targeting. The patient undergoes a regular standard of care transplant, but then immediately following the transplant, about three weeks after the transplant, we infuse those patients with engineered T cells, T cells from the donor that we've engineered to recognize their residual cancer. What we've seen to date, we included a control arm in our phase one study. In the control arm, we had, this is referring to the data that we presented in December at ASH, we had 12 control arm patients, and at that time, four out of those 12 patients, so 33%, had relapsed. In contrast, we had 26 treatment arm patients in the trial, roughly split between our two products, TSC-100 and TSC-101. At that time, we had two out of 26 relapses in the treatment arm, so 8% versus 33%. Clearly, a reduction in the rates of relapses that we're seeing. I think one of the reasons this program's been so successful is we're catching the patients when their disease burden is very, very low. They've just undergone a transplant. Any residual cancer is very low in those patients. If we can come in at that time and give them engineered T cells that target those residual cells, it gives us an opportunity to truly eliminate them and prevent relapse in the patients. As it relates to the control arm, is the relapse rate in line with what you would expect historically? Yeah, so we have done a large analysis of the CIBMTR registry. This is a registry of all patients that undergo transplant in the US. From that analysis, just a quick point of clarification, we're addressing transplant in the context of what's called reduced intensity conditioning, where patients could either get myeloablative conditioning, which is a very harsh regimen. Only young and fit patients are able to tolerate that. The majority of patients actually get a reduced intensity conditioning regimen, and that has a much higher relapse rate associated with it. What we'd expect, looking at the data in CIBMTR, is that about 22% of patients undergoing RIC transplant relapse by the six-month time, about 33% at one year, and between 38%-44% at two years, depending on the type of cancer. So far, we are seeing data very much in line with what we would expect based on that analysis. We've seen a 33% relapse rate and about one-year average time patients on the control arm. So very much in line with what we would expect. You're going to provide another update at ASH. What level of separation should we expect at that point, given historicals? Yeah, we are planning to update at the end of this year, as you said, at ASH. At that point, we will have had eight patients that will have been on therapy for over two years, but many more patients that have been on therapy for various lengths of time between that. At that point, obviously, we'll report on the two-year relapse rate that we're observing, but also on just the overall relapse-free survival curve that we see on the treatment arm versus the control arm. What we're looking to do in our pivotal trial is to achieve a hazard ratio of about 0.6 with respect to relapse-free survival. RFS is our primary endpoint in our trial, and that has been verified by the FDA to be an approvable endpoint for this patient population. What we're looking at at the end of the year is to see a hazard ratio of 0.6 or below in RFS of our treatment arm relative to our control arm. You're probably about to ask this question, but just to clarify, we are moving only one of our products forward. TSC-101 targets the antigen HA-2. 98% of the patients that we're currently addressing are addressable by TSC-101. It makes sense for us to just move TSC-101 forward. Our focus at the end of the year will be on how TSC-101 is performing relative to the control arm. In fact, right now, we're only enrolling patients that receive TSC-101 into our current phase one study. As it relates to the pivotal study, you guys have guided for second half 2025 for initiation with a potential readout in 2027. Can you explain or walk us through the timeline here in more detail? Yeah, so right now, we're, as I said, continuing to enroll into the study with TSC-101, continue to build up the safety data set and prepare for that pivotal trial. There's really three things we need to do prior to launching the pivotal study. One is that we have now developed a commercial manufacturing process. We're switching over to using that commercial process or commercial-ready process in this trial to gain some experience using the commercial-ready process and transfer that to an external CDMO that has the capability to do commercial manufacturing when the time comes. That's the first step. The second is that, and I'm sure we'll get more into the details of the pivotal trial, but we had a preliminary meeting with the FDA last year, and very much to our joy, they agreed with us that we could use an external control arm in the study. This is a control arm in which every patient that we treat, we will match to three patients in the CIBMTR registry that match that patient's disease and risk factors. We have a meeting coming up with the FDA to really discuss the details of that control arm. Finally, we need to also meet with the FDA with an end-of-phase one meeting to reach agreement on the statistical analysis plan, the final protocol, all the things that you need to do prior to launching a pivotal study. Those are really the three key activities that we're engaged in this year. We are still on track to launch the pivotal trial in the second half of this year. Based on the RFS endpoint with the hazard ratio of 0.6, we anticipate needing about 140 treatment arm patients matched to three times as many control arm patients. Based on an event-driven trial, our current estimates with the enrollment rates that we're seeing now and what we would have with the additional sites that we're adding lead to a top-line readout two years from when we treat our first patient in that study. That is why we are still guiding to top-line readout in the second half of 2027. One thing that we've seen with some approved therapeutics in a transplant setting is that they've seen pushback on their cost, specifically because a lot of hospitals do homebrew as it relates to transplant. I know this is early, but how should we be thinking of potential pricing? Yeah, so our thoughts around pricing right now is that we've seen two key, what's the word, well, examples, I guess. Data points. Yes, in the field. Amtagvi, the TIL product out of Iovance, priced at $505,000 per therapy, and then Tecelra coming out of Adaptimmune priced at $727,000. We are expecting a similar sort of range in terms of pricing. We do feel that the TCR-T cell product can be decoupled from transplant. We have recently hired Stephen Camiolo. He comes to us most recently from Iovance, where he played a key role in launching Amtagvi. We are already starting our pre-commercial work here in anticipation of our readout and ultimate approval in probably the second half of 2028, and really with a focus on what is the path, what is the argument that we need to put together to justify pricing in the range of $500,000-$700,000. As it relates to your next program in the heme space, TSC-102, how should we view timelines of development there? Yeah, so just a brief description of what TSC-102 is. Right now, TSC-101 can address, as I said, 98% of the patients we're currently enrolling in our trial. The key point is that any patient that we enroll has to have the HLA type A0201. About 42% of people in the U.S. have that HLA type. Right now, we can address about 42% of the U.S. population, about 47% of the European population. However, we'd like to expand that to ultimately all patients that undergo transplant therapy. To do that, we need to introduce new products that address other HLA types. Our strategy now moving forward is because what we've learned from TSC-101 is that we can identify patients that qualify, donors that are negative for the antigen by finding donors that are negative for the HLA type. Based on that strategy, all products moving forward will actually target different antigens on the protein CD45. CD45 is a protein that's expressed in all hematopoietic cells, but not any non-heme tissue. It's expressed at very high levels, and it's a large protein, so there's many different antigens on that protein. TSC-102 A0301 is our first product to address antigens from CD45. It's targeting the HLA type A0301. We're on track to filing an IND in the second half of this year on TSC-102 A0301. We're also developing additional products, and the next one to come along will be TSC-102 A0101, which will address the HLA type, obviously A0101. We are planning to continue phase I development as we introduce these new products to add these to the pipeline so that ultimately we can address the majority of patients that are undergoing transplant therapy. As we move TSC-101 into pivotal studies, we will continue to develop the TSC-102 series to address these other HLA types. I do want to shift gears to solid malignancies, which has been a particular area of focus for investors. Maybe a quick overview of the reasoning behind using more than one antigen targeting T cell. Yeah, I think the key reason to do this is that, as I said earlier, solid tumors are heterogeneous. If you stain a solid tumor for some of the targets that we're looking at and other companies are addressing as well, there are many targets that you don't see uniform expression across all tumor cells. For example, the antigen PRAME is actually fairly uniformly expressed in melanoma, which is why I think we're seeing such success with PRAME, TCRs, and melanoma. In other tumor types like lung cancer, PRAME is more heterogeneously expressed. Maybe 50% of the tumor cells will express PRAME. The other 50% will express another antigen like MAGE4, for example. Because of that heterogeneity, we're really, again, taking our cue from nature. Nature doesn't express just a single T cell clone when it mounts an immune response against cancer. You see an oligoclonal response, right? You see multiple different T cells addressing the tumor cells. Based on that, we're building up this collection of TCRs so that when we stain a patient's tumor for these different antigens, we can then give them the appropriate TCRs based on what antigens are expressed in their tumor. Right now, our clinical trial enables us to treat patients with two TCR-T cell products at a time, but we anticipate potentially expanding that to three once we get experience with multiplex therapy. That is really the logic behind the strategy that we're taking of doing multiplex therapy. Maybe to kind of reiterate this as it relates to natural T cell responses, is it driven primarily by, let's say, a couple of clones of T cells, or is it like, I don't know, 50? Yeah, so I mean, that's a great question. We have studied the T cells of many different cancer patients now. For a start, it's a very large collection of TCRs that you find in the TILs of a patient. However, as you start to study those TCRs, what we found is that very few of them actually have very strong anti-cancer activity. There's a lot of bystander TILs that are present in a tumor. We clone our therapeutic TCRs out of patient T cells. As I said, when we screen all these T cells, very few of them actually have that core anti-cancer activity. Secondly, if you look at TIL therapy products, they're very often dominated by two or three clones, right? Maybe 80% of the product comes out of three clones, and then the remaining 20% of the product is another 100 different types of TCRs. Based on both of those observations, we believe that most of the anti-cancer response is really driven by a relatively small number, just a handful, two or three different T cell clones. We do not feel like a multiplex product needs to be 50 different clones, which is good because our manufacturing team would lose their minds if I told them that is what we were doing. Overall, we do think that more than one clone is going to be necessary to address that heterogeneity. The data you've seen in your heme program shows relatively limited immune-mediated toxicity. Do you think this has something to do with the TCR-T cells having less tonic signaling because they're just less common antigens? Is it reasonable to expect this tox profile in the solid tumor programs? Yeah, I think there's two reasons why we're not seeing high CRS rates, for example, in the heme program. One of them is that naturally occurring TCRs are tuned to have the appropriate signaling properties. There's very little tonic signaling, which is signaling in the absence of antigen. When they get activated, they do signal appropriately. We've seen historically that TCR-Ts show a much milder tox profile than CAR-T because you don't have that very strong initial burst of signaling that you do with a CAR product. Overall, TCR-Ts just haven't had those same CRS rates that we've seen with CAR-T products. The other reason with the heme program is that the disease burden is extremely low following transplant. The fewer target cells there are, the less chance there is to have a very strong burst of T cell activation, which would lead to that CRS. Certainly in the heme program, it has not been a problem. In solid tumors, there is definitely a larger disease burden. The T cells are going to see more tumor cells. We have seen CRS rates from other companies in their solid tumor programs, but none of them have been really limiting those programs, right? Because of that, I would say slower ramp-up of the T cell response with TCR-T relative to CAR-T. You mentioned a couple of engineering features of your T cells to improve their resilience. What other strategies are you using to improve T cell health, specifically because we're sourcing T cells out of cancer patients? Yeah, I mean, I would say the biggest impact is actually in the manufacturing process. When we get the T cells out of particularly a patient with cancer, which is the case for the solid tumor program, those T cells are pretty beat up, right? A lot of them are in an exhausted state. The advantage of ex vivo engineering is that you now provide an appropriate environment for those T cells to get rejuvenated and develop a younger T cell phenotype, stem cell memory phenotype. That is really from the mix of cytokines that you give those T cells during the manufacturing process. One, we're optimizing that mix. We're actually about to, with our heme program, move to our commercial manufacturing process that addresses some of that. With solid tumors as well, we're constantly refining our process and improving it to promote more of a stem cell phenotype in those T cells. The second big thing that you can do to increase the stem cell memory phenotype is to shorten your manufacturing process. We've seen an enormous impact that the Novartis TCharge program has had on their Kymriah product, right? Because the first generation product was a longer two-week manufacturing. They shortened that to two days. I may be getting the details wrong in terms of the actual time with the manufacturing, but that shorter process leads to a much more potent product that has much greater persistence. Similarly, we're focused on reducing the manufacturing time to really promote that stem cell memory phenotype. Currently, your clinical development program is looking at each TCR individually from a safety perspective. When you reach TILs level two, you're going to start combining them. Once you clear that safety bar, do you think we'll see one study with many different kinds of combinations, basically? Yeah, so just to reiterate what you're saying, our clinical trial design is that each TCR first gets tested at two different dose levels, and then once the TCR is cleared, dose level two becomes eligible to be combined with any other TCR at dose level three. Dose level three is really what we consider the therapeutic dose of our T cells. That's where we're introducing the multiplexing as well. Our focus this year is to treat as many patients at dose level three as we can with multiplex therapy to start generating that clinical efficacy data set that everyone's looking for. As we move forward, how do we imagine pivotal trials or expansion cohorts that are focusing on particular areas? Yes, ultimately, the vision has been that a patient would get a customized multiplex product based on their tumor biology. Our vision has always been that the product is unique for each patient, but manufactured from a collection of TCRs. What we're seeing in the clinic is that certain antigens are much more prevalent than others, right? In particular, PRAME and MAGE4 are very prevalent antigens. We now have a focus on lung cancer, head and neck cancer, and sarcomas with PRAME, MAGE4, and MAGE1. Functionally, what we're seeing is actually much lower prevalence of MAGE1, much higher prevalence of MAGE4 and PRAME. We anticipate that PRAME plus MAGE4 is going to be a very common combination in our clinical development path. We may just choose to move single combinations forward. Our other core product is a TCR that addresses HPV-16. In HPV-driven cancers, which is about 25% of head and neck cancer, but then the majority of anal and genital cancers, there, again, we're seeing very high expression of PRAME and MAGE4. We anticipate that HPV plus PRAME and HPV plus MAGE4 will be two very common combinations. Although in principle, a patient could get any combination of TCRs, there are some that are turning out to be much more common than others. It is possible that we would just focus on some of those core combinations in a regulatory path moving forward. From the indication end, is there potential for a pivotal basket study? Is this something regulators are discussing, or what do you think is a path forward for a tumor agnostic label? Yeah, so by basket study here, you're referring to the different types of cancers? Yeah. Yeah. I would say it really depends on the data, right? If we see very similar response rates across different cancer indications, that argues strongly for a basket study. If we're seeing very different response rates, we may have to separate that. I would say the greatest chance of a basket study would be in our HPV program, right? It makes a lot of sense to do all HPV-16-driven cancers in a single basket to combine head and neck cancer with cervical cancer, with anal cancer, all in a single study. In the non-HPV-driven cancers, again, it's really based, do we see the same response rates in lung as we see in head and neck? If we do, that would argue strongly for a tumor agnostic study. If they're quite different, but both clearly outperforming standard of care, it may be that those need to be separated. We are expecting some first data later this year. As you mentioned, this is not going to be the data of your actual effective dose. Where do you think the efficacy bar is here? Yeah, as I said, we do expect that dose level three is an effective dose. The data that we present at the end of the year will focus on dose level three or higher dose levels. We are looking to actually get our first signals of efficacy when we report data out at the end of the year. What's the bar? I think the bar is different again, depending on what type of cancer you're addressing. Right now in lung cancer, in third and later lines of lung cancer therapy, there's just really no good products. We're seeing about 20-22% response rates with current therapies in that area. If we can double that, obviously, that's a huge impact on lung cancer. In other areas like the HPV-driven cancers, if we see a 50% response rate, like what we've been seeing coming out of VNCI in their study that was performed several years ago, that would clearly meet the bar for regulatory approval. It really depends on what the bar is. I would say it's different, again, depending on what type of cancer you're going after. In the other half of the equation, there is durability of response. This has been a challenge, and CAR-Ts that target solid tumors. When do you think we'll have sufficient follow-up to really be able to define this? Yeah, so I'd say realistically, at the end of this year, we're aiming for around a dozen patients treated at dose level three and with multiplex therapy. Many of those patients will have just been dosed or have just reached their first CT scan, 6-week, 12-week scans. I would say the durability data is more mid-next year and then end of next year for a substantial number of patients with one-year follow-up. I would say that data is going to continue to mature as we get there. Our goal is to get at least a dozen patients in it at multiplex therapy by the end of this year so that we can start to see long-term durability mid and at the end of next year. Thank you. Very clear. I do want to spend a minute on manufacturing, which you've mentioned. Can you give us an idea of what the lead-in times are for your heme product or for your solid tumor product? Are they very different? Yeah. I'm actually going to focus on what we call our second-generation manufacturing process. For heme, this is this commercial-ready process that we're rolling out this year and obviously launching the pivotal trial with. That process, we're reducing manufacturing time down to about 11 days. One, that makes a better, younger product. Two, manufacturing time is not the rate-limiting step in the heme program. The reason for that is that we initiate manufacturing before the patient gets transplanted. The patient needs about three weeks post-transplant to recover from the transplant before we give them their first infusion of engineered T cells. In that program, the T cells are ready before the patient's ready to receive them. Manufacturing is not the rate-limiting step in the heme program. In the solid tumor program, it is because patients get apheresed, and then we manufacture the product. Once the product is ready, the patient then undergoes lymphodepletion followed by T cell infusion. We have been focused on reducing the manufacturing time in that program. We anticipate being able to get that time down to between 9 and 11 days. With about a week to do release testing and QA approval, we will be down to certainly under three weeks from when the patient gets apheresed to when the T cells are ready for them to initiate the therapeutic process. I think that is pretty much in line with what most other companies are doing in this space and is both commercially feasible and in the best interests of the patient. How rudimentary is antigen profiling in solid tumor biopsies? Would you need to change current standard of care to increase patients getting their tumors assessed? Yeah, actually, that brings up a great point. In our phase one study, we are actually prospectively selecting patients based on antigen expression in their tumor. That way, we're only giving product to patients that we know have a chance of benefiting from the product. In the commercial setting, it's becoming more and more common for patients to have extensive analysis of their tumor sample. Certainly, next-gen sequencing is occurring on almost every patient in different types of cancer to understand cancer mutations that are driving their cancer and being able to give them appropriate targeted therapies. More and more, we're seeing RNA-seq being applied to tumor cells as a standard of care in cancer treatment. Although we're using immunohistochemistry in our phase one study, this is a potential. We are also assessing RNA-seq levels for each of our targets. If that proves to correlate very highly with the immunohistochemistry results, we could anticipate shifting over to that assay since that's something that is being performed routinely as part of cancer care. In that setting, if we can get a companion diagnostic approved, that's something that people are getting done automatically anyway, that lowers the bar substantially to doing a targeted therapy in this fashion. As it relates to the practice of getting a biopsy, we spoke of tumor heterogeneity. Is the biopsy size big enough to really capture the antigens you're looking for? Yeah, you can, from an 18-gauge core needle biopsy, which is routine in the hospitals, get the data from both RNA-seq and the next-gen sequencing to get. I should point out that the other thing we're doing is we're also testing for HLA loss in the tumor cells. Obviously, a patient's not going to benefit from a TCR if they've lost the HLA. The HLA loss of heterozygosity assay that we're doing is based on next-gen sequencing from tumor samples. We're getting that routinely from biopsies. We don't need surgical resection for that. You mentioned that you're currently using external manufacturing. Is there any thinking of bringing manufacturing in-house at some point? Yeah, just to clarify, we do all our own manufacturing in-house for our early-stage clinical development. In fact, every patient we've treated to date at TScan has been from product manufactured at TScan. For the heme program, for commercial manufacturing, our current strategy is to use a commercial CDMO. Do we think ultimately we would bring commercial manufacturing in-house as well? That's certainly not out of the question. I mean, I think companies have really benefited from that strategy. Just looking at the CAR-T world, obviously, manufacturing is the key issue in this space, right? You can have a great product, but if you can't routinely manufacture it and manufacture it in spec, you can't get reimbursed, and the commercial success is going to be low, right? That is something that we're taking a very close look at. Thanks for the clarification. Release criteria have also been a challenge for cell therapy in this space. Iovance is an example that comes to mind. How are you guys thinking about addressing this potential issue? Yeah, so we're obviously very focused on having a robust manufacturing process where as close to 100% as possible of product manufactured meets specifications. You need to meet specifications to get appropriate reimbursement. In terms of the assays themselves, we do not suffer from the same challenge that Iovance has in terms of a potency assay. Our product, we know what the target is, right? I mean, it's a TCR-T that's addressing a particular target. Our potency assay is relatively straightforward. We have cells expressing that target, and it's a cell-based assay to assess potency. We have already reached agreement with the FDA on what those potency assays would look like. Excellent. One last question before I open it up for the audience. What is the current cash resources and projected runway, and how well does this align with company's catalysts? Yeah, we ended 2024 with $290 million in cash. That cash provides us runway into Q1 of 2027. That enables us to execute on all of the milestones that we've publicly disclosed, right? Solid tumor data by the end of this year and launching the heme pivotal trial and the enrollment rate that we need for the heme program. Again, we're targeting 140 patients in total in that pivotal trial. That trial would read out in the second half of 2027. We do not currently have cash runway to get us to the end of the pivotal trial. The cash runway we have enables us to fully execute on that pivotal trial with the projected enrollment rate that we need to reach that point. That carries us into Q1 of 2027 with a slight funding gap from Q1 to second half of 2027 to reach that top-line readout. Okay. I'll stop there. We'll pull for questions for a minute and see if there's any other questions from the audience. Currently not seeing any added questions. Gavin, thank you so much for attending today. Very interesting year ahead of us, and looking forward to the solid tumor data at the end of the year. It should be exciting. Yeah, thank you. Thank you again for inviting me to give this fireside chat.