Ladies and gentlemen, thank you for standing by. Welcome to Gracell Biotechnologies' third quarter 2023 conference call. At this time, all participants are in a listen-only mode. After opening remarks, we will open the call for questions. Instructions for queuing up will be given at that time. I will now turn the conference call over to Dr. Kevin Xie, Chief Financial Officer. Please go ahead. Good morning, and welcome to Gracell's third quarter 2023 corporate update conference call and webcast. With me today are Gracell's founder and Chief Executive Officer, Dr. William Cao, and our Chief Medical Officer, Dr. Wendy Li. We're excited to discuss the advancement of the trials underway with our CAR-T candidate on today's call. We're looking forward to sharing with you our recent business developments and upcoming objectives as we have six weeks remaining in 2023 and are looking forward to 2024. As a reminder, we'll conduct a question and answer session following our formal remarks. This morning, Gracell issued a press release announcing unaudited financial results for the third quarter ended September 30, 2023. We encourage everyone to read this press release and would like to remind you that this call is being recorded for replay. Please note that for certain information discussed on the call today, including financial data, clinical data, future plans of our program, Gracell's management will be making forward-looking statements. Actual results could differ materially from those stated or implied by those 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 SEC for a full disclosure of these risks and the factors. This conference call contains time-sensitive information that is accurate only as of the date of this live broadcast, November 13, 2023. 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, Kevin, and again, welcome everyone to today's call. I will begin with the key pipeline and corporate updates. I will then turn the call over to our CMO, Dr. Wendy Li, to provide insights into GC012F clinical data that were recently presented at the 20th International Myeloma Society, IMS, annual meeting. Next, our CFO, Dr. Kevin Xie, will discuss our third quarter 2023 financial results. After our prepared remarks, we will open the call to questions. The past few months have been exciting, both for Gracell and the CAR-T field at large. At Gracell, we have achieved several important milestones, including the initiation of patient dosing in our first company-sponsored U.S. trial, the presentation of the latest update of FasTCAR GC012F at the recent IMS meeting and upcoming American Society of Hematology annual meeting, the advancement of the investigator-initiated clinical study in systemic lupus erythematosus, SLE, and also release of preclinical data from our solid tumor program at a Society for Immunotherapy of Cancer, SITC, annual meeting. This period marks a crucial juncture for the CAR-T field. Some of the most significant hurdles faced by CAR-T in the treatment of blood cancers are being addressed by innovative next-generation CAR-T candidates. Aspirations such as rapid manufacturing, achieving a cleaner safety profile, and enabling deeper, more durable responses were shared by all CAR-T researchers and were also personal motivators for myself that led to the founding of Gracell. It was a journey with a vision to push the boundaries of what's possible in cancer treatment. The progress we have made is a testament to the entire Gracell's team's relentless pursuit of innovation. We are also finding ourselves at the forefront of a pivotal era in medical science, where the application of CAR-T therapy is expanding beyond hematological cancers. The unmet need in autoimmune diseases and solid tumors are massive. At Gracell, our approach is anchored in rigorous scientific research and commitment to innovation. I am pleased to see strides we have made in these disease areas, reflecting our dedication to addressing areas of high unmet need with cutting-edge solutions. Today, we will share some initial findings in our translational research on GC012F for the treatment of SLE. I look forward to sharing our ongoing progress and I remain confident that our journey will lead to meaningful advancement in the field. Now, I hope to provide a more detailed overview of what we have achieved in the third quarter. In September, we announced dosing our first patient in the U.S. phase Ib/II investigational new drug, IND study, evaluating our lead candidate, BCMA CD19 dual targeting FasTCAR, GC012F, in the treatment of relapsed refractory multiple myeloma, RRMM. One clinical site is currently recruiting patients, and we look forward to activating a handful additional sites in the U.S. in the coming months. As a reminder, the phase Ib portion is designed to evaluate safety and the tolerability of GC012F, as well as determine the recommended phase II dose. We anticipate enrolling approximately 12 patients across two dose levels in the phase Ib portion. We estimate that it will likely take approximately 9-10 months to complete patient enrollment. In China, we expect to commence patient enrollment this quarter in the phase I/II IND study in RRMM. The guidelines for clinical research on somatic cells trial, newly enacted in August, has impacted our timeline, but we are happy to report that we have now received all the required approvals and are ready to launch the study in China. In late September, at the IMS annual meeting, the updated clinical data was presented from the ongoing phase I IIT, evaluating GC012F as a frontline treatment for patients with transplant-eligible, high-risk, newly diagnosed multiple myeloma, NDMM. In this 19-patient data set, with a median follow-up of 15 months, 100% of patients achieved MRD-negative stringent complete response, MRD-negative sCR. Dr. Wendy Li will elaborate on the key findings in a few minutes. Longer-term follow-up data from this study, including additional patients, will be presented at the 65th ASH annual meeting in December. We are continuing to see compelling efficacy data and a safety profile and look forward to sharing more details in San Diego next month. To this date, we have reported clinical data of GC012F on 60 oncology patients in three IITs, including 51 patients with multiple myeloma and nine with diffuse large B-cell lymphoma. The consistent findings provide good evidence supporting our strong scientific rationale in leveraging the power of dual targeting and validating the superior qualities of FasTCAR. Also, the very favorable safety profile demonstrated in these studies, including no neurotoxicity observed in any of the 60 patients, could potentially provide a critical differentiation, early line settings and additional indications. We are very encouraged by the profile of GC012F and have high confidence that this therapy could bring profound benefits to the patients worldwide. In the second quarter of this year, we were thrilled to launch a new IIT evaluating in CD19, BCMA dual targeting GC012F in refractory SLE or RSLE. This new direction is inspired by the groundbreaking clinical discovery shared by Professor Georg Schett's group. We see immense opportunity here and believe twelve F is ideally positioned as a potential treatment for many autoimmune conditions, including SLE, combining its safety track record, CD19 BCMA dual targeting capability, and faster and consistent product delivery. In the field of autoimmune disease treatment, safety stands as a critical factor for defining success. As oncologists learn ways to better manage the adverse events, the safety of CAR-T has become less of a concern in cancer applications. However, we believe the focus on safety will be renewed when the industry seeks to potentially adopt CAR-T as a treatment for autoimmune conditions. Any successful therapy must demonstrate exceptional tolerability and safety profile. So far, GC012F has been used to treat 60 cancer patients, including those who are frail and battling advanced cancer. We have observed a consistent safety profile characterized by mostly low-grade cytokine release syndrome, CRS, and notably, no incidences of neurotoxicity to date. It is important to point out these encouraging results have been derived from the same compound currently being investigated in the IIT underway for SLE. This consistent track record of safety gives us confidence as we expand our studies to a new field, where the standards for safety are exceptionally high. On the efficacy side, the promise of CAR-T is to induce a complete immune reset.... where all the autoreactive cells are eliminated and newly generated cells are expected to be healthy. For B-cell-mediated diseases such as SLE, some were hoping to complete depletion of B-cells could reset immune system. Based on this theory, CD19 is considered a valid target for CAR-T, as it is expressed throughout the early and the mature stage of B-cell. However, we think it's important to remember, the SLE is a disease in which autoantibodies attack a patient's own tissues. So in addition to resetting B-cells, our view is that an effective therapy should also address the disease-causing autoantibody-secreting cells, or ASC. ASC populations could be CD19 positive or CD19- negative, and are BCMA- positive. So the use of CD19 single targeting CAR-T therapy alone may not be sufficient to eliminate all the autoantibody-producing cells in all patients. Therefore, we feel there is a strong scientific rationale to support targeting both BCMA and CD19, which aligns with GC012F design in order to provide a more effective and a long-lasting therapeutic approach for refractory SLE. In recent months, we have been working on preclinical and translational studies to support this rationale. Today, we are delighted to share some preliminary findings. First, we analyzed the samples from 4 initial patients treated with GC012F at 1 × 10^5 cells per kg dose. After the 3-month follow-up, we can see B-cells have been restored to naive phenotype in these 4 patients. This provides very encouraging early evidence that GC012F is inducing an immune reset. Secondly, we ran studies with bone marrow samples collected from our SLE IIT patients, and demonstrated that the CD19/BCMA dual targeting CAR-T showed a more efficient elimination of ASC compared to CD19 single targeting CAR-T. Taken together, we believe that our CD19/BCMA CAR-T addresses both B-cell and ASC, and is designed to achieve a deeper and a wider elimination of disease-causing B-cells, as well as plasma cells. You can find the details of these findings in our latest corporate presentation deck, and we look forward to sharing more at upcoming Cell Therapy for Autoimmunity Summit later this month. Lastly, on the manufacture side, we believe that GC012F is positioned favorably with overnight manufacturing and enhanced cell fitness, combined with our team's significant experience accumulated over the years. Although SLE is a chronic disease, faster CAR-T delivery is still highly meaningful for better clinical outcome. To ensure optimal CAR-T expansion in the patient body, patients typically need to stop SLE treatment before the apheresis and also during the wait for CAR-T production, except for the use of low-dose steroids. Fast and consistent delivery of CAR-T therapy would help to shorten this period of suboptimal disease control and greatly reduce the risk of disease flare-up and additional organ damage during the wait. In short, we believe GC012F is a highly differentiated candidate, backed by outstanding safety record, novel and strong scientific rationale, and fasT CAR technology, as well as supported by our team's extensive experience in manufacturing and optimizing the process. We eagerly anticipate advancing the clinical development of in autoimmune disease. Currently, the IIT evaluating GC012F in SLE continues to enroll patients. More than a handful of patients have been treated, and the goal is for patient enrollment to progress into double-digit range. We expect to release the first public readout from this ongoing IIT in the first half of 2024. We are currently on track to submit IND filings in the U.S. and China in 2023 for the planned phase 1 clinical trial. The U.S. submission will be the second IND for GC012F to be reviewed by the U.S. FDA and will be an important milestone as we continue to advance our efforts to provide innovative and effective treatment options to patients with autoimmune disease. Beyond the FasTCAR platform, we are also continuing to advance our SMART CAR-T technology for the treatment of solid tumors. At the SITC annual meeting in early November, we presented the preclinical data evaluating SMART CAR- T-cells in solid tumor models. SMART stands for Suppressive Molecule Activated and Rejuvenated T-cells, and our novel SMART CAR-T technology includes a proprietary switch receptor targeting the suppressive tumor microenvironment. The inhibitory TGF-beta signal is blocked and converted into a pro-T cell signal in CAR-T cells. Our studies have shown that SMART CAR-T cells are younger and more resistant to TGF-beta mediated apoptosis and exhaustion. Upon repeated challenges of tumor cells, SMART CAR-T cells showed more potent and durable tumor-specific lysis than the conventional CAR-T, both in vitro and in vivo, in the presence of TGF-beta. Especially in mouse models, SMART CAR-T exhibit better killing activities in tumor rechallenge studies and higher tumor burden studies compared with conventional CAR-T. Earlier, in fourth quarter, we initiated IIT in China to evaluate our SMART CAR-T candidate, GC506, in patients with Claudin 18.2 positive solid tumors. We decided to further streamline our pipeline during the first quarter by continuing our focus in devoting our resources on the programs that have been potential to be the best-in-class and address large unmet needs. We suspended China phase two trial evaluating GC007g for the treatment of B-cell acute lymphoblastic leukemia, or B-ALL, considering the limited commercial opportunity for this niche candidate. As a reminder, we have seen compelling data in the phase one study with GC007g, including 100% MRD negative CR/CRI among nine ALL patients. GC007g is HLA-matched, donor-derived allogeneic CAR-T, and does not leverage our FasTCAR and TruUCAR technology platform or SMART CAR-T module. The updated pipeline chart will be found in the corporate presentation posted to Gracell's IR website. We significantly strengthened our financial position in August 2023, as we completed a private placement transaction, raising $100 million upfront and up to $50 million in additional funds if the warrants are fully exercised within 24 months. With the support from the top-tier roster of institutional investors, this capital raise extend our cash runway into the second half of 2026, assuming the full exercise of warrants, and is intended to support us through critical upcoming milestones planned for the clinical development of GC012F in multiple myeloma and SLE. Now, I will hand the call over to our CMO, Dr. Wendy Li, to highlight updated data from the ongoing IIT in NDMM. Wendy, please go ahead. Thank you, William. As highlighted, we're continuing to amass clinical evidence supporting the tremendous potential of our lead candidate, BCMA CD19 dual targeting FasT CAR GC012F. In late September, at the IMS annual meeting, we presented long-term follow-up data from an ongoing phase 1 IIT evaluating GC012F in newly diagnosed multiple myeloma. These patients have not received any anti-myeloma therapy before they are enrolled to our study. All patients in this study had one or more high-risk features, of which 89% were classified as stage two or three based on the Revised International Staging System, and 63% extramedullary plasmacytoma. GC012F demonstrated a 100% ORR and a 100% MRD-negative stringent CR rate among the 19 transplant-eligible high-risk NDMM patients as of the data cutoff date of August 1, 2023. GC012F also continued to show a favorable safety profile, with around 70% patients not having CRS of any grade and no patients reporting neurotoxicity or ICANS. We think these data are highly compelling, suggesting a potentially ideal profile for the frontline application of CAR-T therapy, combining both deep response and high tolerability. In December, updated results from this ongoing study will be presented at the 65th ASH annual meeting. As highlighted in the abstract available on the ASH website, we plan to share updated data, including 22 patients with a favorable efficacy and safety profile consistent with prior data sets.... The ASH data set includes 3 additional patients that were not in the IMS data set, because those patients were not dosed or assessed when we first submitted the abstract to IMS. I will now hand the call over to our CFO, Dr. Kevin Xie. Kevin? Thank you, Wendy. Turning to our financial results for the third quarter ended September 30, 2023, I'd like to touch on a few financial trends. As of September 30, 2023, the company had RMB 1,707.9 million, or $234.1 million in cash and cash equivalents and short-term investments. We expect the cash use this year to be approximately $100 million, primarily to fund our R&D and the clinical programs in the U.S. and China. As announced in early August, we completed a private placement financing with $100 million raised upfront and up to an additional $50 million in the event that the warrants are fully exercised within 24 months after closing of the upfront purchase. With this, we have extended our cash runway significantly and now expect our cash position to be sufficient to cover our operational plan and R&D activities into the second half of 2026, if the warrants are fully exercised. For the three months that ended September 30, 2023, net loss attributable to ordinary shareholders were RMB 67.6 million or $9.3 million, compared to RMB 171.9 million for the corresponding prior year period. The decline in net loss is primarily a result of decrease in the fair value of warrant liabilities. The warrants issued in the August private placement are measured and recorded at fair value at the time of issuance. The fair value of the warrants decreased by RMB 39.9 million, or $5.5 million, as of September 30, 2023, and was recorded as a gain in the income statement. Research and the development expenses for the three months that ended September 30, 2023, were RMB 90.1 million, or $12.3 million, compared to RMB 133.4 million in the corresponding prior year period. The decrease was primarily due to the decreased spending on research, development, and the clinical trial as a result of timing of project spending and our strategic pipeline alignment. With that, I'd like to turn it back to the operator to open the session for your questions. Operator? At this time, if you would like to ask a question, please press star followed by the number one on your telephone keypad. If you would like to withdraw your question, again, press star one. Your first question comes from the line of Yigal Nochomovitz from Citi. Please go ahead. Yeah. Hi, William and team. Thank you for taking the question. You mentioned the antibody secreting cells in a certain population may be CD19- negative, which would be helpful with your dual construct. Could you provide a little more color on the percent of antibody secreting cells that may be CD19- negative? Yeah, it's widely reported, but the percentage of CD19- negative ASC in human, you know, we haven't found a very rounded report. But it is a fact that antibody-secreting cells are CD19- negative for sure, and BCMA- positive. If you need, we can send you a reference for that. Okay, that, that would be great. And then with the translational research you mentioned with the four patients, could you provide a little more quantification as to how much more B-cell antibody suppression you saw with the dual construct versus the CD19 CAR-T alone? The assay is ELISpot. So, basically, what it does is we take the PBMC of bone marrow cells from the patient prior to the treatment, after treatment, and we put these cells in the ELISpot device, and with our CAR- T. I mean, CAR- T is the treatment, with the CAR- T ex vivo, and see how many antibody-secreting spots that are formed. Based on that, the difference is the CD19 single CAR and the BCMA CD19 dual CAR, GC012F, it's tenfold. More than tenfold. Okay. Okay, got it. And then final question is: I was just curious, you mentioned, William, you've treated, I think, 60 myeloma patients so far with GC012F. Was there, were there any- No, 51 plus 9. 51 myeloma patients, 9 DLBCL patients. Okay. Yes. Thank you. So, amongst those, amongst those 60 in total, did any of those patients have an underlying autoimmune condition that may have improved with the treatment? We have not paid attention, we, you know, discovered the... Yeah, we, we don't notice that there are certain percentage of autoimmune patients. No, but sometimes it could have happened for liquid tumor. Okay. All right. Thank you very much. Sure. Your next question, your next question comes from the line of Ben Burnett from Stifel. Please go ahead. Hey, thank you very much. I also wanted to ask about the SLE study and some of the early signals you're seeing from the IIT cohorts. Encouraging to hear that B-cells are recovering by three months, but I guess could you talk about the degree of B-cell aplasia that you're seeing? Is this comparable to what you've seen in the oncology studies? Compare with Georg Schett studies? Comparable to what you've seen with 12F in your myeloma studies, just in terms of the amount of B-cell aplasia. I see. Yes. B-cell depletion is similar, although, you know, the SLE study is still needed to be further followed and evaluated. But what we're seeing is the declining curve is similar, and the recovery time or persistence of B-cell depletion, we need to have more time to make a conclusion. B-cell, naive B-cell recovery so far from these four patients looks very similar to other SLE studies. Does that answer your question? Yeah, that's great. Thank you very much. I also wanted to just ask about the newly diagnosed multiple myeloma study. The data you've had is interesting. We're looking forward to the ASH update, but I guess could you maybe frame for us what the regulatory path is or, or could be in the U.S. for this asset in newly diagnosed multiple myeloma? Like, what would constitute a pivotal study in this setting? It, you know, it's too early to give you that perspective. You know, how do we design the study for newly diagnosed and also pivotal studies? But I, you know, based on our understanding of what the regulatory agencies view toward kind of a post-progressive development of a CAR- T therapy to early lines, it's all about safety and of course, efficacy. And this product, I mean, so far, we're convinced it's very robustly safe across different indications, you know, late and early line of multiple myeloma and DLBCL, now SLE. I think, you know, given the data we collected and when we have 1b, RRMM study data, I think that will be the time we'll communicate it with U.S. FDA. By the time we shall have a detailed design, how do we approach the early line or the first line? But we are not excluding anything. We definitely will move forward in the early lines for sure. Okay, great. Thank you. You're welcome. Your next question comes from the line of Kelly Shi from Jefferies. Please go ahead. Hi, this is Dave on for Kelly Shi. Thanks for taking our question. So my question is on SLE. So maybe if you can set up a expectation, what type of data company is planning to release in first half of 2024, and related to that, what cell dose level you are studying? And can it shorten the dose level that you will be studying in U.S. trials similar to RRMM, or it will be dose escalation starting from the smallest dose? Thank you. Yeah. Yeah. We are dosing as more SLE patients, so we expect it's going to be double digits when we present the data first half of 2024. We expect majority of patients will have at least 3 months, and some of the patients will have 6 months evaluation. Now, the dose, we start with the dose very similar that we have treated RRMM patients or newly diagnosed patients, too. So, you know, I can't predict what's going to happen for dose level 3, but now we are dosing up, see what happens. And, based on what we see today, it's, it's very consistent. The PK and the CRS and the neurotoxicity, just preliminary, it seems very similar. We will move up to 300,000, which is still very low compared to others in the industry. And I don't expect to dose higher than 300,000, but we'll see. Right. ... Thank you. Your next question- Did I answer all your questions? Bye. Your next question comes from the line of Eric Schmidt from Cantor. Please go ahead. Thanks for taking my question and the added information. Also a question around the SLE translational data. William, did all four patients achieve deep B-cell aplasia or deep B-cell lymphodepletion with no detectable B-cells? B-cell aplasia after CAR-T therapy. That's what we can say. Your second half of question is, did we see B-cell aplasia after lymphodepletion? No. Okay. What was the duration? Most of it is not. Sorry. Okay. Thank you. What, what fludarabine dose are you using? It's very similar to Dr. Schett's group. Okay. And what was the duration of the- It's similar. It's similar to multiple myeloma regimen. The duration of the B-cell depletion was similar to what you've seen in myeloma? Oh, B-cell lymphodepletion is very similar. B-cell aplasia, at this moment, I mean, the longest we have seen so far is a couple of months of hope after CAR-T infusion. So to make a claim that how long the B-cell aplasia, I think it's still too early. The, I mean, complete recovery, I think it's, it needs more time. You know, I'm, you know... Right now, the declining of B-cells is very similar compared with multiple myelomas. But when are these patients comes back with a meaningful readout, I think we need a couple of months to see. And then, you know, I have to remind that these first four patients are low doses. It's a 1 × 10^5 per kilo, and now we're moving up to 2 × 10^5 and 3 × 10^5. Okay. We need to give them an opportunity. Thank you. I think you mentioned that you saw elimination of antibody-secreting cells. Did you also measure autoantibodies themselves and see elimination of autoantibodies? Oh, yeah. Yeah. I mean, in vivo, I mean, in human, we, we certainly measure as many types of autoantibody we can if those autoantibodies are high or were high prior to therapy, right? Now, what I mentioned is ELISpot is ex vivo study. So we measure typical, for example, double-stranded DNA antibody. You saw that- There are 20 autoantibodies to measure. It's yeah. For clinical, it's doable, but for preclinical, we wanna have a consistent system to compare. Sorry, I missed your second part. In the patient, the SLE patients with double-stranded DNA antibodies, you did see those decline? Yes. Although I do not want to give out any data related to efficacy. Yeah, but... Okay, that's it. Thank you very much. Thank you, Eric. Your next question comes from the line of Emily Bodnar from H.C. Wainwright. Please go ahead. Hi, good morning. Thanks for taking the question. There is an ASH abstract out, also on a dual CD19 BCMA CAR- T for SLE. I was curious if, if you've seen that and maybe if you can comment on some initial thoughts from there on the efficacy and safety side. And then if you could provide any guidance for timing on initial data for the Claudin 18.2 positive solid tumor study in China, and maybe if you'd also talk about the design there. Thanks. Yeah. Thanks for the question. I mean, it's still early for us to release or to share the data, especially efficacy. Safety, because, you know, as you know, you're going to see safety in the first 28 days. It's unlikely the typical CRS or neurotoxicity will happen after 15 days. So within 28 days, we are comfortable to you know to share, even though it's, again, I have to warn, this is early data. It's a first low dose, 1 × 10 to the fifth per kilo. It's about 66 million total CAR-T cells, 6 million. But it's very, very encouraging. I mean, we see all the signs of safety and efficacy. Now, a reasonable set of data readouts will be the first half year, 2024. By the time we'll have a double-digit patients and with at least three months, and hopefully, you know, half of them are six months follow-up. So that, that's what we shall expect. Sorry, I think maybe you misunderstood my question. I meant there was an abstract that was released to be presented at ASH from another CD19 BCMA CAR-T therapy for SLE. I was just curious if- Mm-hmm. ... seen that and what your thoughts were on what they present or what they showed in the abstract? Yeah, I saw that abstract that has been presented somewhere before. It is good to see another dual targeting CAR-T that is being applied to autoimmune disease. You know that, but every construct is different. We don't know the details of their construct, and we don't know much of about background, particularly the safety of the same compound, the same CAR-T for other indications, for example, oncology. But based on what we saw from the abstract, the data looks reasonable. I think, you know, when we compare with Dr. Schett's group, the patient background is different. I think everybody would agree that the patient that involved with this group tend to be younger, and the time from the diagnosis is short. And this abstract seems the patients are more diversified. The SLEDAI index seems it's I would say similar because there are more than I think 10 patients. So the mean is similar, median is similar. The age seems to be more diversified. And then some patients with active lupus nephritis may not be fully recovered, which is not surprising in our opinion, because when in the real world, when the patients are older and the time from the first diagnosis is much longer, and they're being treated more standard care, and it all depends on percentage of patients have active lupus nephritis, and that will, you know, give a different flavor of readouts. The last thing I want to remind, you know, everyone who is interested, you got to look into the product, the format of final product, whether it's a fresh CAR-T cells or it's a frozen. You know, as we all appreciate, if it's a frozen CAR-T cells, it's more robust in the real world for delivery, for shipping, and if anything happened to the patient right before the dosing, the cell can be stored in the proper conditions. If it's a fresh cell, it's going to be challenged. Okay, that's helpful. Thank you. And if you could just comment on the Claudin and 18.2 positive study and when we might see initial data there. Yeah, we just launched, so there is really not much to share. Yeah, I mean, any specific questions I would be happy to share with you. Okay. Got it. Thank you. You're welcome. Your next question comes from the line of Yannan Zhu from Wells Fargo Securities. Please go ahead. Great, thanks for the questions. I also have a question on the translational study for the SLE patient bone marrow ELISpot assay. I was wondering whether the inhibition that you saw in the assay was due to CD19- negative, BCMA- positive bone marrow cells, or could it be due to greater inhibition of the CD19 positive cells? And also, I was wondering, is it possible to quantify the percentage of CD19- negative, BCMA- positive cells, ASCs in a bone marrow, in these bone marrow samples? Thank you. Let me answer the first question. We do have a CD19 with the same sequence, same binder from the GC012F. So the single CAR-T, CD19 CAR-T, in comparison with the dual CAR-Ts, and so the comparison is very clear. If you know, the inhibition of CD19 positive cells by the dual CAR-T, you know, yeah, we can always suspect when a single CAR-T become a dual CAR-T, it might change certain characteristics. But at least from the single binding perspective, the dual targeting, in theory, should hit CD19 and BCMA. So the effect of what we see is more than additive. It's about 10 times. So either it's additive or synergistic, because of the dual targeting. We need to, you know, do more studies to illustrate that. But the observation is very clear that the dual targeting does inhibit autoantibody-secreting spots, significant. What was your second question? ... is it possible to quantify the percentage of CD19- negative BCMA- positive, positive ASCs in these samples? Good question. We are doing it. It varies a lot, from patient to patient, as you would, you know. So far we collected 4 patients, which is not easy to collect the bone marrow cells from those treated patients, but we need more data. Got it. And then, I was wondering if you have, you could provide any update on the partnership front, both regarding the myeloma perhaps as well as the new SLE initiative. Thank you. Yeah, we continue to engage the conversation with potential partners. There are partners interested in both oncology and immunology, and but there are particular partners only interested in immunology. That's all, as much as I can share. But yes, we are busy engaging conversations. Great. Thanks for the updates. Thank you. Your next question comes from the line of Joe Catanzaro from Piper Sandler. Please go ahead. Yeah. Hey, guys. Appreciate you taking my question. Great. Thanks for the updates. Maybe two for me. First one, William, I think I heard you say that you're going to have a presentation at the Cell Therapy for Autoimmune Disease Summit later this month. Just wondering maybe if you could elaborate a little bit on what you expect to present there. Will there be any more additional translational work from these first four patients that we might see there? And then my second question: I know it sounds like you continue to expect the U.S. myeloma study to complete enrollment in about 9-10 months. Just wanted to know if you have any updated thoughts around when you may have an initial data disclosure from that study. Thanks. Yeah. Regarding the translational studies, I think the data to be presented at the summit is going to be similar, you know, what I said. It's—I think it's about 10 days from now or less than 10 days, so I don't think you should expect significantly more information from our presentation. We are in 1B for our MM trial, and it's in U.S. We have to wait the EOP1, end of phase 1 report submitted to FDA and get consensus or discussion with them to for next phase. So, I don't believe that we can release, you know, data prior to that, but that's my understanding. But as far as for the study, it's ongoing. You know, so far, so good. Okay. Thank you. Thanks for taking my question. Thank you, Joe. Your next question comes from the line of Justin Zelin from BTIG. Please go ahead. Hi, thanks for taking the questions. So on the SLE data for the update, can you remind us what we should expect, obviously, safety and what we should expect from a clinical efficacy standpoint? Yeah, expect, meaning, predict. You know, so far, all I can say, so far, so good. And it takes time to have a meaningful efficacy data for safety because it comes in short, coming, you know, within 15 days, you pretty much see them all. Neurotox takes a couple more weeks, but so far, again, it's very... Our impression, all I can say, it's not really data. Our impression, it's very consistent what we've seen before. Yeah, I mean, as I answered on the question of the other caller, you know, next year you should expect double digits of patients. The readout on the double digit patients will be mostly at least 3 months, and some of them will be 6 months, which is more meaningful. And our patients are very diversified. I think it's a more - it's actually, it's the real world. The SLEDAI is, based on SLEDAI, it's the patients are having more severe SLE and that age older, and that's, you know, all I can say at this moment. Great. And maybe, William, if you could just give us an idea of what you would think an impactful durability would be for a CAR-T for SLE. I think that would be helpful. Yeah, I mean, that's an interesting question. It's just, I mean, this is a very difficult to answer. You know, it's, it's a balance between the length or the persistence of B-cell depletion, but in the meantime, you don't, you don't want them to be, you know, disappear for too long. You want the B-cell coming back with new phenotype, young phenotype, and we call it B-cell reset. And how long is it good enough to... I think, you know, our theory is we always see, in oncology side, we always see very deep B-cell depletion, and what's translating to readout is the MRD negativity. It's, it's always, you know, at the top 100. So we expect B-cell aplasia in immunology will be very deep as well. But how, how deep, I mean, how long, particularly? What is the persistence we want? We'll see. I mean, we are doing those escalation, and we'll evaluate, and then, of course, efficacy. Great. Thanks for taking my questions. We have no further questions in our queue at this time. I will now turn the call back over to Dr. William Cao for closing remarks. Thank you again to everyone for joining us on the call. We are focused on advancing our highly differentiated and most competitive candidates, including the FasTCAR GC012F. The U.S. IND trial in RRMM is now underway, and we look forward to submitting IND filings in the U.S. and China for the planned phase one clinical trial in RSLE this year. We remain committed to pushing the boundaries of medical innovation and improving patient outcomes through our transformative therapies. This concludes today's conference call. 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