Great. Well, we're very excited to share our ASH summary for you. Joining us today is our chairman and CEO, Dr. Dajun Yang, our chief medical officer, Dr. Yifan Zhai, and our senior vice president of clinical development, Dr. Zhichao Si. I will now turn it over to Dr. Yang to begin the presentation. Good morning. Can everybody see my slide in the full screen mode? Yes. Now we can. Great. Thank you all for attending. This is a disclaimer. We are very excited to attend this year's ASH. I just want to highlight a few pictures we were doing at ASH. This is the first time we had a really prime location of the booth and a really nice design and a really central location just behind the ASH. We hold several advisory board meeting near the conference center, and many oral presentations and posters. The team are very excited. One of the largest advisory MDS have about 60 PIs over the world coming. This conference, we have multiple presentations, but focus primarily on two late-stage assets or partner, the lisaftoclax. We highlight, distribute a lot of information about our four global registration trials. We will go through each one of them today, especially those presented at ASH. First, I'd like to present the De Sova class. This is something we take 30 years, from lab to clinic to market. As a team, actually, we were the first one to put AT-101, the really first small molecule inhibitor of BCL-2 and BCL-xL, Mcl-1 into clinic back 2004. Okay. Throughout the 21 years, we have put three compound in the clinic. The second one was actually dual BCL-2 BCL-xL inhibitor, Pacifica class. Then we have the third generation, the BCL-2 selective deSova class, finally made to the market. AT-101, as I show here, was the first IND cleared by FDA back 2004. 2005, 20 years ago, the leading PI, Tom Kipps, was actually our leading PI on AT-101 for the CLL. I had a picture with him during the ASH. We were at a session together. That was already 21 years ago, from the very beginning. Of course, just to highlight a few preclinical activities we have done. The APG-2575 in the preclinical setting. In some of the assays, we have a lower IC50 and more potent. I think significantly, maybe in certain models, where the venetoclax has no activity and APG-2575 show strong activity. I think more importantly is from the day one, when we designed the phase I trial, we try to be different than venetoclax. This is a very important differentiation from day one. Venetoclax, as you know, is using this lead in for BTKI and also four weeks or five weeks, a weekly dose turn up to the target dose. From day one, we designed this daily dose turn up, only take five days to the target dose and no BTKI lead in. Okay. This is very important for the CLL/SLL patients, especially in U.S., most are outpatients setting. This is our approved label and using the daily dose turn up, July in China. This is the only daily dose turn up schedule on the market. As you can see, we have only three dose strengths and take five days to target dose. In the current monotherapy approval, the target dose actually is 600 milligrams. We can start introduce a combination right away. This year's ASH, we had an oral presentation from the leading PI, Professor Zhu, and also the AML/MDS as a poster from the U.S. leading PI, Dr. Kadia. This is really the first time we release the full clinical data of the pivotal phase II registration trial in the BTK inhibitor failed RR/CLL SLL patients. I'd like to mention, actually, it's good that CDE approved our pivotal phase II trial four years ago, at the same time, also gave us a very high bar that require every single patient have to fail both chemo immunotherapy and the BTK inhibitor. That time actually is very hard to recruit the patient who fail the BTKI. This is not just the RR/CLL, but also the BTK inhibitor failed RR/CLL SLL patients. As you can see, this is a daily dose ramp-up design. In the presentation, we actually highlight the details of patient characteristics. It turned out those are really high-risk CLL/SLL patients, especially complex karyotype accounts more than 40%. The 17p deletion and the TP53 mutation is very high. It's much higher than many trials in this patient population. More importantly, their patients actually have multiple, complex karyotypes and also the 17p deletion and the TP53 mutation. Also, actually, more than 50% are unmutated IGHV. As you can see, historically, all these CLL registration trials are much lower risk than what we have enrolled in this registration trial. Despite this high risk, very late stage, heavily pre-treated patients, we did achieve a very excellent OR, over 62%. Also, in the MRD negativity test, the patients actually are also very high. Also presented very nice PFS and OS. More importantly, we did some subgroup analysis, such as those with 17p deletion, TP53 mutation, and also complex karyotype, demonstrated very excellent efficacy. Overall safety was really well tolerated and no tumor lysis syndrome reported in this trial. Also, no drug-related deaths. If you look at the hematological-related TRAEs, this is much less than other BCL-2 inhibitors, especially in this heavily pre-treated patient group. Overall, we consider lisaftoclax to have optimal efficacy-safety balance with the daily dose ramp-up, shorter T1/2, and no tumor lysis syndrome reported in this trial, and no DDI. In summary, we take this word, less is more. Basically, the approval actually is for one systemic therapy CLL patients, and without the emphasis on the RR/C LL. I think this is really the first time globally that lisaftoclax is the single agent with the CLL after one therapy. Basically, lisaftoclax could offer CLL/SLL patients better option as a monotherapy and/or in combination with the BTK inhibitors. The second presentation is from this updated report on lisaftoclax in the AML and high-risk MDS patients. This actually took a while to recruit the patients because the product is optimal. As you can see, we had the two-part design. The first part is just a dose escalation to determine the MTD and the DLT. It took about 22 patients. After that, we did a dose expansion to evaluate efficacy and safety and determine the dose. Overall, we treated more than 100 patients, and especially in the R-AML patients or the R high-risk MDS patients, there is a high response rate. It is worth to mention in the high-risk MDS patients, we actually achieved a 40% CR, 40% bone marrow CR. Overall, we achieved the 80% OR. This is very impressive. In the R MDS patients, we also achieved the 50% OR. More importantly, in the venetoclax-resistant AML or MDS patients, just by combination lisaftoclax with Aza, we achieved about 31% OR. This really offers the potential for the ven-failed patients in the AML setting, which is really unmet medical need right now. We also did some genomic analysis looking for potential biomarkers. This is a heat map, as you can see, that we actually treated patients, more than 50% have TP53 mutation. Despite those, we actually also saw a pretty decent response. More importantly, at this conference, we had a really high interest from investigators around the world for our GLORIA-4 high-risk MDS trial. I think, you know, partially because the VERONA trial failed, and currently, our leading PI is Dr. Guillermo Garcia-Manero and also Dr. Xiaojun Huang. Dr. Guillermo Garcia-Manero was actually the leading PI for VERONA trial. We are very pleased that the FDA, EMA, and also China CDE, cleared this global phase III registration trial for the first-line high-risk MDS patients. I think if we successfully carry out, we could be the first Bcl-2 inhibitor approved for the treatment of high-risk MDS. This is a highlight of a trial design and well-received by the PIs around the world, actively recruiting patients. Let me turn to the olverembatinib data highlights. At the conference, we have overall about seven posters. I think a really important one is this Polaris-1. Just before the ASH meeting, we have announcement that the Polaris-1 global phase III registration trial for the first-line Ph-positive ALL cleared by FDA and EMA. We presented part one of this global phase III registration trial, demonstrated really favorable efficacy and tolerance. The overall trial design is a 2: 1 randomization, with a dealer's choice, investigator choice, TKI. At the end of the induction, three months, looking for the MRD negative CR rate as the primary endpoint for approval. We are very excited to present as a part of the Polaris-1 study. As you can see that MRD negative CR rate is as high as 64%. Overall CR rate is about over 94%. I think that this is really the best in class in terms of response rate and also tolerance. The historical data on the imatinib at that time was not looking for the MRD negative CR rate, and the bosutinib probably often used off-label in the real world, the CMR rate is only 24%. The ponatinib trial, the MRD, this is the most relevant one as the same patient population, the first line had only about 34% MRD negative rate. Of course, it's double the imatinib in that registration phase III trial. We also demonstrate the overall good safety and the similar PK in combo with low-intensity chemo. Another really important study is update the second-line treatment options for the CML patients after failing either the first generation or second-generation TKI. I think you can see the overall MR rate is really favorable and also improve over time. In the subgroup analysis, we actually find out that if the patient in the first line using the second generation TKI actually have responded better. Of course, the baseline is important for those with less than 10%, BCR-ABL is actually responding better. That you see the baseline patients population is important determine the response rate. Another poster presentation is those of the registration trial. We had a four-year follow-up for the pivotal phase II registration trial in patients who failed three TKIs. At that time, this is the full approval registration trial. We enroll over 144 patients, and this is a 2: 1 ratio against the best available treatment, which is mostly just some not very effective treatment options for patients. After failing three TKI, including the first generation and the two second generation. At that time, China do not have any third generation TKI or asciminib. Overall remain very favorable EFS and also the safety profile. I think it's interesting, it's important to know that over the time during the treatment, okay, after this is a four years follow-up, the prevalence of hematological AE actually reduce over time. Okay. This is looking for the grade 3 and the plus hematological AEs. You can see thrombocytopenia, neutropenia actually reduce over time, probably by clear the cancer cells in bone marrow. If this is any grade, primarily grade 1 or 2, non-hematological AE also reduce over time, except the only one is skin pigmentation, which is not a really important non-hematological AE. This actually result is consistent with our phase I study, and also the pivotal conditional approval study. Another important application of the olverembatinib is actually in this rare Heme disease, myeloid lymphoid neoplasm with FGFR1 rearrangement. This is one of a rare malignancy with a poor prognosis and no really effective treatment. It takes 16 centers over three years to recruit 20 patients. Actually, this is the first time we report that olverembatinib actually have a very promising efficacy. Just at two months, 76% of patients achieve a CR, CRh, or cHR. The best response actually is about five receive a Complete Molecular Response. Some of them eligible also did a transplant, and three had still CMR, no disease detected. This is a really significant option for patients with these rare disorders and no effective treatment. There's another poster presented looking at the blast crisis CML patients. Actually, olverembatinib also offer a good response. I think that it's important at this conference that there are other TKIs or asciminib, like allosteric inhibitors. Actually, we want to share with you, in this same cell line that we develop asciminib-resistant BCR-ABL mutations, highlighted here. The other TKI actually could also offer some response. Of course, olverembatinib, among all, is the best one against the T315I mutation, compound mutation, and those asciminib-resistant BCR-ABL mutations. One last highlight I'd like to share is our APG-5918 is the EED inhibitor. EED is a part of the PRC2 complex. Another notable target is EZH2. EZH2 has many approved drugs on the market, but so far, no EED inhibitors approved yet. The EED inhibitor also have potential to treating some of the anemia, like sickle cell anemia, thalassemia. At this conference, you probably noticed that Fawcraft have demonstrated the clinical efficacy with sickle cell anemia. In the preclinical model, we actually did additional oncology study. In the cell line, we demonstrate combination with ponatinib, a really good synergy. This is actually resistant cell line to both our EED inhibitor or ponatinib, but a combination of a good synergy. In the animal model, we demonstrate very good synergy in these resistant models and also the another third-generation IMiD, CC-92480, even show better synergistic effect. Just to highlight, we did have presented before our drug in the preclinical setting, demonstrating also similar activity as a Fawcraft compound, and in some extent, probably better in the same model, looking for the in vivo efficacy in the anemia model. Overall, I think that we demonstrate that really potential for the SOHO class combination of our olverembatinib will really offer synergistic effect in the AML and also with our another really promising compound, MDM2-p53 inhibitor, synthetic lethality MOA. The synergy in the AML and the DLBCL. This is just to highlight more potential of our targeted small molecule drugs. In conclusion, the take-home message is that the first time we released the full clinical data of a registration trial in the BTK inhibitor-failed RR CLL patient, really high-risk, and demonstrated really excellent efficacy and safety profile, and highlighted those two global phase III trials cleared by the FDA and EMA, especially the first-line MDS, GLORIA-4. There is huge interest in our upcoming BCR-ABL2 inhibitor in the global market. Olverembatinib, we demonstrated POLARIS global registrational trial part A in the first-line Ph-positive ALL, and we are looking forward to a registrational trial with the clearance now by the FDA and EMA. Overall, olverembatinib offered a very excellent MRD-negative CRa today and also demonstrated multiple efficacy and safety, and especially 4-year follow-up in the resistant TKI patient population from the registration trial. Also, we demonstrated another potential efficacy with EED inhibitor in multiple myeloma and emerging data coming out with this drug in anemia and oncology, including the previous one we presented for the prostate cancer. This is really the last slide I would like to share with you all. We have multiple late-stage hematologic malignancy-focused novel compounds in the global clinical development. The highlight at this year's ASH presentation, we are very excited. We had many discussions and meetings with the investigators around the world. As you can see, our targeted drugs cover majority of hematologic malignancies, including anemia. We are looking forward to working with investigators around the world. I will probably stop here. I will be happy to answer any questions you may have. Thank you, Dr. Yang. We are now open to questions. Just a reminder, if you would like to ask a question, please use the raise hand icon found at the bottom of this webinar application. When you are called on, please unmute when asking your question. Just give a minute. Our first question comes from Brian Cheng from JP Morgan. Hey, Brian. Hey, guys. Can you hear me? Yes. Great. Well, thanks for doing this recap for us. Maybe just first on the POLARIS-1 trial. Dajun, I'm wondering if you can speak to your thinking around the reliability from this early POLARIS-1 data cut as your study proceeds. How should we think about the data flow in the coming year or so? Can you remind us also how your enrollment is going in the POLARIS-1 trial, and when could we expect a top line? I have a quick follow-up. Thank you. Thank you, Brian. Very good question. I think the POLARIS-1 is very significant in two aspect. First of all, globally, there's no very effective target drug for the Ph-positive ALL. Imatinib was initially entered the guideline, but then was not very active. In the real world, dasatinib probably widely used, but also off-label. The ponatinib probably by far, from the PhALLCON trial, demonstrate best the response. Three months CMR rate or MRD-negative rate about 34%, double that of imatinib. That's really the similar patient population, first line for the Ph-positive ALL. As you can see from our part A of the POLARIS-1, we got a 64% three months of MRD-inactivity rate of more than 50 patients. We are very happy that globally FDA, EMA also cleared that registration trial. We are actively enroll. We have multiple countries regulatory agency clear and multiple sites. I think that the enrollment for this one could be very fast, and because we're actually using the investigator choice TKI, the control arm. It's a low-intensity chemo. This is only three months induction CMR rate or MRD-inactive rate. I think that the readout can be very fast. Hopefully, we could see enrollment complete by the early 2027, and then we can file the NDA to the regulatory agency of the same year. Got it. Maybe just one quick follow-up on the lisaftoclax. Clearly there are several differentiation here. I think one of them is the ramp-up in dosing. You can do it much faster than venetoclax. The lack of tumor lysis syndrome. On the tumor lysis syndrome front, I'm curious if you can kind of give us a little bit more color on the significance of that side effect. What are you hearing from the ground when your treating physicians are using the lisaftoclax? Thanks for taking our questions this morning. Good questions, Brian. I think that the early days of BCL-2, especially venetoclax in the CR patient population, tumor lysis syndrome was quite serious. Then, of course, taking the prophylactic measurement like hydration, also in the case of venetoclax, actually also sonrotoclax, they are taking this weekly dose turn up, right? Also with the BTK leading to debulking, I think all tumor lysis syndrome is well under control. Probably not as serious as early days. Unfortunately for venetoclax and also the sonrotoclax, the registration trial was using the weekly dose turn up. Their approval label, they can only use that weekly dose turn up. I think that overall we offer the patient really good convenience, which is important for the CR/SR patients in U.S. Secondly, I think another thing very important, we and others now demonstrate that the BCL-2 inhibitor, especially for us, have a shorter T1/2, which is a really favorable advantage. That not just less tumor lysis syndrome, but more probably importantly, is less marrow toxicity, right? In our drug, another important advantage is no DDI. That really offer the better option for combination, not just with the BTK inhibitor, but also with other antifungal antibiotics. I think that taken together, the tumor lysis syndrome is probably well under management now, but the marrow toxicity is a probably major differentiation, also no DDI. Great. Thank you. Thanks, Dr. Yang. Thank you, Brian. Our next question comes from Wangbing Zhu of Citi. Hi, Wangbing. Thank you. Thank you for taking my question, and congratulations on the progress. Maybe I have only one quick question on the lisaftoclax in the first-line MDS. venetoclax failed in the VERONA. Do you have any insights for this ASH, for this trial and differentiation in our first-line MDS? We know that we have got the clearance from the FDA and EMA for our GLORIA-4. What's our trial design and enrollment progress and the potential data readout timeline? Thank you. Maybe we can have our CMO, Dr. Zhai, to answer this question. Hi. Good morning, good evening, everyone. It's a good question. It took us more than 1 year, probably 18 months, to get all the health authority, especially FDA, and gave the clearance on the GLORIA-4 design because multiple reason. One is the Project Optimus, right? You need to require multiple data, not just the efficacy, safety data, your analysis, the exposure response comparisons. We're very happy announce that multiple health agencies, including actually FDA, EMA, and also China. This GLORIA-4 study, actually, if you may remember, we received clearance from CDE first, and then take a while to go through all the major other health agencies, including FDA and EMA. It's a great progress. Meanwhile, because VERONA failed, at that time when we initiated, actually nobody know VERONA will fail or success. You ask a very key question, fundamentally, why we feel we have a confidence we'll win, because compared to venetoclax, actually, we have show very different safety profile and a much shorter T1/2 and also have no DDI, and much translate into the clinical setting and demonstrate much less marrow suppression. Actually, we released part of the data and then from the AU101 study, we conducted two studies in China, AC101 plus the AU101, clear demonstrate a very dose-dependent efficacy. Of course, it's not the long-term. We don't have the long-term overall survival data yet. At least compare the data, the safety data, the efficacy data, we feel confident our compound will do better than venetoclax. Especially, they already released the data in SOHO and in ASH, right? Dr. [audio distortion] released their data. Compared to their data, we feel confident we're able to do better job, our compound. Maybe I can add a few more extra points here. I think it's important to know the VERONA trial failed is not because of the target, right? The target in BCL-2, especially selective one, already approved for the CLL and especially AML. AML, I mean, some of the high-risk MDS will actually eventually become the AML, right? Basically, they're already treating the worst case MDS, AML well, or widely used. Second, I think that in the real world, off-label use of venetoclax are actually quite common for patients with MDS. In the data released at both SOHO and ASH this time, I think you do see a couple notable differences here. Those differences add up together, maybe the reasons make the VERONA trial negative, right? One thing, this is a randomized phase III trial, and you can notice that the Aza reduction occurs much more in the combination group, right? Of course, this may be first that is consistent with the notion that the venetoclax has more marrow toxicity. In the randomized registration trial, you don't know patient receive placebo or venetoclax. When the toxicity occurs, you can only reduce the drugs you know, which is Aza, right? If you reduce the Aza too early, too much, that may actually lose some of the activities. Another thing noticed is that the patient may actually have a little higher TP53 mutation, and also the blasts less than 5, et cetera. I think that there are several important differences. Actually, at this conference some of the European group presented the data showed pretty good efficacy and safety profile when they dose the venetoclax just seven days instead of 14 days in the VERONA trial. In the seven-day trial reported by the investigators, they actually demonstrated good efficacy and safety, and everything else is good. The talking at the conference is that if the VERONA trial was able to turn to the seven-day trial, that may be positive. Anyway, that's too late. To be honest, the VERONA trial negative result is kind of surprising and, of course, disappointing. At the same time, that's also why many MDS experts, KOLs around the world are very excited, highly interested to join our GLORIA-4 trial. We all have the same goal, to help the patients with MDS globally. Hopefully, we could have a very good enrollment and have a quicker readout of GLORIA-4. Thank you. Great. Very clear. Thank you. Thank you, Wangbing. Our next question comes from Matthew Biegler from Oppenheimer. Hi, Matthew. Hey, guys. Thanks for doing this event. I'll ask about CLL. Can you talk about the pivotal GLORIA trial and the decision to use ibrutinib as the control arm while some of your competitors are choosing to use ven-based regimens like IV or VO? That's number one. Also number two, do the results of the CLL17 trial change anything in terms of the treatment landscape or physician's propensity to use one combination over the other, and how does that affect your thinking for lisa's development strategy? Thanks. You mean the GLORIA trial design, right? Clear by FDA. Correct. I think that's a very good question, especially with the CLL17. I think that we have to consider this from two sort of angle. To be honest, clinically, with all the data, clearly show the combination of a BTK inhibitor with a BCL-2 inhibitor is probably the best for the CLL patients, especially the fixed duration, right? Our GLORIA trial looking for is more just add-on strategy. Part of the reason is that in the CLL right now, BTK widely used, especially the combo already in the first line. All actually the result is pretty good, right? Just a single agent. If you do the registration trial randomized, most likely you have to do the BTK inhibitor alone as a control arm, which nobody want to do that, including BeiGene, right? We took this add-on strategy. Actually, the BTK inhibitor can be investigator choice. Okay? Can be ibrutinib, can be acalabrutinib, can be zanubrutinib. Okay? That's number one. Number two, I think as you can see, more and more BTK inhibitors and degraders enter the market. The CLL patients will have more options. There's one thing also very clear is that single agent BTK inhibitors, especially in the high risk of patient population, is not sufficient, okay? Our goal is really to look in these suboptimal responders of a CLL with BTK inhibitors and add it to the BCL-2 inhibitor. Okay? This add-on strategy will clearly offer patient a benefit, and more importantly, this is a trial design agreed by the FDA. Okay? I think that the more BTK inhibitors used in the CLL is actually good for us, and we don't have DDI issue. We have a very good safety profile, really easy, quick combination to benefit the patients from the really early on is the key advantage. I think part of answer to your question is in the GLORIA trial currently, we are not looking for the fixed duration. Partially is because of the control arm BTK inhibitor alone is not fixed duration, right? That's why in the combination, we have to be continue with the BTK inhibitors. I think in reality, after we have more clinical data, we probably could talk with the regulatory agency that after, let's say maybe 18 months, that's actually the design of our GLORIA-2 trial, is a combination with acalabrutinib for fixed duration, 18 months. Okay? I think the data readout in a while probably will help us to discuss with the regulatory agency. Maybe actually fixed duration is the way to go. We don't need that for both arms. I think that's really possible. Actually, CLL17 support that fixed duration may actually offer better response to patients without continued treatment. Thanks, Dr. Yang. Thank you. Thanks, Matthew. Our next question comes from Justin Zelin of BTIG. Hi, Justin. Thanks for taking our questions, and congrats on these data presentations. I'll ask a question on all your ASH data sets here, you showed deep molecular responses as well as broad activity across resistance mutations developing on asciminib treatment. I'm curious to hear your thoughts on how you view your agent here fitting within the landscape of next-generation TKIs and development across both CML and ALL, including those in development, and how you view it strategically fitting in within the landscape. I'll ask a follow-up. A very good question, Justin. I think first of all, right now, of course, there are more allosteric and the TKI enter the CML development and potentially to the market. I think let's look at two set of data. Number one, in the CML, the BCR-ABL, one of what the so-called gatekeeper mutation is T315I. On top of that, there's the compound mutation, which means there's more than one mutation in the single cell. The most commonly are those T315I plus like E255 and others. Okay? We demonstrate clearly in the preclinical and also in the clinical setting for the BCR-ABL with T315I and other compound mutations, olverembatinib is the most potent one. Okay? The best one. We have a really good deep response and also broad response. Okay? You can see that the current data from 10-701, they actually do not have that activity in the phase I trial data so far. They didn't enroll those patients or have a very minimal number of those mutation patients. Okay? I think for the lay line CML, especially those with the T315I mutations, asciminib or terms, and another one, the Enliven's, do not have a very strong activity. I think that is the major differentiation we have in the CML space, the lay line, the CML with mutations. In the ALL, asciminib and all other allosteric inhibitors because of the mechanism action, they are very selective, but they're not very potent against the specific fusion protein, which is same target, BCR-ABL, but is more P190, okay, not P210. Overall, all these allosteric inhibitor do not have much trials for the Ph-positive ALL. I think the Ph-positive ALL deserve a more potent TKI and also really good safety. I think that's the advantage we have. You can see even though it's a small number of patient, over 50 still, that we demonstrate we double actually what the ponatinib was able to demonstrate in the three months MR rate. I think a combination, the lay line CML with the mutation, which is account at least 40%, and a really excellent efficacy and safety overall in the Ph-positive ALL, especially this is the first line. I think the significance of the POLARIS-1 clearance by FDA EMA is that this is the first line ALL patients. We really want to offer the patients the best benefit, and then they also can continue in the maintenance treatment. In China, we have ALL patient taking our the longest one more than three years. ALL is a really high prevalence in Asian countries, in China, Japan, and Korea. It's like the CLL in the West, in U.S., Europe. There's a huge unmet medical need, and we probably offer the best one. Another I think important aspect is that this data by other companies presented at ASH, we actually had a similar data of even probably better because we take a patient in the U.S. by MD Anderson PI, the same PI Dr. Jabbour, four years ago. We have data of patient who fail ponatinib, who fail asciminib, who fail even both ponatinib, asciminib. All the PI at that time says, "Dajun, you guys should talk to the FDA. Do the pivotal phase II trial." By that time Project Optimus already started. Great. FDA really want you do more dose optimization, looking for the best safety efficacy dose. Number two, they really require you to do the RCT. When you do the RCT, you can think about what could happen to those compounds right now. I think we're probably the last one to use bosutinib as a control arm in the RCT trial design. Great. If I could just ask a follow-up question on lisaftoclax. Just given the practical advantages you're seeing here over standard of care. Are you seeing increased interest amongst investigators in exploring additional combination regimens here? If there are any specific partner therapies or fixed-duration doublets that are emerging as the most compelling that you'd like to highlight based on that interest? Yeah, I think this is an important question. Definitely in the CLL/SLL patient population, fixed duration is the way to go, right? It's just regulatory-wise, you need the BTK inhibitor as a control arm. That's where is the hurdle. We take this add-on strategy, which is actually more BTK inhibitor-approved or degrader-approved, is better. It doesn't matter which inhibitor or degrader, as long as it has the same target, same pathway. Switching between the BTK inhibitors or even degraders will not help the CLL patient much. Especially those high-risk, 17p deletion, TP53 mutation, those BTK inhibitor alone will not benefit, will not reach the optimal response. That's at least suboptimal responders is at least 50-60 patient population in the CLL, right? Add-on strategy and eventually fixed duration of the BTK inhibitor with the BCL-2 inhibitor is probably the best way. In that case, you need to looking for the BCL inhibitor have a favorable PK properties, and safety profile, and also no DDI, okay? I think that's where, especially in the CLL community, KOL really like our drug. It is a daily dose ramp-up. That's important for CLL patients. Probably not so much for the AML/MDS, because that only need a two days dose ramp-up, start from the 200 milligrams. Overall, I think this, the CLL class really offer the additional better option for the CLLs in the CLL community and benefit the patients more than any other therapies. Great. Thanks for taking our questions, congrats again. Thank you. Thank you, Justin. We have time for one more set of questions. I have a question from Greg Renza from Truist. Great. Thanks, Yifan. Thank you, Dr. Yang and Dr. Zhai, for a great weekend and great presentation. Dr. Yang, maybe just on lisaftoclax, just in keeping with respect to the full release of the clinical data from the China registrational, just wanted to give you an opportunity to just remind us of the key highlights there that supported the approval in China, especially in the context of what other BCL-2s are showing at ASH and up to date. Maybe for Yif, just how this is translating with respect to sales in China and any help on how we should be thinking about the trajectory there. I do have a follow-up. Thank you. Yif, go ahead. You can answer. Yeah. No, thank you, Greg. As it relates to sales, we haven't given public guidance, as you know. We have made the investments for a sales force in China to drive first-mover advantage of lisaftoclax in China. We have the people in place. We're increasing our market penetration as we speak. The uptake is going well. We'll have the numbers reported in our next upcoming annual report. We'll be sure to give detail to the public as it relates to the sales trajectory. I think we're positive as we speak right now with the way things are going. Maybe I can add a little more here. I think with the launch in July, in the first four months already, we do see a really good uptake, high interest, not just from the CLL/SLL approved indication, but also from the AML, MDS, myeloma, DLBCL, and also the Ph-negative ALL. I think as we mentioned before, BCL-2 selective inhibitor is really considered the small molecule of a PD-1, have multiple indications, multiple combinations. I think the first four months or first 100 days sales from our experience commercial team, which they had launched the BTK inhibitors in China, really see the huge uptake, penetration. Of course, also offer the patient more benefit with this approval in China. I think that moving forward, we clearly demonstrate our advantage differentiation over another class, especially in the case of MDS and potentially also multiple myeloma, which we had an oral presentation last year at ASH. BeiGene is the one. I think that they're also behind us in those indications. Overall, I think we probably offer the balance of potency, safety, and also convenience as the preferred BCL-2 selective inhibitor. Great. Thank you. Just a last one, as we look into your pipeline, especially with several protein degrader developments occurring at ASH this past weekend, how do you see your own protein degrader pipeline developing and being positioned for competitiveness? Thanks again. Good question. We do in our pipeline especially, put a major effort in the degrader, the PROTAC. We do look in carefully for each target, whether inhibitor or whether the degrader. I think it's really first looking for the specific target that's more like a driver for the disease. Our EED inhibitor is also allosteric inhibitor, and we do have upcoming, the one example we can give is the MDM2-p53 degrader. Our APG-115, the MDM2-p53 inhibitor have been in the clinical trial in multiple indications, including combination with PD-1. To be honest, we and other MDM2-p53 inhibitor all run into same bottleneck that is related to the mechanism action that the inhibitor, when you release that interaction blocking the p53, you upregulate p53. Then the same time when you upregulate p53, they will come back to upregulate MDM2. Accumulation of MDM2 will then block the p53 tumor suppressive function. I think that may be part of reason we and others have been working on this target for more than 10 years in the clinic now, still no approved MDM2-p53 inhibitors to the market. That's part of the reason we develop a degrader, and in the case of MDM2-p53 degrader, you completely lock out the target protein MDM2. At least in the preclinical setting, one dosing, just one shot in the animal model is sufficient to cause and maintain complete tumor regression. Okay. I think we do have a serious pipeline upcoming for each of the degraders we're working on. We do think these, some of the target, the degrader would offer advantage over the inhibitors. Great. Thank you, Dr. Yang. I think that's all the questions for now. I'd like to conclude by thanking everybody for joining this session and your support. Very excited to share the data with you. Please write us and contact us for any follow-up. We'll see you at JP Morgan next year, and in the meantime, wish you all happy holidays and a healthy happy 2026. This is a wrap. Bye, everybody. Thank you all. Thank you. Thank you. Bye.