Ladies and gentlemen, thank you for standing by. Welcome to the Gracell Biotechnologies clinical update conference call that is being held at the European Hematology Association 2022 hybrid congress. At this time, all participants are in a listen only mode. After opening remarks, we will open the call for your questions. Instructions for Q&A will be given at that time. I will now turn the conference call over to Rebecca Rodriguez, ICR Westwicke Investor Relations. Go ahead. Good morning, and welcome to Gracell's clinical update conference call and webcast. With me today are Gracell's Founder and Chief Executive Officer, Dr. William Cao. Chief Medical Officer, Dr. Martina Sersch, and Chief Financial Officer, Dr. Kevin Xie. The team is excited to discuss the clinical data from three investigator-initiated studies that were shared at European Hematology Association 2022 hybrid congress. After our formal remarks, we will conduct a question and answer session. Gracell presented three clinical updates over the past few days at ASCO and EHA 2022 annual meetings, and issued two press releases highlighting the data. We encourage everyone to read these press releases and would also like to remind you that this call is being recorded for replay. The team will be reviewing a clinical update presentation in conjunction with today's prepared remarks, and this presentation has been posted to the events and presentation page on Gracell's IR website. Please note that for certain information discussed on the call today, including data and future plans of our programs, Gracell's management will be making forward-looking statements. Actual results could differ materially from those stated or implied by these forward-looking statements as a result of various important factors, and please refer to the Risk Factors section of our latest 20-F filing with the SEC for a full disclosure of these risks and factors. This conference call contains time-sensitive information that is accurate only as of the date of this live broadcast, June 13th, 2022. Gracell undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this conference call, except as may be required by applicable securities law. I will now turn the call over to Gracell's CEO, Dr. William Cao. William? Thank you, Rebecca, and again, welcome everyone to our clinical update conference call. As shown on slide three, Gracell is dedicated to bringing game-changing cell therapies to cancer patients with high unmet medical needs. We have developed two proprietary technology platforms to address the key challenges faced by conventional CAR- T. Our FasTCAR platform enables next day manufacturing for autologous CAR- T. Our allogeneic TruUCAR platform is utilized in a novel strategy to address the rejection of CAR- T cells by a patient's body, a major challenge in developing safe and effective off-the-shelf CAR- T. Built upon these two platforms, we now have a rich pipelines, including five product candidates in clinical development with multiple clinical trials underway, including two IND approved trials and several investigator-initiated trials or IIT. In our opinion, there are three key factors that contribute to the potential development and commercial success of a CAR-T candidate such as GC012F. The three factors span safety, efficacy, and CMC, which is short for chemistry, manufacturing, and control. We believe that our first-in-class BCMA and CD19 dual-targeting autologous CAR-T candidate, GC012F, is highly competitive and differentiated across the three key metrics. First of all, on the CMC and the manufacturing front, GC012F is manufactured on a FasTCAR next-day manufacturing platform, which affords two key advantages. First, as shown from our preclinical data, GC012F cells are younger and less exhausted. Second, our next-day manufacturing process has the potential to reduce vein-to-vein time for patients to less than two weeks, and may eliminate the need for bridging therapy that both adds a few weeks delay and may impact CAR-T overall outcome and efficacy. In addition, GC012F showed a favorable safety profile in two indications. In our relapsed refractory multiple myeloma data sets, we have treated 29 patients so far and observed mostly Grade 0-2 CRS, and no immune effector cell associated neurotoxicity syndrome, ICANS, of any grade. To put this into context, BCMA targeted agents have seen in other studies around 15%-20% ICANS and neurotoxicity overall, including high-grade neurotoxicity. The safety advantage will be even more important as we potentially move towards treating earlier stage patients, especially in a frontline setting. Next, on efficacy front, GC012F continues to generate very compelling and highly competitive results in a hard-to-treat, predominantly high-risk population. We have been reporting very deep responses, with 75% MRD negative sCR rate and a 100% MRD negative rate in all patients treated. The original response is highly competitive when comparing to the high-risk subgroups from other studies. Dr. Sersch will elaborate on our latest data shortly in more details. We are very encouraged with data we have so far and are dedicated to continuing advancing our clinical pipeline. However, we look forward to opening our first U.S. study in the near future after our IND filing later this year. Now, I will hand the call over to our CMO, Dr. Martina Sersch, to discuss very compelling data in greater detail. Martina, please go ahead. Thank you, William. We are very excited to present to you today the clinical updates that have been shared with the scientific community during the past two weeks at ASCO and EHA 2022. We presented two oral abstract presentations for our lead candidate, GC012F, at both ASCO and EHA, and updated clinical data from 29 relapsed refractory multiple myeloma patients. At EHA, we have also presented the first initial data from an IIT in the second indication of GC012F in BNHL and updated clinical data from an ongoing IIT with CD19, CD7 dual-directed allogeneic CAR- T GC502 in B-ALL. The rationale for dual targeting CD19 and BCMA stems from the concept of potential antigen escape with BCMA-targeted therapy alone, as well as the findings that early myeloid progenitor cells express CD19 and targeting CD19 can eliminate those malignant cells, as shown in our pre-clinical data. This may lead to deeper responses as measured by MRD, minimal residual disease. This is important as deeper response, including a high rate of MRD negativity, is a concept well-established, leading to longer PFS and extended overall survival in multiple myeloma. The FasTCAR platform is the manufacturing platform positioned to tackle the unique challenges of CAR- T manufacturing, including, but not limited to faster vein-to-vein time based on the concept of concurrent transduction activation steps, as well as expansion in the patient's body, which leads to a significant time saving for the overall vein-to-vein time. In addition, the shorter manufacturing process has the potential to avoid bridging therapy, a therapy needed to bridge between CAR- T availability and apheresis. In some studies, over 75% of patients treated with conventional CAR- T therapies needed bridging therapy and has led to a few controversial discussions. Bridging therapy can introduce additional risk to patients and could potentially adversely impact the overall outcome of CAR- T therapy and, on the other hand, artificially inflate early overall response rate. Moreover, lengthy washout times are needed after a bridging therapy, which adds to the duration of vein-to-vein time. Our FasTCAR manufacturing platform enables 22- to 36-hour manufacturing, has the potential for significantly reducing the need for bridging therapy or even avoiding it altogether. The multi-center open label single arm investigator-initiated study enrolled 29 patients between October 2019 and January 2022 into three different dose levels of CAR- T cells from 1x10^5 to 3x 10^5 per kilogram body weight. The study now completed enrollment. We reported data at EHA 2022, with the most recent data cut-off of June 8, 2022. Due to COVID lockdown situation in Shanghai, China, some most recently enrolled patients are still undergoing first response evaluation, and their follow-up visits could just recently been rescheduled. Patients with a minimum of three prior lines of therapy that were either refractory to PIs and IMiDs or primary refractory patients after two lines of therapy were eligible for enrollment into the study. The primary endpoint was safety, and secondary endpoints included overall response rate, best overall response, minimal residual disease assessment at pre-specified time points, and PK/PD, among others. As shown on the baseline characteristic slide, it is important to point out that 90% of patients were evaluated as high-risk patients according to mSMART 3.0 criteria with 10% double hits and 28% extramedullary plasmacytomas. High-risk patients are hard-to-treat group of patients that are usually associated with poorer outcomes, including much shortened duration of response. Median prior lines of therapy was five, ranging from two to 11. 97% of patients were triple-exposed, with 93% IMiDs refractory and 93% PIs refractory. 34% of the patients had received an anti-CD38-targeted therapy, and 83% were refractory to their last therapy. As outlined on slide 10, 100% of the patients achieved a reduction in paraprotein, with most patients achieving a 100% reduction in paraprotein at time of data cutoff. Overall response rate at time of data cutoff of June 8 was 93.1%, with the best response achieved at data cutoff was 75.9% MRD negative stringent complete response. 86% of patients had achieved VGPR or better at time of assessment. Of note, most recently treated patients only had one month of efficacy follow-up based on the schedule of assessment. Median duration of follow-up was 11 months, ranging from 4.9-34.5 months. It is important to note that during the past five months of follow-up, due to the COVID-19 pandemic and the lockdown situation in Shanghai, China, not all patients could attend their scheduled follow-up visits to reassess depth of response at time points of two, three, or six months and beyond. Hence, the overall response that might have deepened could not only be assessed in some of the patients. Median duration of response at time of data cutoff was 15.7 months, with a confidence interval of 7.5-33.1 months. This is a very encouraging durability so far, considering the difficult to treat predominantly high-risk patient population treated on study. 100% of all assessable patients for minimal residual disease showed MRD negativity measured either by flow cytometry or EuroFlow. This is very meaningful as a deeper response, including MRD negativity, is a concept well-established, leading to longer progression-free survival and extended overall survival in multiple myeloma. There was no difference observed in dose levels, and 29 out of 29 patients had at least one MRD assessment post-infusion. As shown on slide 13, assessing MRD by EuroFlow, looking at landmark analysis at one month, six months, and 12 months post-infusion, showed that 18 patients had a one-month assessment, 13 were available at the six-month assessment, and eight patients had a 12-month assessment completed. At the 12-month assessment, 87.5% of the patients assessed by EuroFlow remained MRD negative. 20 out of 20 patients had at least one MRD assessment per EuroFlow post-infusion, and all patients treated on study achieved MRD negativity. On slide 14, as you can see, the safety profile is similar to previous findings and showed mostly low-grade CRS, with 14% of patients experiencing no CRS at all. 48% of patients experienced a Grade 1, and 31% experienced Grade 2 CRS. Only 7% of patients had a Grade 3 CRS, and we did not observe a Grade 4 or Grade 5 CRS on study. No ICANS or neurotoxicity were observed in any patient. Most common hematological adverse events were neutropenia, lymphopenia, leukopenia, and thrombocytopenia. No bleeding events were observed on study. Pharmacokinetics showed that GC012F expanded well in all patients at all dose levels and showed long persistence with a limit of detection at 30 copies per microgram DNA. Cmax was day 10, and median peak copy number was 96,438 copies per microgram DNA. As shown on slide 16, there was no difference observed between the dose levels for AUC, day zero to 28, with a median of 553,943 copies per microgram DNA in all 29 patients. AUC 0 to 28 mean values ranged from 331,920 to 758,989, with no difference observed between the three dose levels. As a conclusion, GC012F continues to show a favorable safety profile with mostly low-grade CRS, Grade 0-2, 93.1%, and no ICANS observed, including multiple patients experiencing no CRS at all. GC012F demonstrated a high overall response rate of 93.1% in a mostly high-risk population at date of data cut-off. Responses are still ongoing and being assessed for deepening over time. 75.9% of patients to date achieved CR or stringent CR. Patients are still being followed for response assessment for best overall response. In addition, most importantly, we saw a very high MRD negativity rate in all treated patients, 100%, with 20 patients out of 29 to date assessed by EuroFlow. EuroFlow assessment showed a 100% MRD negativity at a sensitivity level of 10 to the - 6, a sensitivity level on par with NGS assessment. Overall, GC012F dual targeting BCMA/CD19 showed very promising activity in relapsed or refractory multiple myeloma patients, including high-risk patients and heavily pretreated patients with prior exposure to anti-CD38 monoclonal antibodies, PIs, and IMiDs, with a median of five prior lines of therapy and being manufactured with next-day manufacturing, enabling faster turnaround and less bridging therapies used. Now I would like to switch gears and show additional data for FasTCAR GC012F in the second indication of BNHL. The concept of targeting CD19 in BNHL is well-established. However, antigen escape and progression are being observed by targeting CD19 alone. BCMA is expressed in a subset of cells in BNHL and could be an ideal target for providing deeper and potentially more durable responses in combination with a manageable safety profile that had been observed for GC012F in the lead indication of RRMM. Per the study design on Slide 20, the first-in-human data of GC012F in BNHL includes an enrollment target of nine to 18 patients to establish safety and preliminary efficacy in BNHL patients. To date, we have treated patients in three different dose levels. As of data cut-off of February 2022, three patients were enrolled and treated, with all patients being diagnosed as DLBCL, including patients with bulky disease, a particularly difficult-to-treat subpopulation of BNHL patients. As illustrated on Slide 22, all treated patients achieved a CR at the first assessment time point at month one, at time of data cut-off of February 2022. Patients one and two, who have been followed for more than three months, showed sustained CR at the three-month assessment. Looking at the tables on Slide 23, the safety profile of GC012F in BNHL was consistent with findings observed in relapsed refractory multiple myeloma patients with mostly low-grade CRS and mostly hematological toxicities. All were manageable with standard of care. As indicated, all patients treated expanded well in all three dose levels. As a conclusion, the first-in-human data of CD19 BCMA dual CAR- T for relapsed refractory BNHL demonstrated a very promising first response rate in DLBCL patients with CAR- T expansion observed in all patients. The early clinical data demonstrate a favorable safety profile, with Grade 1 CRS observed in patients in the lower dose group and one Grade 3 CRS observed in the higher dose group, which reverted to Grade 2 within two days. No Grade 4 or 5 CRS and no ICANS of any grade were observed in any dose level. We observed potent and fast activity with a 100% CR rate at one month in all three patients with relapsed refractory BNHL, including patients with bulky disease. The study continues enrolling patients. Last but not least, let's turn to TruUCAR GC502. As you may recall, the data had been previously presented at AACR 2022. The data now presented in the poster presentation at EHA features a slightly longer follow-up based on the abstract submission deadline. As illustrated on Slide 27, GC502 is our first dual-directed allogeneic CAR- T manufactured on the TruUCAR platform. The concept of dual-directed CAR- T targets the CD7 on patient T-cells in combination with TCR knockouts to allow adequate expansion, preventing host versus graft, as well as CD19 to target malignant cancer cells, in this case, B-ALL malignant cells. As per the study design shown on Slide 28, the study is enrolling patients with relapsed refractory B-ALL in three different dose levels to observe DLT, as well as preliminary efficacy over response rate and duration of response. To date, four patients have been enrolled in treatment on study, with all patients heavily pretreated with four prior lines of therapy, including CD19 and CD19/CD22-targeted CAR- T therapies. Three out of four patients achieved MRD-negative CR/CRi, with one out of four patients who only obtained a PR did proceed to ASCT stem cell transplant at day 39 post-treatment. However, unfortunately died due to complications post-transplant. Two different formulations were administered. Formulation A, two out of two patients observed Grade 3 CRS. Formulation B, two out of two patients, we observed Grade 2 CRS. GC502 showed robust expansion in three out of four patients, with one patient who achieved a partial response, not showing adequate expansion. GC502 showed manageable and reversible adverse events in two different dose levels and two different formulations with no ICANS or Grade 4 or Grade 5 CRS observed. In summary, early results of TruUCAR GC502 in patients with relapsed refractory B-ALL showed a very promising rate of month one MRD negative CR/CRi in combination with a manageable toxicity profile. The study is continuing enrolling patients. Gracell has made significant progress in delivering results on our pipeline assets in China, investigator-initiated studies, which are part of our overall strategy to de-risk the IND programs moving forward. We have a rich pipeline with currently two IND studies open and enrolling patients in China on top of our multiple IIT studies. Our registrational phase I-II study for our donor-derived CAR- T GC007g is ongoing and enrolling patients moving towards the goal of opening the phase II part of the study very soon. Now, I would like to turn it back over to William. Thank you. Thank you, Martina. Gracell has a significant track record of achieving clinical and regulatory milestones. During the first half of 2022, we have reported many exciting data, and we look forward to an equally prolific second half, including submitting our first U.S. IND and advancing our clinical and pre-clinical pipelines. With that, operator, please open the line for questions. Thank you. To ask a question, you will need to press star one on your telephone. To withdraw your question, press the pound key. Please stand by while we compile the Q&A roster. Our first question comes from Kelly Shi with Jefferies. Your line is open. Hi. Actually, thanks for presenting such a great data. This is Dave Wan from Jefferies instead of Kelly Shi. Just a couple of questions. One is for GC012F multiple myeloma IND, are you looking to add options for outpatient administration as well when you file the IND? Martina. Sure. It's better for you to answer. Yeah. Usually in a controlled study, when you basically kick off your IND study, that would not be something you would be doing for the filing, right? However, it all depends if it's feasible, pending on the safety profile. Now, looking at our excellent safety profile with mostly low-grade CRS, some patients even experienced no grade CRS at all, I think there is definitely an opportunity to administer in an outpatient setting. Okay, great. One more thing for NHL cohort. I'm just thinking too, for as a fast-to-market strategy, are you thinking of trial in post-CD19 CAR as a first indication before going into early line? Is this for BNHL, the question, right? Yes. Yeah. Yeah. We think we are highly competitive. With our dual targeting strategy, including our excellent safety profile, we wouldn't not wanna position ourselves post another CAR- T therapy. Now, in BNHL, however, CAR- T therapies are moving into earlier lines. Now, the question is, could we position or could we treat patients who have been pre-exposed to CD19? We would definitely include those patients into our study. With our dual targeting strategy, even, you know, considering certain relapse, we would need to have CD19 BCMA positivity, mostly the CD19 to treat BNHL patients. Relapse is not always caused by antigen loss. Some patients relapse CD19 positive. To answer your question, we would not, in general, consider positioning ourselves post such CAR- T therapy, but we would also not necessarily exclude those patients if they want to be enrolled in our study. Okay. Got it. Thank you. Our next question comes from Louis e Chen with Cantor. Your line is open. Hi. Thanks for taking my questions. I had a few for you here. First one I wanted to ask you is, have you scheduled a pre-IND meeting with the FDA? What are the gating factors to filing that IND? Did you say that you're gonna actually start U.S. trials this year? If you do, when do you think we'll actually see some U.S. data? The last question I have for you is if you could speak to the durability of GC012F. Thank you. Those are pretty big questions. Martina, why don't you pick first? Yeah, thank you. First of all, we will use all the basic help that FDA provides, and that includes having a pre-IND meeting. That's a very critical step in any IND filing because FDA can provide guidance and also provide feedback on the strategy for any company. Now, secondly, we are planning, everything is going very smoothly with our all the steps that we need to conclude to file the IND. Currently, the Lonza tech transfer is ongoing. All the data are being collected with the target of filing the IND in the second half of 2022. The U.S. study is going to be started as soon as possible after the IND is accepted. That usually takes at least three months post-IND acceptance because that is the gateway for getting additional approval at the different sites. Now to your other part of the question, when can we expect to see U.S. data? Now, pending enrollment and pending the endpoint confirmation and how long that endpoint would have to be measured, we can expect to see data internally probably as early as 2023. However, for external, since this may be a pivotal study, depending what FDA is going to approve in the end, that data will not be made public until the BLA filings and all those activities are considered to be final. So for external, seeing data, would be as early as 2024, but that all is pending, obviously, what type of study FDA is going to grant us and what type of study we then can start. Last question was durability question, I believe, correct? Correct. Yeah. The durability of 15.7 months is highly competitive considering that we are treating high-risk patients. I wanna remind the audience here that high-risk patients are a very different type of patient population as opposed to standard risk. In any study who basically enrich their patient population like we did for over 90% for high-risk patients will see a difference in median duration of response. However, also important to consider here that there is a range. Now, as you can see in our data, the confidence interval is as high as 33 months. The true duration of response could be much longer than the 15.7 months. In addition, we have treated more patients just very recently. Now those patients are being followed, and those patients' assessment will also impact the median duration of response. Those patients now have been followed some for six months or less, and some of those patients could not get a follow-up assessment due to the COVID situation in Shanghai, China. That assessment point is missing currently, also for the overall response rate. Did that answer your question? Yes, it does. Thank you very much. Sure. Thank you. Our next question comes from Joe Catanzaro with Piper Sandler. Your line is open. Hi. This is Sam on for Joe. Just a couple of quick questions from us. How are you thinking of enrolling the relapsed multiple myeloma patients in the U.S. given the crowded BCMA market? Would you focus on this high-risk and mSMART CRi population, or do you intend to target like an all-comer population? Very good question, obviously. Martina? Yeah. Thank you. Yeah, great question. We will be going for all-comers, and we are already in contact with multiple sites. I can, I can say that everyone is very excited. And the reason for that is that we have an excellent advantage that no one else has, and that is our fast manufacturing in 22-36 hours. That brings so many advantages and empowers the treating physician to treat the patient much faster than with any other CAR- T therapy out there. Having said that, obviously also the dual targeting has significant advantages. And last but not least, our current safety profile is highly differentiated from all the other CAR- T therapies. Now, there is competition out there. You know, there's many studies ongoing. What we've been hearing is that a CAR- T study, especially with the data we have been presenting, is very encouraging, and we should not worry about enrollment. That is what I've been hearing over the past two months. We are very enthusiastic starting the study. Perfect. Thank you. Just a quick follow-up. Have you reported what the vein to vein time was in this population, and would you expect it to be similar between China and the U.S.? The vein-to-vein time is the concept that is complex by itself. I wanna point out again, our manufacturing time is significantly shortened from all the other CAR- T therapies because we do concurrent transduction, and the expansion is not ex vivo, it is basically happening in the patient. Now, what's also very important here, the vein-to-vein time is something decided by the PI, and it is based on a couple of factors, including how long he has to wait for the therapy. If it's longer than, let's say, two weeks, three weeks, and the patient progresses fast, he has no chance with, you know, treating physician to apply bridging therapy. With the new data coming out showing that bridging therapy can adversely impact CAR- T outcome as well as kind of taints the picture of the outcome of the overall study, it will be something that we definitely wanna avoid in our study in the United States. The vein-to-vein time could be as short, depending on release and everything else, as 11 days. Now, we definitely gonna try to have the shortest vein-to-vein time possible given all these, you know, evidence and facts that speak for themselves. Thank you for taking our question. Thank you. As a reminder, to ask a question at this time, please press star then one on your touchtone telephone. Our next question comes from Justin Zelin with BTIG. Your line is open. Hi. Hi, team. Thanks for taking the questions, and congrats on these data. Martina, the very high MRD negativity rate for GC012F is quite striking. Could you speak to your thoughts on how the MRD negativity will translate to durability responses? Yeah. Thank you. Great question. You hit the nail on the head, right? MRD was actually the topic at ASCO and EHA. The community all agrees that MRD will be the future decision-maker for treatment choices as well. Now, we have the striking 100% MRD negativity rates in actually all the patients that we treated. They were assessed, and they were MRD negative. Now, we even have a very high sensitivity level of MRD negativity to 10 to the -6, which is higher than most reported. They only report 10 to the -5. Now, achieving MRD and maintaining MRD is a very critical part of success in even providing potentially functional cure in multiple myeloma. Our follow-up assessments to show that MRD can be sustained over 12 months and even longer is a predictor of preferential outcome in regards to progression-free survival and overall survival. Some even say, for example, if you have landmark at 12 months and a patient can sustain it at 24 months, the risk of relapse is substantially decreased. All of that encourages us even more for our dual targeting approach, and in addition, the additional fast path with the fast manufacturing to believe that we have a one-of-a-kind, the highly competitive autologous CAR- T therapy here. Great. That makes a lot of sense to me. I did notice that there were two patients that had they were not included in the overall response rate that had maybe a partial response, but they were MRD negative. Do you expect those patients could have a deepening in their response as time goes on in subsequent assessments? Absolutely. The way response works so far in multiple myeloma, and I believe that will be changing, was IMWG overall response rate, which measures protein in urine and blood. That protein has a half-life. That is why you seem to see deepening of responses. In fact, the response is already there. We just need to clean and clear all the protein in the body. MRD negativity is a really good indicator to see that patient already cleared the tumor out of the bone marrow. Now, we expect that to display later, but also obviously in the overall response assessment. We've been seeing that a lot in the patients we've treated. That's why it's really important to follow the patients and assess them in addition to see that deepening of response, hopefully at the next time point, even a stringent complete response. Excellent. Maybe just the last one from me is during the ASCO presentation. I believe a presenter noted that typically the vein-to-vein time was about two weeks. I just wanted to see if we could confirm that. I know it obviously differs between PI to PI, but just wanted to hear your thoughts there. Thank you. Since it's a POC study, and you may appreciate that study started in 2019 when, you know, it was a new dual targeting approach. No one had ever done this before. The reason actually why the vein-to-vein time may have not been 11 days, for example, is multifold. One could be longer release criteria, but the second was also the PIs would be very cautious. They have a new drug in their hands. They may wanna debulk the tumor first, also in consideration of potential CRS. Giving bridging therapy in some of these patients will artificially inflate the vein-to-vein time because now you have to treat the patient with bridging therapy, then you have the washout period of two weeks, and suddenly you are at, you know, three weeks perhaps, while you could have treated the patient much sooner. The really important part here is the release time. Also, again, I want to stress that factor. Our manufacturing time remains always 22-36 hours. That advantage cannot be taken away and no one can do this. We are the only one. It's really we empower the physician now to make the better decision for some patients, to treat the patient and avoid bridging therapy, which adds additional, you know, toxicity perhaps, and could also impact CAR- T outcome adversely. Thanks for taking all my questions. Thank you. As a reminder, a t this time, please press Star then one on your touchtone telephone. Our next question comes from Nick Abbott with Wells Fargo. Your line is open. Oh, good afternoon. Thanks for taking my questions. The first one, Martina, just on definition for loss of response. Is that an MRD, loss of MRD, or is it a more traditional measure? A patient progressing is not measured per definition in MRD. Treatment choices could start to happen when you see a patient turning MRD positive. That happens, right? That MRD positivity could then turn back into MRD negativity, by the way, which shows if you have a potent CAR- T that's still working. That's a very interesting concept, right? You still have an active drug, which is amazing. A patient progressing is based on overall response rate, and that is the M-protein that you measure in blood and urine. If you have BM lesions, it could be that the BM lesion, for example, didn't respond to target lesion or the BM lesion starts growing again. Just to be clear, your median duration of response, then this is based on reappearance of M protein or progressing like extramedullary lesion, for example. Exactly, yes. Just so I'm clear here, so we've got a median duration of response. Do we assume then that at least 15 patients have progressed? It's a little bit more complicated because nine patients have just been recently treated. Those patients are not really contributing to the median duration of response because their assessments are still ongoing and it's very early on. Our data set is more complex because we enroll patients over such a long period of time, and we continue to report on that data, and that kind of distorts a little bit that picture as opposed to one study, you finish enrollment, you finish looking at the endpoints, and then you have basically all the data in to calculate median duration of response. We can't really. Right. Calculate it on all patients yet. Right. Right. Right. Now, we consider all the patients, and that's why we believe, you know, this may change. The confidence interval, you saw that too, right? It's up to 33 months. The true median duration could be as long as 33 months. Right. That's what I'm trying to get to. Is this being influenced by, you know, early failures versus a more of a representative? Like, should we expect median duration response to stay around this level or? Because it, as you say, it's easy to do the math and, you know, if the next group of patients progress very quickly, unfortunately, then median duration response is gonna go down. But if at the moment it's being overly influenced by patients that for whatever reason are not doing as well on treatment, then it could go up as the better patients stay on treatment. That's what I'm trying to get. How many patients is this based on this median? We calculated it on all the patients. The patients we have on study who have not progressed would not, you know, and the patients who- Yeah. Have progressed so far. Every single patient we treated, the 29 patients were included. What can happen though now, because some of the longer the patients who have been followed for almost three years, we couldn't get their assessment in. They were considered having progressed, which then adversely impacts the median duration of response because now you calculate it as if they had progressed. We don't know. They could still be happy living, which we believe, by the way, because usually if they don't come back to the hospital, they are doing well. If they have a problem, we know it because then they came back to the hospital. Now we are trying to get all those, you know, assessments in, especially for those very long responders, which we have. Which again, I want to stress the fact that these are high-risk patients, cannot be compared with an overall normal, you know, risk patient population or even a patient population where only 20% of the patients are high risk. As I know, a lot of, you know, we always want to compare, but these 15.7 months are onward in high-risk patients. You can even look at the subgroup analysis of some of the other data sets. They have lower values, actually. Just so I'm clear, Martina, with 29 patients, to define a median, you have to have at least 15 progressions, progression events. Whether they're real progression or not, you know, that's what it's based on. It's a Kaplan-Meier distribution. It's not that you have to have half your events must have happened to be able to calculate it. Okay, it's more of a I get it now. Then- Yeah. If you didn't- Plus the distribution than half of the patients progressed, and now you can calculate, if that makes sense. Yeah. Okay. It's not logical. You didn't report a median PFS, but presumably, given 100% response rate, it's gonna be similar to DOR. The study is not powered for median progression-free survival. That is, by the way, true. Okay. For many of the other studies. That is why you only see the percentage of patients who did not progress at a certain time point. You see the 12 months, you see the 18 months, something like that, right? You can do that for bigger sample sizes, but this 29 patients is still a very small sample size. We definitely Sure. We're gonna look at that in our future study in the United States. Okay. Just this last one. Progression, is it coincident with loss of GC012 F or antigen escape? That question is one of the biggest questions, right? Why do patients progress on CAR- T therapy? I believe Johnson looked into this, you know, I'm sure BMS looked into this. It's not always necessarily an antigen loss. That is why we also believe we could potentially treat patients who relapse after CAR- T therapy, which is not where we wanna go. I responded to the question earlier, right? We believe with the dual targeting, we have that potential that we could treat those patients, and they will respond again. Because BCMA is so uniquely and widely expressed in plasma cells, and on top of that, we have the CD19 component here as well. You could retreat your own patients. You might not wanna retreat somebody who's seen a different product, but are you considering adding retreatment into your, you know, your protocols under your IND? From a physician perspective, you would not necessarily wanna retreat with the same drug. That they don't like to do that, even if you have convincing data that you could. They like to change, whatever, you know, if it's a different CAR- T or if it's a different antigen. I don't think that's gonna be something that would be necessarily viable. I don't think so. Okay. Fair enough. Thank you very much. You're welcome. Thank you, Nick. Thanks. Thank you. I'm showing no further questions at this time. I'd like to turn the call back over to Dr. William Cao for closing remarks. Thank you again, everyone, for joining us on the call. We are very excited about the data from our two lead programs in three indications that were recently presented at ASCO and EHA. I hope to take this opportunity to thank our team, PIs, and also the trust from patients. In summary, Gracell is well-positioned to deliver breakthrough CAR- T-cell therapies capable of overcoming major industry challenges by leveraging our proprietary FasTCAR and TruUCAR technology platform. We look forward to further advancing our clinical programs, and we'll keep everyone updated along the way. Thank you. Ladies and gentlemen, this concludes today's presentation. Thank you once again for your participation. You may now disconnect.