Gracell Biotechnologies Inc.

Ladies and gentlemen, thank you for standing by. Welcome to Grace Albiotechnology's 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 Shea, Chief Financial Officer. Please go ahead.

Good morning, and welcome to Gristel's third quarter 2023 corporate update conference call and webcast. With me today are Gristel's founder and chief executive officer, Dr. William Tao, and our chief medical officer, Dr. Wendy Li. We're excited to discuss the advancement of the trials underway with our CAR-T candidates 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, Grisel issued a price release announcing unaudited financial results for the third quarter ended September 30, 2023. We encourage everyone to read this price 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, resource management will be making forward-looking statements. Actual results should 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 20F filing with SEC for a full disclosure of this risk 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. Green Cell 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 Green Cell CEO, Dr. William Tao.

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 Lee, 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 Schiff. we'll discuss our third quarter 2023 financial results.

After our prepared remarks, we will open the call to questions.

The past few months has been exciting, both for Gracell and the Clark ECOs 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 FASCA 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 the Society of Immunotherapy of Cancer annual meeting. This period marked 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-P researchers and were also personal motivators for myself that led to the funding of Gray Cell. 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 Gray Cell 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 chronic therapy is expanding beyond hematological cancers. The unmet need in autoimmune diseases and solid tumors are massive. At Gray Cell, 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'll 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 of first patient in the U.S. Phase 1B-2 Investigational New Drug IND Study, evaluating our lead candidate, BCMA-CD19 dual-targeting FASCAR 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 1b portion is designed to evaluate safety and the tolerability of GC012F, as well as determine the recommended Phase 2 dose. We anticipate enrolling approximately 12 patients across two dose levels in the Phase 1b portion. We estimate that it will likely take approximately nine to 10 months to complete patient enrollment. In China, we expect to commence patient enrollment this quarter in the Phase 1-2 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 Evaluation GC012F 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 minimum residual disease, negative, stringent, complete response, MRD negative, SCR. Dr. Wendley 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 FAST-CAR-T cells. 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 in 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 RIT-evaluating E19 BCMA dual-targeting GC012F in refractory SLE, or RSLE. This new direction is inspired by the groundbreaking clinical discovery shared by Professor George Schett's group. We see immense opportunity here and believe 12F 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 today. It is important to point out these encouraging results have been derived from the same compounds currently being investigated in the IIT under way 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 systems. Based on this theory, CG19 is considered a valid target for CAR-T, as it is expressed throughout the early and mature stage of B-cell. However, we think it's important to remember that 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 clotting 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 four initial patients treated with GC012F at one time 10 to 5 cells per kilo dose. After the three months follow-up, we can see B cells have been restored to naive phenotypes in these four patients. This provides very encouraging early evidence that GC012F is inducing an immune reset. Secondly, we run studies with bone marrow samples collected from our SLE-RIT patients and demonstrate that the CD19-B-SMA 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 Autoimmune Disease Summit later this month. Lastly, on the manufacturer 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, Fast CAR-T delivery is still highly meaningful for better clinical outcomes. To ensure optimal CAR-T expansion in the patient body, patients typically need to stop SLE treatment before the aphoresis 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 12F is a highly differentiated candidate backed by outstanding safety records, novel and strong scientific rationale, and fast car key technology, as well as supported by our team's extensive experience in manufacturing and optimizing the process. We eagerly anticipate advancing the clinical development in autoimmune diseases. 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 R&D filings in the US and China in 2023 for the planned phase one clinical trial. The US submission will be the second R&D for GC012F to be reviewed by the US 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 five-car platform, we also continue to advance our smart car technology for the treatment of solid tumors. At the city annual meeting in early November, we presented the preclinical data evaluating smart car T cells in solid tumor models. stands for Suppressive Molecule-Actuated and Rejuvenated T-Cells. And our novel Smart CAR-T technology includes a proprietary switch receptor targeting the suppressive tumor microenvironment in which the inhibitory TGA 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 exhibits better killing activities in tumor re-challenge studies and higher tumor burden studies compared with conventional CAR-T. Earlier in fourth quarter, we initiated an IIT in China to evaluate our smart CAR-T candidates, GC506, in patients with collagen 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 II trial evaluating GC007G for the treatment of B-cell acute lymphoblastic leukemia, or BALL. Considering the limited commercial opportunity for this niche candidate, As a reminder, we have seen compelling data in the Phase I study with GC007G, including a 100% MID-CR-CRI among 9 DLL patients. GC007G is HLA-matched donor-derived allogenetic CAR-T and does not leverage our fast CAR and 2U CAR-T technology platform or smart CAR-T module. The updated pipeline chart will be found in the corporate presentation posted to Grayscale'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 internet institutional investors. This capital raise extends 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. I will hand the call over to our CMO, Dr. Wendy Li, to highlight updated data from the ongoing RIT 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, sewer targeting FOSCAR-T-GC012F. In late September at the IMS Annual Meeting, we presented long-term follow-up data from an ongoing Phase I IIT evaluating TC012F in newly diagnosed multiple myeloma. These patients have not received any antibioloma therapy before they are enrolled to our study. And all patients in this study had one or more high-risk features, of which 89% were classified as stage 2 or 3 based on the reverse international staging system, and 63% after medullary plasma cytoma. EC012F demonstrated a 100% ORR and a 100% MRD-negative and CR rate among the 19 transplant eligible high-risk NBMM patients as of the data cutoff date of August 1st, 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 this 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 the favorable efficacy and safety profile, consistent with prior data sets. The ASH data sets includes three additional patients that were not in the IMS dataset 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 Hsieh. Kevin?

Thank you, Wendy. Turning to our financial results for the third quarter ending 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 for U.S. dollar $234.1 million in cash and the cash equivalent 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 risk upfront and up to 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 ended September 30, 2023, Net loss attributable to ordinary shareholders were RMB 67.6 million or US dollar 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 warrant issued in the August private placements are measured and recorded as fair value at the time of issuance. The fair value of the words decreased by RMB 39.9 million or U.S. dollar 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 ended September 30, 2023, or RMB, 90.1 million, or U.S. dollar, 12.3 million, compared to RMB, 133.4 million in the corresponding four-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 question. Operator?

At this time, if you would like to ask a question, please press star followed by the number one on your telephone keypad. And if you would like to withdraw your question, again, press star one. Your first question comes from the line of Yigal Nachumovitz from Citi. Please go ahead.

Yeah, hi, William and team. Thank you for taking the questions. 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 humans is You know, we haven't found a very rounded report, but it is a fact that there are antibiotic screening cells that are CD19 negative for sure and BCMA positive.

If you need, we can send you a reference for that.

Okay, 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 at its spot.

So basically what it does is we take the PBMC bone marrow cells from the patient prior to the treatment. of the treatment. And we put these cells in the helispot device with our CAR-T. I mean, CAR-T is the treatment with the CAR-T ex vivo and see how many antibodies secreting spots that are formed. Based on that, the difference is you see the 19 single CAR

BCME-C19 dual-card, GC012F, is 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 012. No, 51 plus 9. 51 myeloma patients, 9 DL-BCL patients. Okay, yes, thank you. So 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 discovered we don't notice that there are a certain percentage of autoimmune patients. but sometime it could have happened for liquid tumors. Okay. All right. Thank you very much.

Your next question comes from the line of Ben Burnett from Stiefel. Please go ahead.

Hey, thank you very much. I also wanted to ask about the SLE study, some of the early signals you're seeing from the IIT cohorts. I encourage you to hear that B cells are recovering by three months. But I guess, can you talk about the degree of B cell aplasia that you're seeing?

Is this comparable to what you've seen in the ecology studies? Compare with George Shep's studies?

Comparable to what you've seen with 12F in your myeloma studies, just in terms of the amount of B cell aplasia. Yes.

B cell is different. Depletion is similar, although the SLE study still needs to be further followed and evaluated. But what we're seeing is the declining curve is similar. And every time, or persistent, we saw 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 studies. 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 could be in the U.S. for this asset in newly diagnosed multiple myeloma? What would constitute a pivotal study in this setting?

It's too early to give you that perspective. How do we design the study for newly diagnosed and also pivotal studies? But, you know, based on our understanding of what the regulatory agencies view toward kind of a 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 indication, you know, late and early line multiple myeloma and DLBCL. Now, SLE. I think, you know, given the data we collected and when we have 1B RMM study data, I think that will be the time we'll communicate with US 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 in 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 an expectation, what type of data are companies planning to release in the 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.

We are dosing more SLE patients, so we expect it's going to be double digits when we presented data first half of 2024. We expect majority of patients will have at least three months and some of the patients will have six months evaluation. Now the dose, we start with the dose very similar that we have treated RMM patients or newly diagnosed patients too. you know, I can't predict what's going to happen with dose level three, but now we're dosing up, see what happens. And based on what we see today, it's very consistent.

The PK and the CIS and the neurotoxin, just preliminary, it seems very similar. So we'll move up to

three times 10 to fifth, which is still very low compared to the others in the industry.

And I don't expect those higher than three times 10 to fifth, but we'll see. Thank you.

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 the question is,

Did we see a pleasure of the lymphodepletion? No. Okay, and what was the duration? Most of them not, sorry. Okay, thank you. What Flucidose are you using? It's very similar to Dr. Scher's group. Okay, and what was the duration of the? It's similar. similar to multiple myeloma regime.

The duration of the B-cell depletion was similar to what you've seen in myeloma?

B-cell, lymphodepletion is very similar. B-cell, aplasia, at this moment, I mean, the longest we have seen so far is a couple months of whole after cartilage infusion. So to make a claim that how long a B-cell pleasure, I think it's still too early. I mean, complete the recovery. I think it needs more time. 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 months

to see. And then I have to remind that these first four patients are low doses.

It's one time 10 to fifth per kilo.

And now we're moving up to two times 10 to fifth and three times 10 to fifth. So 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 certainly measure as many types of autoantibody we can if those autoantibodies are high or were high prior to therapy. Now, what I mentioned is ELISPOT is ex vivo study. So we measure typical

For example, double-stranded DNA antibody. And you saw that? There are 20 autoantibodies to measure.

For clinical, it's doable. For preclinical, we want to have a consistent system to compare. Sorry, I missed the second part.

So in the patients, the SLE patients with double-stranded DNA antibodies, you did see those decline?

Although I do not want to give out any data related to advocacy. Okay, that's it. Thank you very much. Thank you, Eric.

Your next question comes from the line of Emily Bogner from HC Wainwright. Please go ahead.

Hi, good morning. Thanks for taking the question. There is an ASH abstract out also on a dual CD19 BCMA core T for SLE. I was curious 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 Quadin 18.2 positive solid tumor study in China. And maybe if you could 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 as you know, you're going to see safety in the first 28 days. It's unlikely the typical CIS or neurotoxin will happen after 15 days. So within 28 days, we are comfortable to to share, even though it's, again, I have to warn, this is early data. It's the first low dose, one time 10 to 5 per kilo. It's about $6 million total CAR T cells, $6 million. But it's very, very encouraging. We see all the signs of safety and efficacy. Now, a reasonable set of data readout will be the first half year 2024. By the time we'll have a double-digit patient with at least three months and hopefully half of them at six months follow up.

So that's what we shall expect.

Sorry, I think maybe you misunderstood my question. 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 you've 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 therapy that is being applied to autoimmune disease. But every construct is different. We don't know the details of their construct, and we don't know much about background, particularly the safety of the same compound, the same CAR-T, or other indication, 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. Shett's group, the patient background is different. I think everybody would agree that the patient involved in this group tend to be younger, and the time from the diagnosis is short. And this abstract seems the patient's more diversified. The Selendi index seems, I would say, similar because there are more than, I think, 10 patients. So the mean is similar, medium is similar. The age seems more diversified. And then some patients with active locus nephritis may not be fully recovered which is not a surprise in our opinion, because in the real world, when a patient is older and the time from the first diagnosis is much longer and they're being treated in more standard of care, and it depends on the percentage of patients who have active lupus nephritis, and that will give a different flavor of readout. And the last thing I wanna remind everyone who is interested, you gotta look into the product, the format of final product, whether it's a fresh CAR T-cells or it's a frozen. As we all appreciate, if it's a frozen CAR T-cells, it is more robust in the real world for delivery, for shipping, and if anything happened to the patient, right before the dosing, that can be stored in the proper conditions.

If it's a fresh store, it's going to be changed.

OK, that's helpful. Thank you.

And if you could just comment on the quadrant 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, any specific questions, I would be happy to share with you.

Thank you.

You're welcome.

Your next question comes from the line of Yanan 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 early spot 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, would you... Is it possible to quantify the percentage of CD19 negative BCMA positive cell ASCs 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 GC012 bag. So the single car, CD19 car, in comparison with the dual cars. And so the comparison is very clear. If, you know, the inhibition of CD19 positive cells by the dual car, you know, yeah, we can always suspect when a single car become a dual car, 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 that 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 do more studies to illustrate that. But the observation is very clear. The dual targeting does inhibit autoantibody secreting spots significantly. What was your second question?

Is it possible to quantify the percentage of CD19 negative BCMA positive ASCs in these samples?

Good question. We are doing it. It's a variable a lot, um, among patient to patient as you would, you know, so far we, um, collected four patients, um, which is not easy to collect the bone marrow cells from those treated patients.

Uh, but we need more data.

Got it. And then I was wondering if you have a, you could provide any, uh, update, um, 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 for our 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 update. Thank you.

Your next question comes from the line of Joe Cantanzario from Piper Sandler. Please go ahead.

Yeah. Hey, guys. Appreciate you taking my question. Thanks for the update. 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 nine to ten 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 to what I said. I think it's about 10 days from now, or less than 10 days. I don't think you should expect significantly more information from our presentation. We're in 1B for our MM trial and it's in U.S. We have to wait the EOP1, end of phase one report, submit it to FDA and get consensus or discussion with them for next phase. So I don't believe that we can release data prior to that.

That's my understanding. But as far as for the study, it's ongoing. So far, so good. Okay. Thank you. Thanks for taking my question. Thank you, Joe.

Your next question comes from the line of Justin Zelen 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?

Expect, meaning predict.

So far, all I can say, so far, so good. And it's 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 is very consistent to what we've seen before. Yeah, I mean, as I answered the question of the other caller, you know, next year you should expect double digits of patient. The readout on the double digit patients will be mostly at least three months and some of them will be six months, which is more meaningful. And our patients are very diversified. I think it's a more, it's actually, it's a real world. The Celenda index is based on, Celenda index is the patients having

more severe SLE and that age older. And that's 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 interesting. I mean, this is a very difficult to answer. It's a balance between the length or the persistence of B-cell depletion. But in the meantime, you don't want to disappear for too long. You want the B-cell coming back with a new phenotype, young phenotype, and call it a B-cell reset. And how long is good enough to... I think our theory is we always see in oncology side, we always see very deep B cell depletion. And what's translated into readout is the MID negativity. It's always, you know, just top 100. So we expected B cell aplasia in immunology will be very deep as well. But how deep, I mean, how long particularly? What is the persistence we want? We'll see. I mean, we are doing dose escalation. We'll evaluate. And then, of course, advocacy.

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 Kao's 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 FASCA GC012F. The U.S. R&D trial in RRMM is now underway, and we look forward to submitting the R&D filings in the U.S. and China for the planned Phase I 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. Thank you for your participation, and you may now disconnect.