Good afternoon, everyone. Welcome to the next session with Kyntra Bio. I'm Ami Fadia, biotech analyst here at Needham. It's my pleasure to be hosting the company, and I have with me today, Thane Wettig, who is the CEO of the company, and David DeLucia, who is the CFO. Thane and David, thank you so much for being here and participating in the conference. Why don't I turn it over to you, Thane, to take us through the presentation, and we'll keep some time at the end for Q&A. Yeah, that sounds good, Ami. Thank you very much, and thanks to the Needham team for the opportunity to provide the update on the Kyntra Bio story, the classic forward-looking statements which you are all familiar with. I want to touch first on the overarching picture of Kyntra Bio, the investment highlights. Toward the end of 2025, we really culminated the transformation of the former FibroGen into Kyntra Bio as we completed the sale of FibroGen China to AstraZeneca for a total consideration of approximately $220 million. This included $85 million in enterprise value for roxadustat, and then AstraZeneca taking over our China accounts, which had $135 million in cash, and offshoring us dollar for dollar that same amount. A total consideration of $220 million. This allowed us to do a couple of things immediately. First, successfully repaying the term loan that we had with Morgan Stanley Tactical Value, which further simplified our capital structure by removing all of the senior secured debt off of our balance sheet and extending our cash runway into 2028. The other thing that it enabled us to do immediately was to begin the Phase II trial for our ADC, FG-3246 and FG-3180, which we are currently enrolling in that Phase II trial. We'll talk more deeply about FG-3246, its target, and why we are so encouraged by not only what we've seen, but looking forward to the results of the Phase II trial, which is ongoing. Importantly, we'll also cover a component of that program, FG-3180, which is a companion PET imaging agent, which is also in clinical development as a potential novel patient selection biomarker. The other thing that we're now also laser-focused on is roxadustat, where we have a Phase III-ready development opportunity in a condition called lower-risk myelodysplastic syndrome. Again, we'll dive deep into this as well, including some recent updates on the current status of that program. In terms of recent and near-term catalysts, we expect to see interim results for the Phase II monotherapy trial of FG-3246 in the second half of this year. We've submitted the final Phase III protocol for roxadustat to the FDA in December for the anemia of low-risk MDS opportunity, with a potential for a Phase III initiation in the second half of this year as well. Now we'll turn our attention to our ADC focused on metastatic castration-resistant prostate cancer. The FG-3246 and the FG-3180 program. I think everybody knows about the seriousness of prostate cancer and how high the need continues to be for treatment options that can extend survival in late-stage metastatic castration-resistant prostate cancer. It's the second most common type of cancer. One out of seven or one out of eight men at some point in their lives will be diagnosed with prostate cancer. There are approximately 65,000 drug-treatable mCRPC cases in the U.S. every year. Unfortunately, the five-year survival is only about 30%. Therefore, there continues to be significant unmet need in mCRPC for therapies that can extend survival in patients who are either ineligible for or who have progressed on androgen receptor pathway inhibitors and/or chemotherapy, and also a significant need for new novel MOAs, such as non-PSMA approaches that can treat patients who have progressed on the available treatment options. In addition to that, and I think that this has been proven with the advent of PSMA PET imaging agents, there is also a great opportunity for predictive tools that can help inform patient selection, and also the ability to figure out more optimal ways to either sequence or combine therapies for mCRPC. Now we'll turn our attention to our target. The target of our ADC is an epitope on the surface of a number of cancers. It's called CD46. It's a novel tumor-selective target. CD46 has been proven to negatively regulate the complement system, and it helps, therefore, tumors evade complement-dependent cytotoxicity. It's a multifunctional protein, which is overexpressed in a number of tumors. In addition to it being overexpressed in mCRPC, which is the focus of our ADC at the moment, it is also overexpressed in colorectal cancer, lung cancer, and a number of other solid tumors. I think importantly, it also has limited expression in normal tissues. The only other place that you see reasonable or expression of CD46 is in placenta or prostate epithelium. That's it. It either has no expression or extremely low expression in all other normal tissues. It is overexpressed in mCRPC, and so CD46 expression is upregulated as prostate cancer progresses from the localized castration-sensitive phase to mCRPC, and it's further overexpressed following treatment with the androgen signaling inhibitors. We estimate that about 50%-70% of mCRPC patients have high expression of CD46. We also know, based upon DNA markers, that CD46 is expressed more homogeneously and at higher levels compared to PSMA. We're really excited about the opportunity to further explore the role that CD46 plays in mCRPC. Turning to now our program, targeting a novel epitope of CD46, we believe has a therapeutic and diagnostic potential. FG-3246 is the therapeutic. It's got the targeting antibody plus the payload. It has an MMAE payload and the linker that goes along with that. This is the Seagen approach that has been approved in a number of other chemotherapy regimens, nothing for prostate cancer at this moment, but a number of other tumors where MMAE plays an important role. The antibody that has been specifically engineered to target CD46 is YS5. It's a fully human, full-length IgG1 monoclonal antibody to the tumor-selective epitope of CD46 that, again, is less accessible on most normal cells, and it does not interfere with the complement system regulation. I spoke about the companion PET imaging agent. It also utilizes the same YS5 antibody, is delivered with a zirconium-89 tracer, and has demonstrated specific uptake in CD46-positive tumors. We'll talk a little bit more about some recent data that has been generated as part of an IST, as part of a combination trial of our ADC with enzalutamide that was recently disclosed at ASCO GU. We do believe that this PET imaging agent has the potential to inform patient selection, and that we do believe that the PET-based biomarker currently is considered to be superior to a CD46 IHC approach in prostate cancer. Our strategy aims to achieve a clinically differentiated profile, again, in this disease, which unfortunately is highly dissatisfied at the moment. We'll talk about a couple of above trials that have been conducted with the ADC. The first one is the Phase I monotherapy study of FG-3246 in patients with mCRPC. It was the classical dose escalation followed by dose expansion study, 33 patients in the dose escalation phase to determine the maximum tolerated dose, and then 23 patients in the dose expansion study. The primary endpoint, again, from the escalation phase was the safety and tolerability and the determination of the MTD. Secondary endpoints were the typical PK and efficacy endpoints. Exploratory endpoints evaluated the potential relationship between CD46 expression and measures of anti-tumor activity associated with the ADC. In the dose escalation phase, the maximum tolerated dose that was taken into the dose expansion phase was determined to be 2.7 milligrams per kilogram adjusted body weight. This is the baseline characteristics. I think it's important to note that this was a heavily pretreated patient population, a median of five prior lines of therapy, which included androgen deprivation, androgen signaling inhibitors. There were some patients who had been previously treated with taxane therapy, but that was in the castration-sensitive phase. Nobody was treated with docetaxel or a taxane treatment in the castration-resistant phase. Now we'll talk about the results from that Phase I monotherapy study, which demonstrated what we believe to be very meaningful clinical activity, again, in a heavily pretreated patient population. The efficacy analysis included 40 patients from both the escalation and the expansion cohorts, 8.7 months median RPFS, a PSA50 decline of 36%, 20% ORR, and associated with that ORR was a duration of response of 7.5 months. I think it's important to note that the 20% of patients, so five out of 25 who were evaluable, all of those patients were at the 2.7 milligram per kilogram dose. Based upon that and some additional post-hoc analysis that we have done with respect to exposure response, we do believe we've seen a clear dose response associated with the ADC. When we compare those results, notably the RPFS results to other programs at a similar stage, in a similar sort of median prior lines of therapy, we believe that our ADC FG-3246 has demonstrated very comparable efficacy in this Phase I monotherapy trial. This is in fact what gave us the conviction to take this into the currently enrolling Phase II trial. In terms of adverse events, the Phase I monotherapy safety profile was entirely consistent with other MMAE ADCs adverse events. What you'll see is Grade 3 and above neutropenia, neutrophil count decrease, white blood cell count decrease, very limited Grade 3 or above adverse events across any of the other adverse events which were noted. I would note that peripheral neuropathy occurred in about one out of three patients, but only one patient had Grade 3 or above peripheral neuropathy. That clearly is an adverse event that is commonly associated with MMAEs. Again, based upon the efficacy as well as on this adverse event profile, that gave us the conviction to further explore the ADC and the companion PET imaging agent as part of a Phase II trial. The other trial, which was recently concluded and disclosed, was the ADC FG-3246 in combination with enzalutamide in a Phase I-B/II IST conducted by the University of California at San Francisco. Again, it was the typical Phase I-B/II trial, the escalation phase followed by the expansion phase. These are patients who had progressive mCRPC and had progressed on at least one prior androgen receptor inhibitor and no prior taxane for, again, the castration-resistant phase. Study endpoints in the escalation phase, again, were the maximally tolerated dose. Secondary endpoints were the typical endpoints that we discussed earlier, PSA50, ORR, RPFS, et cetera. We also had an exploratory endpoint in evaluating the potential relationship between CD46 expression and anti-tumor activity of the combination therapy of enzalutamide with FG-3246. On the left, you'll see the results from the entire patient cohort across the I-B and II population. What we've seen is an RPFS of seven months and a PSA50 response of 22%. I think it's important to note that a majority of the patients in this trial, so over 60% of the patients in the trial, had progressed on two or more prior ARPIs. When the investigators looked at the results of the patients who had progressed on one prior ARPI, the RPFS was 10.1 months and an encouraging PSA50 response of 40%. Rahul Aggarwal concluded in his ASCO GU disclosure that FG-3246, again, has demonstrated encouraging anti-tumor activity in patients with mCRPC, notably for those who have progressed on only one prior ARPI. In terms of the adverse event profile, again, classic or typical adverse events consistent with not only the monotherapy, Phase I monotherapy trial, but also, again, the MMAE-associated adverse events. The one thing I would like to call out is the rate of neutropenia. As I highlighted in the Phase I monotherapy trial, there was a large percentage of patients, about over 30% of patients, who had experienced Grade 3 or above neutropenia in the Phase I monotherapy trial. You see here that there has been a marked decrease in the number of patients who experienced Grade 3 or above neutropenia, as denoted in the orange part of the neutropenia column there. The reason is because Dr. Aggarwal, in his IST, introduced G-CSF to mitigate the neutropenia that is common with this MMAE approach. In fact, every patient in the dose expansion cohort received G-CSF, and it markedly reduced the incidence of Grade 3 neutropenia. The reason that that's important is because in the Phase I monotherapy trial, those patients who had experienced Grade 3 or above neutropenia, most of them had to be either dose interrupted or downward titrated from the expansion dose of 2.7 milligrams per kilogram. This is an important design element of our ongoing Phase II monotherapy trial. I'd also like to highlight one additional data point from the IST that was again disclosed at ASCO GU. This is the demonstration for the first time of an association of PSA50 response with higher tumor uptake of FG-3180 or the PET imaging agent. What you'll see on the right is a PET scan. This is a patient who was treated with FG-3180 or PET46. Six days later, they came back, and they were scanned, and then the ADC was administered. What you see in the table on the left, and pay attention to the bottom row, because that is what measures the standard unit volume, the maximum average over the standard unit volume mean blood pool. It's designed to basically normalize the background CD46 expression. What you'll see is those patients who had a higher uptake of CD46 or higher expression of CD46 were more likely to have a PSA50 response than those that had a lower level of CD46 expression. For the first time, we have demonstrated the potential of FG-3180 as a PET imaging biomarker for potential patient selection. We're going to further evaluate this in the ongoing Phase II monotherapy trial. Now turning to a summary of what we've seen in both the Phase I monotherapy trial and the combination trial with enzalutamide that was just disclosed at ASCO GU in patients who were on one prior ARPI. Again, we believe that FG-3246 has demonstrated encouraging anti-tumor activity, and it gives us the conviction to take this again into the Phase II portion of the program. I think probably the best thing to highlight here would be the PSMAfore trial from Novartis for Pluvicto. This is a trial that was concluded in 2024. In 2025, Novartis received their second indication for Pluvicto in mCRPC. In this case, it was in the patients who were post one ARPI and pre-chemotherapy. There was an RPFS of 9.3 months. We believe that in our Phase II monotherapy trial, that we need to hit about a 10-month RPFS in order to have an encouraging and competitive efficacy profile that would give us the conviction to take it into then the Phase III portion of the program. Now I'll talk about the Phase II trial, which is again, ongoing and enrolling patients in the United States right now. We do expect interim results in the second half of this year. We're studying 75 patients, 25 in each one of the three dose cohorts, 1.8, 2.4, and 2.7 mg/kg. 50 of the 75 patients are at a higher dose relative to what was administered in the IST, which was 2.1 mg/kg. Again, 2.7 mg/kg was the expansion dose from the Phase I monotherapy trial. The interim analysis is going to be conducted after 12 patients in each arm undergo 12 weeks of therapy. We're going to be looking at a composite response rate of PSA50 and ORR. We're going to be most interested in, as the trial progresses, in seeing more mature RPFS, which would allow us to then determine how competitive we believe the profile is relative to not only currently available therapies, but also those that are in development. Each one of the patients will receive prophylactic G-CSF. As we think about the Phase II monotherapy trial relative to the Phase I monotherapy trial, there are some important design elements that we believe give us an opportunity to build upon that 8.7 months of RPFS, which was demonstrated in the Phase I trial. First is use of three of the highest doses that were used in the Phase I monotherapy trial. Again, this is given the exposure-response relationship that was established in that Phase I trial. Utilization of primary prophylactic G-CSF to mitigate the MMAE-associated adverse events like neutropenia, again, the goal here is to ensure that patients can stay on their dose early in the course of therapy when the maximum cytotoxic effect is provided from the ADC. We believe that based upon Dr. Aggarwal's experience in his IST, which was recently disclosed, that we've got the ability to knock that Grade 3 or above neutropenia adverse event rate way down and allow patients to continue on therapy without dose interruption or dose reduction. Finally, we're going to be studying a patient population which is more upline. Instead of a median of five prior lines of therapy, these are patients who have progressed on one prior ARPI. Think about it in either the first-line or second-line status in mCRPC. Based upon that design, which we believe will allow us to conclude whether or not we have a competitive product to take into a Phase III, we've designed the trial to select the dose for the optimum benefit-risk profile. We talked just a moment ago about the three factors which we can hope to drive RPFS in this all-comers population. We're also going to be able to see data on a large number of patients who will have been treated with the PET46 imaging agent to see if, in fact, it can perform as a predictive patient selection biomarker. Again, we believe that this unlocks multiple registrational pathways, either sequentially or in parallel. Multiple lines of therapy in prostate cancer monotherapy and/or combination therapy approaches, and either an all-comers population or in patients who have a high expression of CD46. The upcoming catalyst is, again, as we spoke, in the second half of this year is interim analysis from the ongoing Phase II trial we expect in the back part of this year. In summary, we believe that we've got a novel mechanism of action with a potential first-in-class opportunity. We're the only ones working on CD46 as a target, and again, we think it's important that we have a non-PSMA approach. We talked about the compelling results from the two previous studies where 3246 demonstrated important clinical activity, either as a monotherapy or in combination with enzalutamide. We have a consistent safety profile with other MMAE-based ADC therapies which have been approved in other tumor types. We believe that, again, this has significant potential opportunity in multiple lines of mCRPC, again, given the sizable unmet need that continues in metastatic castration-resistant prostate cancer. Importantly, we will be investigating the PET biomarker imaging agent to determine if we can see a correlation between expression of CD46 and response to the ADC. More to come on this toward the back part of this year, and then the RPFS data, which will be generated ongoing, and we'll see it more fully mature in 2027. Now turning to our roxadustat program. For those of you who are familiar with roxadustat, you'll know that it has been approved in more than 40 markets for anemia associated with chronic kidney disease. This was the business that we sold to AstraZeneca in China, where it generated peak revenue of $340 million in China in 2024. The science behind roxadustat is hypoxia-inducible factor prolyl hydroxylase inhibitor. This science led to the 2019 Nobel Prize in Physiology or Medicine. It increases hemoglobin by mimicking the body's natural response to low oxygen. Again, it's been approved in more than 40 markets for the treatment of patients who have anemia associated with chronic kidney disease, patients who are both on dialysis and not on dialysis. Our focus for the program is in a different indication than anemia associated with chronic kidney disease. This is anemia associated with lower-risk myelodysplastic syndromes, which we believe represents a sizable opportunity. Anemia is a hallmark symptom of MDS that gives rise to significant morbidity and quality-of-life issues. 75,000 patients are diagnosed with MDS in the U.S. 58,000 of these have low-risk MDS, and about 50,000 of these live with anemia. Despite recent approvals, there remains a significant unmet need in this refractory population, given the fact that the currently available agents are effective in leading to transfusion independence in less than 50% of patients. This relief is often temporary, with limited treatment options in the second-line and beyond setting. In addition, the currently available agents can be challenging to either dose calibrate or administered. The currently available therapies are administered in office in either a sub-Q injection or an IV infusion. We believe that there's an opportunity to come forward with a product like roxadustat with its oral mode of administration, which can be a meaningful benefit to a number of patients, again, given the morbidity associated with this patient population. There was a previous Phase III trial that was run by FibroGen in collaboration with Astellas and with AstraZeneca. It was the MATTERHORN trial. It looked at anemia associated with lower-risk myelodysplastic syndrome. In that total cohort, we demonstrated a numerical advantage of transfusion independence but did not reach statistical significance because of an abnormally high placebo response rate that was driven by the enrollment of a number of patients who had a low transfusion burden at baseline. These are patients who would require one or two units over an eight-week period of time. Many of these patients just spontaneously become transfusion independent because of the low requirement that they have. At the vocal request of a number of thought leaders who believe that roxadustat showed promise in this MATTERHORN trial, we did a post hoc analysis in looking at patients who had a high transfusion burden at baseline. These are patients who had four or more RBC units in two consecutive eight-week periods prior to randomization. This is the patient population that, for the most part, are being treated with the currently available therapies in the real-world setting. In that post hoc analysis, the eight-week RBC TI within the first 28 weeks of the trial was 36% for roxadustat and only 7% for placebo, which was a nominally statistically significant p-value. Some very similar results when looking at eight-week RBC TI within the entire length of the study, the entire 52 weeks, 45% for roxadustat and 13% for placebo. Again, this is what gave us the conviction to approach the FDA through a Type C process to determine the path forward for another Phase III trial of roxadustat in this high transfusion burden patient population. We believe that if we can show a benefit in this particular patient population, that we could elevate the standard of care in second-line or third-line lower-risk MDS anemia. Typically, physicians make treatment selections based upon either the del(5q) or RS status, ring sideroblast status, of either being RS positive or RS negative. Luspatercept, which is REBLOZYL from BMS, which in 2025 was a $2.3 billion product, 80% of that value in the U.S. and the majority of that for the treatment of lower-risk MDS, has really solidified itself in the RS positive population as a first-line setting based upon a head-to-head trial conducted against ESAs. In the RS negative setting, luspatercept does get utilization, even though it really hasn't demonstrated much of a benefit in the RS negative population. We believe that roxadustat can effectively compete in the second-line setting and beyond, and in doing so, not only provide an important treatment option for patients who don't achieve transfusion independence on the currently available agents, but also represents a sizable commercial opportunity as well. I spoke about the Type C process that we undertook with the FDA in the middle of last year, where we reached alignment with them on essentially all of the important design elements of a Phase III trial. The patient population, those that would require four or more RBC units in two consecutive eight-week periods that are refractory to, intolerant to, or ineligible for prior ESAs. Importantly, the ability to manage potential thrombotic risk through eligibility, dose modification, and discontinuation criteria, looking at either eight or 16-week RBC transfusion independence. Final analysis is performed when all participants have completed about 12 months of treatment or discontinued therapy. Again, the dose regimen, oral route of administration 3x a week with a starting dose and a maximum dose of 2.5 and 3.5 milligrams per kilogram respectively, which mirrors the starting dose and the maximum dose from the previous Phase III trial. Again, we submitted the final protocol to the agency in December, and we expect to hear back comments from them in the very near future that would then allow us to finalize the protocol and continue to proceed toward the Phase III trial. In summary, we believe that there is a substantial unmet need in this lower-risk MDS patient population despite recent approvals. There is no other oral treatment for anemia of lower-risk MDS commercially available or in late-stage development. We believe that we can demonstrate a highly differentiated profile, especially given how physicians make these treatment selections, either in RS positive or RS negative patients. We think that there is a sizable unmet need in the RS negative population, which again represents more than 50% of patients with low-risk MDS. We did receive Orphan Drug Designation for roxadustat in December from the FDA, which gives us at least seven years of regulatory exclusivity in the U.S. Again, this worldwide MDS market is expected to exceed $4 billion in the next five years. It's got an attractive pricing opportunity, an efficient commercial model in the U.S. with the potential for, we think, much greater than $0.5 billion in peak U.S. sales. That is it. Ami, we'd be happy to take any questions. Okay, great. Thank you, Thane, for that thorough presentation. Maybe if you can talk about the three doses that are being tested, and can you help us think about some of the trade-offs on the efficacy plus sort of the tolerability side across the three doses? What would you need to see, or what would you like to see, in terms of PSA50 from the data? Yeah. No, thanks. That's a good question. What we've decided to do was really stretch the doses out, have a low-end dose of 1.8. Again, we're trying to walk that line between the classic MMAE adverse events and then the efficacy that we believe we need to be competitive to take it into that Phase III portion of the program. I think what we would hope to see is better responses and acceptable safety at the 2.4 or the 2.7 milligram per kilogram doses. Again, 2.7 was what was used in the Phase I monotherapy trial. A number of those patients had to be downward titrated to 2.4, though, due to the neutropenia. This mitigation of neutropenia with prophylactic G-CSF is a really important component of the program. We think that by looking at the three doses, we'll be able to determine, even perhaps through the interim analysis, is there a dose that could perhaps is shining better than the others, or perhaps maybe the lower dose might fall out. If we don't see the responses at 1.8 like we're seeing with 2.4 and 2.7, and 2.4 and 2.7 are also demonstrating acceptable safety, we do have the ability to drop that 1.8 dose and then enroll the remaining patients all at either 2.4 or 2.7. In terms of PSA50, Ami, because of the non-PSMA approach that we have, we don't think that PSA50 is the best marker, right? It's a biomarker, if you will, but I think there's been enough evidence generated, even in the past kind of 12-18 months, which looks at PSA50 not necessarily being correlated with rPFS. I think the Janux example is a great example of that. You've got a very promising T-cell engager approach with startling PSA50 and PSA90 responses that didn't hold true with the rPFS. Their rPFS was 7.4 months in, I don't know how many patients there were, 15, 20, 25 patients. We're going to use the PSA50 results as instructive, along with ORRs, through this interim analysis. We've set a fairly low bar to continue on, a bar that is consistent with our Phase I monotherapy, PSA50, and ORR results because, again, we're most interested in getting to the more mature RPFS data because that ultimately is the data point that we're going to look at to say, "Do we move it into the Phase III portion of the program?" Coming back to the PET imaging agent, seeing these results from the IST for the first time, which showed a correlation between CD46 expression and response to the ADC, that's going to be a really important efficacy measure that we're going to be looking at as well. If there is a correlation between RPFS and response to the ADC, so you get a higher RPFS, the higher the expression of CD46, that would then allow us in the Phase III portion of the program to self-select patients who are higher expressers and enroll those patients with the potential to get an even higher RPFS, again, in order to have a targeted selection and not treat patients who don't have the CD46 expression that they need in order to get a response to the ADC, and then drive that RPFS up in that patient population that can respond the best to the therapy. At the interim data, how many scans would have been done on the patients? Maybe sort of, in the Phase I-B/II, did you see sort of deepening of response over time? I'm trying to understand at what point will we be seeing that data cut. Yeah, we aren't having patients undergo multiple CD46 scans. This was the same way that Rahul Aggarwal did it in his IST. Patients came in in the expansion cohort. They received the PET imaging agent. It wasn't used as a screener. It was only used to determine what their level of expression was. Everybody then got enrolled into the IST. It was an open-label trial. We're doing the same thing for our Phase II. The open-label trial, all 75 patients will get the PET46 or FG-3180 at baseline. They'll come back six days later and get the scan and then immediately get the ADC. We'll be able to assess the expression levels of CD46 based upon the PET scans, and then be able to do a correlation assessment over time of the efficacy measures relative to the expression levels of CD46. There were about 25 patients worth of data in the IST. When we think about the 75 patients that we're going to add in our Phase II monotherapy, we think we're going to have a really nice, robust data set at 100 patients in how we need to think about tumor uptake of the PET versus correlation to exposure to the ADC. Ami, if we are able to show correlation and then drive that RPFS up, we think that's kind of the golden ticket, if you will. We could also not necessarily see a correlation, but yet see an RPFS in an all-comers population, which gives us encouragement. In fact, I think if you look at the PSMA PET imaging agents and the expression levels of PSMA that have been determined by the PSMA PET agents and the response to Pluvicto, there has been a correlation, but only, it seems like, in the top quartile of PSMA expression. Everybody who gets Pluvicto has had to undergo a PSMA PET imaging agent and a PET scan to determine if they are positive for PSMA, okay? That is a defined criteria in the label of Pluvicto. The PSMA PET imaging agent, so these come from companies like Lantheus and Telix. Those are the two market leaders. They generate a $1.5 billion just in revenue on the PSMA PET imaging agents. We believe that there could be an important commercial opportunity for our PET46 or our FG-3180 as well. Again, even if we don't show a correlation and if the FDA then requires patients, before they get our ADC, to undergo a PET scan after having been treated with FG-3180 or PET46, and if we run that same play, there could be a really important commercial opportunity for us as well with the PET agent. Have you engaged with the FDA on whether FG-3180 would be required as a companion diagnostic for the patients in the regulatory trial, in the registrational trial? Yeah, we do. I'm sorry, keep going. I didn't mean to cut you off. No, I think that was my question. Go ahead. Yeah. FG-3180 has its own IND, and so there is a separate development pathway for FG-3180, just as there is for FG-3246. Again, we would anticipate a parallel path, not only of clinical development, but a regulatory pathway as well of FG-3180, similar to FG-3246. Mm-hmm. This current ongoing study will help you determine what might be the cutoff for the CD46 expression level that you can incorporate in your future studies? That's exactly right. There will be a lot of analytics associated with trying to determine who is a non-expresser of CD46, a low or moderate or a high expresser. Dr. Aggarwal in his IST did have a few patients who had no expression of CD46. They didn't respond to the ADC. We're going to continue to further evaluate and characterize the expression levels across, as Dave pointed out, instead of just 25 patients like we've seen to date in the IST, another 75 patients. We'll have a substantial amount of data within the next probably 12 months or so. Mm-hmm. With regards to roxadustat, you are waiting for a final response and alignment with the FDA on the trial. Maybe help us think about how you're thinking about moving this forward, and of course, you have your ADC program that you need to continue to fund. What are some options that you're exploring with regards to roxadustat? You bet. Dave, why don't you take that one? Yeah, sure. Great question, Ami. As Thane stated earlier, when we closed the sale of FibroGen China, we were able to significantly recapitalize our balance sheet, and that really allowed us to fully fund the Phase II study for FG-3246. That brings our cash runway into 2028. However, if we were to take on the cost of the Phase III roxadustat trial ourselves, we would need to bring in some incremental funding to support that. Our cash runway into 2028 just contemplates funding the Phase II for FG-3246. Right now, as we think about roxadustat, we're going down a concurrent pathway where we can either think about bringing in some additional capital and funding the study ourselves or partnering it with a strategic that has a presence in hematology or hem-onc that would be a good fit for their portfolio. At this point in time, we are running a parallel process to see what would be best for shareholders and the way to bring this forward, to bring roxadustat and fund it into the Phase III, and that process is currently ongoing. We're looking at all options, and in the end of the day, we're going to do what's best for shareholders. I'll add to that. Thanks, Dave. That was well said. Ami, we will add to that we are doing these Phase III-enabling activities, so we're not waiting until this parallel process culminates. We are undertaking the enabling activities. We're at the tail end of the CRO selection process. We've procured all of the clinical supply for the Phase III trial. We're continuing to advance the protocol, and we'll be ready to respond to the FDA when we hear back, which we think will be, again, very shortly. The plan is to continuing to do these, what we would call low-cost, value-added opportunities before you have to start to spend the sizable amount of money. We think the cost of the trial will be in the $70 million range. That probably gives you an idea of the magnitude of the capital that we'd have to bring in. Yeah. Okay. All right. Well, those are all the questions I had. Thank you both for joining today, and thanks to all our listeners as well. Yeah, thanks for the opportunity. Thank you so much, Ami. I appreciate it. Thank you. Take care now. All right. Bye-bye.