As a reminder, this conference is being recorded. I would now like to turn this conference over to your host, Ms. Monique Kosse, Investor Relations, LifeSci Advisors. Ma'am, you may begin. Thank you, operator. Thank you everyone for joining today's call. I would like to advise listeners that comments made on today's call may reflect forward-looking statements that are related to such matters as BeyondSpring's clinical and pre-clinical research and development activities and results, regulatory and commercial plans, industry trends, market potential, collaborative initiatives, and financial projections, among others. While management believes that its assumptions, expectations, and projections are reasonable in the view of the currently available information, you are cautioned not to place undue reliance on these forward-looking statements. The company's actual results may differ materially from those discussed during the call for a variety of reasons, including those described in the forward-looking statements and risk factor sections of the company's 20-F and other filings with the SEC, which are available on the investors section of the BeyondSpring's website. Joining us on today's call is Dr. Lan Huang, BeyondSpring Co-founder, Chairman, and Chief Executive Officer, Dr. Ramon Mohanlal, Executive Vice President, Research and Development, and Chief Medical Officer, Richard Daly, Chief Operating Officer, and Elizabeth Czerepak, Chief Financial Officer. It is now my pleasure to turn the call over to Dr. Lan Huang. Lan, please go ahead. Thank you, Monique. Next slide, please. Thank you everyone for joining the call today to spend your precious morning with us. Today we're going to share with you the exciting and positive data of our DUBLIN-3 study, the Top line, which is using the OS as the primary endpoint in the late stage non-small cell lung cancer. This slide is showing you the plinabulin, which is the first-in-class selective immunomodulating microtubule binding agent, which is called SIMBA. It is a potent antigen-presenting cell, or APC inducer. We have been developing plinabulin in the last 10 years. Plinabulin actually is a new chemical entity. It binds in a very differential pocket in tubulin, with that it depolymerize the tubulin, releasing a very important immune defense protein, GEF-H1. With GEF-H1 upregulating the downstream signaling transduction pathways, it leads to the DC maturation and then the T-cell activation, which give us the durable anticancer benefit, which we are using DUBLIN-3 to confirm. In addition, plinabulin can also protecting the neutrophils in the bone marrow and currently we are also working on the CIN indication for plinabulin. Through our 10 years effort, we have been working with leading scientists globally at Mass General, Fred Hutch, MD Anderson, and University of Basel, to understand this mechanism, and we have published in five leading journals, including two cell subjournals shown here. Next slide. As you see that in the immune cycle, you really have to hit a few different steps in the immune cycle to show the optimum immuno-oncology response. It starts with number one, the radiation or chemotherapy could potentially generate a tumor antigen. Plinabulin, as this very important APC inducer, is a key step in initiating the anticancer durable response. It could mature the central cell and then have this antigen presentation and leading to the tumor antigen-specific T cells, which we call hit the gas into the system. With the checkpoint inhibitors, which release the brake, the car would go faster, and that's what we're currently using the IO combo treatment studies to confirm this optimum response. Next slide, please. To prove plinabulin's anticancer benefit, the first indication we choose is in the second line and third line non-small cell lung cancer, EGFR wild type, which we believe is still severely unmet medical needs. It's a huge population with limited treatment options. As you see in the EGFR wild type patient, it consists around 85% of the Western lung cancer patients and around 70% of the Asian lung cancer patients. You all know now with the immunotherapies moving into first line, docetaxel-based therapies are the mainstay in this indication. We also know from the TAILOR study, TKI actually are worse than docetaxel in the EGFR wild type patient population. However, with docetaxel-based therapy, it still has limited efficacy in limited survivor, but also has severe side effects, including over 40% severe neutropenia. Since nivolumab was approved six years ago, and currently there's no new agent with novel mechanism has been approved in this indication. A few important trial has failed to meet the OS primary endpoint. Next slide, please. We decided to use plinabulin to target this population to really is to develop an agent which can address this unmet medical need. The scientific rationale is the following. Because plinabulin is activating the GEF-H1 through the depolymerization of tubulin, GEF-H1, actually according to our cell report paper, with the high immune signature of GEF-H1, actually do let patients live longer in various cancer types. That give us the foundational benefit for this agent. Based on our understanding of plinabulin's immune mode of action, Ramon, our chief medical officer, has been spearheading in designing the DUBLIN-3 study to select prospectively patients with measurable lung lesion, and those patients are more responding to this plinabulin from its immune mechanism action. Next slide, please. With that said, I'm going to turn the baton to Dr. Ramon Mohanlal to walk you through the design and also execution and also the exciting data of DUBLIN-3. Ramon. Thank you, Lan. At the start, I would like to go through the design of the study, as a refresher, if you will. This study was a global randomized single-blinded study, was conducted in different regions, in the U.S., in China, and Australia, which was comprised of 60 study sites. The study was conducted in non-small cell lung cancer, in EGFR wild-type patients in second and third line. I will walk you through the design that you see in the middle, where you see that patients were randomized in a 1:1 ratio to either docetaxel and plinabulin, on the top on the right, or the comparison arm, which is docetaxel and placebo. You will be aware that today with checkpoint inhibitors having moved into first-line non-small cell lung cancer, you will be aware that now the docetaxel and docetaxel-based treatments have become the standard of care in second and third line. Here we also have docetaxel as the comparator arm. Quickly to remind you regarding the patient population. On the left, we can see that, in the box on the left, we can see that we included non-squamous or squamous patients, stage III-B, IV, ECOG status was zero, one, or two. It was required that the patient had received a prior line with platinum. It also was required that the patient must have at least one measurable lung lesion in the lung. Prior checkpoint inhibitor therapy was allowed in this trial. At the bottom, you can see the protocol endpoints summarized. The primary endpoint was overall survival. We had a number of secondary endpoints, ORR, PFS. Importantly, we looked at Grade 4 neutropenia on day 8 in cycle 1. Plinabulin, as Lan pointed out, being an immune agent, is expected to have a long-term benefit, which is typical for immune agents. We also look at the 24 OS rate, 24-month OS rate. In addition to that, the 36, and we also looked at 48 months, which is four years. We looked at DOR and a number of quality of life and safety-related endpoints, to include Q-TWiST, standard quality of life assessments, the proportion of patients with a certain cycle number to include eight cycles, 10, 12, or more. Next slide, please. Here I would like to walk you through the data as we currently can share with you. We plan to submit an abstract of this top-line data with DUBLIN-3 in a major conference. That limits us somewhat what we can share with you and what we cannot. Here, I believe, we have summarized the key data set that you would find very useful, I believe. I would like to start off with making the key points as a key summary that is shared in the slides. First of all, the OS primary endpoint was met. Secondly, all key secondary endpoints were met. Importantly, the efficacy data as we see, the efficacy data results as we see is consistent. It all goes in the right direction and reaches significance for the key predefined endpoint. Importantly, we see a doubling of OS rate if we look at the time points 24 months, 36 months. There also, at the bottom, that I will walk you through in more detail, we also look at four years, 48 months, where we see a benefit for the combination. Lastly, we see and confirm the Grade 4 neutropenia benefit, which you will be aware is topic of a separate NDA that currently is under review with the FDA. Let me go through the rows one by one. The top row shows the primary endpoint OS rate. Regarding mean OS, the P-value is 0.03. If we look at OS log rank, the P-value is less than 0.04. With this, we met the protocol pre-specified criteria to call the study a positive study. The protocol P-value that was required was 0.046, which took into account the adjustment prompted by the interim analyses that we have conducted. These tests were done as two-sided. You can now see in the table that summarizes the secondary endpoints that I will go through line by line. For ORR, we met the significance in terms of P-value less than 0.03. PFS, P-value less than 0.01. Grade 4 neutropenia frequency on day 8 in cycle 1 with docetaxel alone, 27.8% of patients. Adding plinabulin to docetaxel, that then comes down to 5.3%, highly statistically significant. 24-month OS rate with docetaxel alone, 12.5% of patients. The plinabulin combination, almost doubling, 22.1%. 36-month OS rate with docetaxel alone, 5.3% of patients. Plinabulin, more than doubling, 11.7%. As I mentioned, we also look at four years, 48 months, where we have zero patients in the docetaxel arm, and a little more than 10% with the combination. In short, the trial's primary endpoint met key secondary endpoint, also met the Grade 4 neutropenia benefit was here confirmed. That also will help us with the CIN application. All data goes consistently in the right direction. Next slide, please. Regarding the next plan for DUBLIN-3, we will be discussing the filing plan with the U.S. FDA, the NMPA this year. Of course, with this data, a potential filing first half next year. We believe we have here a data set that will be highly attractive in second and third-line non-small cell lung cancer EGFR wild type for the following reasons. With checkpoint inhibitors having now moved into first-line, in effect, that has created a vacuum in second and third-line because patients who fail checkpoint inhibitor in first-line will not be considered typically in second and third-line, so also to receive checkpoint inhibitor. Therefore, docetaxel has become the dominant player in second and third-line, with docetaxel, as we know, and we know docetaxel very well because it has been used for very long. It is very effective, but it has severe side effects, in particular neutropenia, and also negatively impacts the patient's quality of life. You will be aware that in second and third-line non-small cell lung cancer patients, these are often very sick patients, and approximately 50% of the patients are opt out of receiving treatment in second and third-line after they fail first-line checkpoint inhibitor, typically out of fear of toxicity and negative impact on their quality of life. For these patients, it's important not only to live longer but to live longer well. That is the profile we believe we offer with adding plinabulin to docetaxel, where not only we offer superior incremental survival benefit over docetaxel alone, but also we make docetaxel safer. We prevent the neutropenia. In previous studies, we also showed that we positively impact the quality of life. That's data that we are still analyzing. I expect that we also here will demonstrate that we have a quality of life benefit with the combination. In the box at the bottom, I would like to point out the important safety benefit that we observed in this trial. If you look at the overall AE profile, what we see, the overall AE frequency between the two treatment arms are approximately the same. However, the severity is less with the combination. We see far less Grade 4 neutropenia, far less Grade 4 AEs in general, in addition to neutropenia. It shifts to lower grade, to Grades 3 and 2. What that is telling us is that we keep the AE frequency the same, but we move it into lower severity, which is an attractive proposition for second, third-line non-small cell lung cancer. Lastly, we didn't see anything that was unexpected in terms of AE signal or AE concern. Next slide, please. We already pointed out during the R&D day that the company will be focusing on building a large portfolio around the triple IO combinations. Some of those studies already have started with the nivolumab, ipilimumab, plinabulin combination. We are now in phase II for small cell lung cancer. The MD Anderson trial has started with radiotherapy checkpoint inhibitor and plinabulin, and we are looking into the next set of trials. Of course, we were all waiting for confirmation from DUBLIN-3 to demonstrate that the drug is effective as an anti-cancer agent, but also that it confirms the IO mechanism of action that we saw because we saw a significant long-term benefit with adding plinabulin to docetaxel. With that confirmation now, we will quickly expand on our IO triple combination portfolio development program. We will be addressing and focusing on the areas of unmet needs in the IO space. As we see that these patients, firstly, who become resistant to IO therapy, who initially responded but then become resistant, and we will aim then to reverse that to make them again responsive to checkpoint inhibitors. We will focus on the immune-related AEs. We see that as a tremendous unmet need in the IO space. Of course, several IO agents will be combined with chemotherapy as well. There we have the neutropenia benefit in addition to the immune-related AE benefit that we hope to confirm, that we believe is very attractive to add to an overall survival benefit. This will be an important focus for us moving forward. I believe you can advance this slide. What I just said is summarized in this slide. That will be the focus of the company moving forward. Next slide, please. With this, I hand this back to Lan. Thank you, Ramon. As you see, we are developing plinabulin franchise. Plinabulin is truly a pipeline in a drug. Currently we're developing three different areas. First is in the prevention of chemotherapy-induced neutropenia. This clinical confirmation has been done in six clinical trials with over 1,200 patients. As you know, plinabulin CIN indication has received breakthrough designation from both U.S. and China NMPA. We also received priority review from FDA, and the PDUFA date is November 30th. Today we are very excited to show you the positive topline DUBLIN-3 study. I just want to emphasize the three points from this positive study. Number one is we met the primary endpoint, the OS benefit statistical significance. We also met the statistical significance for the key secondary endpoint, so which shows the internal consistency. Secondly, we also show a significant reduction in severe neutropenia in DUBLIN-3. This is further confirms plinabulin's prevention of CIN benefit. This can support the future potential launch of plinabulin into the CIN indication. Lastly, very exciting, we saw the doubling of the OS rate in the 24 months and also 36 months in the plinabulin arm compared to the docetaxel arm. This is truly underscoring the plinabulin's immune anti-cancer benefit. Which gave it the gateway into the transformation opportunity on the right, which plinabulin is in the different studies in combining with the IO regime to look at multiple solid tumor indications. We definitely think plinabulin's future is bright, and thank you so much for staying with us and supporting us along the way. We owe you big deal, and we hope that we can bring this talented child, plinabulin, to patients in need in the very near future. Thank you. Now we are opening up for question and answers. At this time, we will be conducting a question and answer session. If you would like to a question, please press star one on your telephone keypad. A confirmation tone will indicate your line into the question queue. You may press star two to remove your question from the queue. For participants using speaker equipment, it may be necessary for you to pick up your handset before pressing the star keys. One moment while we poll for questions. Our first question comes to the line of Josh Schimmer with Evercore ISI. You may proceed with your question. Great. Thanks so much for taking the questions. Congrats on the results. Such an exciting outcome for the patient community. A couple of questions, if I may. First, was this designed as a registration enabling study? Any reason why it couldn't support label extension? Yeah, this is a registration study. What's your second question for the label extension? Yeah, just any reason or anything about the design that may preclude the FDA from considering it for addition to the label? I think it will be having its own label. The first is this is a different dose from the CIN indication, right? This is a 30 mg, day 1, day 8 dose, then with the CIN is the 20 mg per meter square dose. They're different dose for this. Then I think we were using this study to file for its own indication and also has its two different IND numbers for the CIN and also for the lung cancer. I don't know if I answered your question. Yep, no, that's helpful. What percent of the patients were enrolled in North America? What's the percentage of patients? Yes, please. Yeah, it's around 20%. Okay. We did discuss with FDA regarding this percentage, and they want us to show the PopPK to make sure the PK is the same among the Western patients and also the Asian patients. If they are same, similar, then you can combine the data. We have shown them to be the same. Okay. You've shown that yet? Yeah. Okay, great. Yeah. We have. Yes. Now that you have a broad CIN prevention drug and one that also looks like it confers a survival benefit in at least the non-small cell lung cancer population, how are you thinking about a pricing strategy that can reconcile those two applications? Yeah. First is, probably I can start with the dosing, because as you see, the lung cancer dose is three times dose of the CIN dose. The CIN can be a little bit less expensive, so lung cancer is more. With this dosing difference, so there is a difference there. With this question, I think the best person to answer would be Rich. Rich, can you answer this question? Yes, I think this is a really good question, and obviously, we hadn't decided on price, so thanks for the question, Josh. We were waiting for these data to make our decision because as the only drug that actually has this opportunity to prevent CIN and with the potential for an anti-cancer benefit along with that, we want to make sure that we're appropriately pricing for value for the practitioner and value for the payer and for the patient. As we think about this, as Lan said, you have this CIN dose, which is dosed the day of chemotherapy, and then you have the dose for non-small cell lung cancer, which is approximately four times the CIN dose. We don't want to get caught in a situation where we're pricing differentially. It's probably going to be a milligram for milligram dose because we think that's the appropriate way to go to market. We want to make sure that we're capturing the true value of the product for all the parties, all the stakeholders involved. We're actively working on that right now. Obviously, with these data, we want to make sure that we're taking these data into account. That's one of the reasons why we've been holding back. Not really answering your question, so I apologize, but we do want to make sure we bake this information into it, because as the only drug with this type of an effect, positive effect, we really want to make sure that we're looking at this appropriately. Understood. Then maybe one last question, if I may. What percent of the patients in the trial were refractory or unresponsive to checkpoint inhibitor therapy in prior lines? Do you have any early sense as to the benefit plinabulin delivered in that population specifically? Yeah. Probably I can start, and Ramon can add. We do enroll PD-1 failed patients and also stratify in both arms. Since we are enrolling a lot from Asia, so those percentage is limited. It's probably around 15% in the population who are the prior PD-1 failures. I think the data is still being analyzed. Ramon, you want to add? Yes. Thank you. The question, of course, is important, about what was the fraction of patients with prior PD-1 and who failed. I would also like to point out is that, generally, when patients move from one chemo to the other, it is well-established that then they start to respond to the new chemo, especially if you take an IO approach like we do with plinabulin, where plinabulin helps to effectively present these antigens to the T cell repertoire. The question is important, but I would like to point out is that the second and third line here has a different chemo, and you will provoke a different response. Irrespective of whether they had a prior checkpoint inhibitor or not, the switching itself will make this treatment applicable for second and first line, irrespective of what they had before. Even if you have only a relatively small fraction of patients who had prior PD-1 inhibitor, the claim still holds that this is a treatment for second and third line generally, irrespective of what they had before. The one caveat is, as I pointed out, is that they should have failed a prior platinum regimen. That is approximately standard in first line anyway. The question is important, but we don't see an impact for us in terms of how this data will be adopted generally in second and third line. Okay, got it. Thanks so much, and congrats again on the results. Well, thank you so much, Josh, for the great questions and also for your strong support. Our next question comes from the line of Jason Gerberry with Bank of America. You may proceed with your question. Hey, guys. Congrats on the update. Just a couple of questions from me. I just wanted to tease out or confirm that the OS hazard ratio is truly clinically meaningful. I know sometimes you can be at kind of 0.85x, just barely touching, I think, what doctors might characterize as clinical meaningfulness. Just wondering if you can speak to the clinical meaningfulness of the data more broadly. As we start to think about a potential halo effect to the utilization of plinabulin and CIN, I believe that CIN used at a lower dose. Do you anticipate that this does have a halo effect on CIN if approved with an anti-cancer benefit in lung? Thank you so much, Jason, for the brilliant question. For the first hazard ratio and clinical meaningfulness, I think I will let Ramon to answer. The second question, your halo effect of the anti-cancer into the CIN, I will let Rich to answer. Ramon, you go first. Yes. Thank you for the question regarding hazard ratio. Firstly, I would like to point out is that the hazard ratio that we have is within expectation. I mentioned we are preparing a major presentation at the major conference so that we can make the biggest impact with presenting this data to the medical and scientific community. I would like to point out is that the hazard ratio that we have is within expectations. I would like to make some additional points. The points that you make, it's very important that hazard ratio is something that a lot of people will look at, but obviously, the key is always to meet the primary endpoint for seeking FDA approval. The next point to make is the primary endpoint for FDA approval, as you know, here is OS rate. Secondly, just quickly to point out is that you will be aware that for IO agents, the agents that have immune effect, typically, we see a relatively more benefit with longer duration, and we see that here as well with plinabulin. With hazard ratios, typically, there is relatively more weight of that earlier data. I can share with you that we are very pleased with what we have, and we will, of course, disclose the full data set at the time of that major conference. Thank you. Yeah. Rich? Yeah, thanks. I think this is one of the fundamental questions that we've been investigating over the last year and a half as we prepare for these data to come out. We've done market research here, and I want to make it really clear, obviously, without a claim, this is not something we can promote, and we would never promote. As we prepare for the next steps and analyze the data, and Ramon and his team do the work that they need to do. Obviously, this data can be in the marketplace, but it's not something the commercial team can touch. With the awareness of this data and the ability to promote it, we think it can have a positive effect on the use in CIN. The physicians, what they tell us in market research is, again, this would be the first drug that would be able to have a positive effect in preventing CIN, chemo-induced neutropenia, and have an anti-cancer benefit, albeit at least in data limited to non-small cell lung cancer. Physicians will do what they will do. The initial feedback we get from market research is that it would have a positive carryover into CIN. We're very excited, incredibly excited about these data and the potential not only for non-small cell lung cancer patients, but also the potential benefits, as Ramon alluded to, in building out the lifecycle management of this and looking at it in a broader aspect as well. Got it. Great. Thanks so much for taking my questions. Thank you so much, Jason. Our next question comes to the line of Andy Hsieh with William Blair. You may proceed with your question. Great. Thanks for taking my question. Really want to congratulate the team. It's been kind of a years-long process, and especially to Lan, I think you really see the value and the potential of this drug years ago, when nobody really believed in that. Congratulations on everybody and on the BeyondSpring team. I have a question regarding the primary endpoint. I just wanted to clarify that for the overall survival, typically, we use median as kind of the primary endpoint, and you alluded to the fact that the significance is really related to the mean. Can you help us understand the primary endpoint and kind of the difference between mean and median? We actually, in our SAP, we're looking into both the mean OS and also median, but it's not really median OS, right? It's the log-rank P value that look at the KM OS graph, right? That's the P value which you are using to get the drug approved. We actually look at both, and both met statistical significance, as you see from Ramon's presentation. Also from, you probably see from the current data, which we can share, the limited number we can share, the curve definitely has OS tail, which is flying at the end, right? The graph is separating a lot more in the later part of the curve. Just to answer your question, both met statistical significance. Right. Okay. That's helpful. Thank you very much. In terms of other geographic regions, now obviously with kind of a double win, right? Double play on two different indications, how has the thinking on other geographic locations such as Europe or Japan kind of come to play as you kind of broaden the plinabulin franchise into a global brand? Yeah. That's a great question. Currently, the study is a global trial. We do enroll globally, in U.S., China, and Australia. I think the China and U.S. filing is obvious from the current data combining together for both countries. For Europe and Japan, I think the next step is for our head of regulatory, Gordon, to also have meeting with EMA and then also have the submission plan, just like what we are doing currently with the CIN indication. The CIN is already paving the way with all those discussions. Yeah. Thank you for this great question. Yeah, definitely, we don't want to stop at the U.S. and China, which are the two largest market in the world, but Japan and also E.U. are also very meaningful, and they also have a lot of patients who we can help. Right. Exactly. Just kind of looking at these abstract submission dates, I think World Lung in September might be a little bit kind of out of reach, but would ESMO be something that you would be very interested in presenting the DUBLIN-3 data? Yeah. That is the plan. Let's put it this way. Yes. It's coming up, right? You got it. The middle of September. Yeah. It's middle of September. That's in the plan. Great. I look forward to that presentation. Lastly, maybe this is kind of a follow-up to Jason's question before. I just was curious about the control on docetaxel. I guess, how would you characterize the performance there within the DUBLIN-3 trial? Is that kind of consistent with your expectation as well, or any sort of comment you want to make on the control arm? Yes, it's consistent with, if you look at nivolumab versus docetaxel, that study, that's similar to the docetaxel, how it behaves there. Yeah. It's similar to the current standard of care, docetaxel, how it's supposed to be. Great. Thanks for answering all my questions and really, it's a great day and congratulations to the BeyondSpring team. Well, thank you so much, Andy. Thank you for supporting us along the way when people are not believing us. In our view, scientific rationale actually is the foundation for clinical evidence, right? Currently, we took six years to confirm plinabulin is an anticancer drug. Thank you for supporting us along the years. Our next question comes from the line of Maury Raycroft with Jefferies. You may proceed with your question. Hi, good morning, everyone. I'll add my congrats. Great to see the news today. I just wanted to confirm and follow up on a question earlier about the hazard ratio. I think it was mentioned that it was within expectation and just wanted to confirm, presumably this means that it will be meaningful as well. Yes. Yeah, it's clinical meaningful. That's right. Got it. Okay. At this point, I'm wondering, do you have perspective into total docetaxel dose that was used in each arm and how this contributed to benefit relative to benefit coming from plinabulin's novel mechanism? I think that is still in tally, but we expect we have more cycles of treatment in the docetaxel and the plinabulin arm. Actually, yeah, we definitely see the direct anticancer benefit from plinabulin, from the ORR data also. Those will all need to wait until a major conference to disclose. Got it. Makes sense. Seeing the overall response rate benefit in this study, that was a surprise to us. Just wondering if you can talk more about what you're seeing on ORR. Is it a different type of response, maybe earlier or deeper because of the different mechanism? Are you seeing similar type of response, but just in a higher proportion because you're able to keep patients on max chemo dose? Yeah, let me just share you some color, but I think definitely the data has to be released at the major conference. For both docetaxel arm and also the plinabulin and docetaxel arm, the PR, right, because this is looking at the PR, and they usually come cycle 3 and cycle 4 in both arms. Our response rate, I cannot tell you how much more, but we are more, right? With higher statistical relevance. Basically, we are adding additional direct anticancer benefit into the combination. It's not because the PR comes from cycle 6 or cycle 8. They all come around cycle 3 and cycle 4. Got it. If there's more responders in the plinabulin docetaxel arm, that basically comes from the direct anticancer benefit of plinabulin, right? Got it. Seeing responses at a similar cycle time point in both arms, but you're getting a higher rate in the combo arm. Yes. Got it. Okay. Last question, just another follow-up on overall survival. Can you comment at all on what you're seeing in terms of months for overall survival and potentially contextualize versus other data sets that are out there? We've been referencing the 2.8 months delta between nivo and docetaxel, are you seeing better, worse, or in line? I think we cannot comment on that, right? Okay. We are saving that for the major conference. Fair. It is clinically meaningful. Let's put it this way, right? Got it. Okay. Well, congrats again, and thank you for taking my questions. Well, thank you so much, Maury. As a reminder, if you would like to ask a question, please press star one on your telephone keypad. One moment while we poll for questions. Our next question comes to the line of Joe Pantginis with H.C. Wainwright. You may proceed with your question. Hi, everyone. Good morning. Let me add my congratulations as well. My first question is probably for Ramon. I just wanted to ask about the proportions of the regions. I know there were, I believe, much higher proportion in China. My second question is probably for both you, Lan, and Rich as well. With regard to your commercial strategy, obviously the variables in the U.S. are quite evident. I don't know if you wanted to comment on that or what your desires might be in the U.S., but I wanted to focus on China. I think it might be a good time to remind us based on the presence that you've had and all the efforts that you've had, Lan, in China, you know, do you need a partner? What role would the national health system play, not only in CIN but bringing plinabulin to lung cancer patients as well, if it is approved? Thanks. Yeah. Thank you so much, Joe. You are the longest analyst for us, so you really see us growing in this arena. Yeah. The first question is for Ramon. I think the percentage of patients in various regions. We answered around 20% of Western patients, but of course, Ramon can add more color to this. Ramon? Yeah. Yes. I think the key of your question is how many patients from China, how many from Ex China. Ex China for us means Australia and U.S., and that was around 20%. Yes. Got it. Joe, your next question is what's our commercial plan in China? Is that right? Yeah. Really, the role, based on all the efforts that you've had and you're in China for all these years, do you need a partner? Can you remind us in what role the national health system will play if plinabulin is approved? As you say that, yes. We do have our boots on ground in China, which also help us in all the quality of the clinical trial conduct. And also plinabulin actually received a 13th five-year grant from the government, which is the innovation grant in government, and that also give us the highest chance to get into the national insurance system after this drug is approved. From a partner point of view, actually, it is also of advantage to have partner in China because it is a vast country. Probably their resources can also help us in reaching to the furthest regions and also in developing the drug in more indications and together. Of course, because China also is very concentrated in Shanghai, Beijing, and Guangzhou. For those local areas, potentially, there is ways of also being able to do it ourselves. There's always synergy in working with a partner in China. Of course, who is the partner in China? That's the key, right? We definitely, if we find the partner for us, it would be the synergistic partner, not only in the commercial way, but also their pipeline would also be very synergistic with plinabulin in multiple different indications. This way, one plus one is greater than two, and that's kind of partnership we would be looking at, right? In addition, I think your next question regarding getting into the national insurance is very important. I think when the drugs get into the national insurance, the vast sales growth. For example, for one of the company, their biosimilar [TECFIDERA], initially before it get into the national insurance, it was selling CNY 400 million. The year after getting into national insurance, it was selling CNY 1.8 billion. That's like four times of difference in one year. Got it. Thank you very much. With our drug, it has a high chance of getting in there. Yeah, thank you for this great question. No, thank you. Ladies and gentlemen, we have reached the end of today's question and answer session. I would like to turn this call back over to management for closing remarks. Well, thank you so much, gentlemen, ladies, for spending your precious morning with us, and you have been with us all through those years. It's all of our dream to bring plinabulin to millions of patients in need. Thank you so much for your support. Have a nice morning. Goodbye. Thank you for joining us today. This concludes today's conference. You may disconnect your lines at this time.