Brii Biosciences Limited (2137) Earnings Call Transcript & Summary

Good morning, good evening, everyone. Thank you for joining our AASLD Data Readout Investor Call today. Before we start, I would like to remind you that statements made during this call may include forward-looking statements. The company is not obligated to update these statements based on new information or events. This is Sarah Qiu, Associate Director of Investor Relations. On today's call from Brii Bio's executive management team, we have Dr. Zhi Hong Chairman and Chief Executive Officer. Dr. David Margolis, Chief Medical Officer; Dr. Qing Zhu, Head of China R&D; and Dr. Ankang Li, Chief Strategy and Financial Officer. Dr. Hong will provide opening remarks, followed by Dr. Margolis discussing our AASLD presentation. Dr. Zhu and Dr. Li will join the Q&A after the prepared remarks. And finally, Dr. Hong will close with final remarks. Now I would like to turn the call over to our CEO, Dr. Hong. Please go ahead.

Well, thank you, Sarah. Good morning, good evening, and welcome to this conference call. I know this is almost towards the end of AASLD. Some of this app show was published on Friday, I wish we can share this information as soon as we could, but we are under daily embargo from AASLD, so this is the timing of this press release and this update conference call is the result of this data embargo. But nevertheless, I want to give you a quick update on this ASRV. I think this is truly a very exciting meaning that where we have seen a lot of things begin to come together. And as you know, over the last 5 years, many companies, including ours, and continue to invest search in the -- for a cure for HBV. I think at this conference, a lot of Phase II data begin to read out. I think you can see -- for those of you, who have looked at the abstract, you will quickly understand that the entire industry has converged onto a number of very important directions, those that focus on antivirals and those are focused on immune modulators, among the most promising antivirals or the siRNA or the antisense oligonucleotide, among the immunomodulators. There's obviously data on [ PEG pegylated interferon ], TRR as well as immune checkpoint inhibitors and also for the [ adapt the immunity ] we've seen data coming out from a therapeutic vaccine, including ours. I have to say that where we are making a lot of progress. I think the journey to where we are today has truly been extraordinary. I can tell you from the data we have seen so far, I continue to support the direction of our HBV cure strategy. If anything, there's more data support, the choice of our investment in this area, specifically on BRII-835, the sRNA and the BRII-877 on the neutralizing antibody and also BRII-179, the therapeutic vaccine. Another main important thing that I want to let you know that together with our partner, Vir, we actually have 10 presentations at AASLD and 4 of which are late breakers making significant progress in both HBV as well as HTV. So we would like to give you some brief update on our program as well as some of the latest development from Vir, our partner's portfolio as well. So without further ado, I would like to turn this to our Chief Medical Officer, Dr. David Margolis, who will take you through on a deep dive in terms of what we have presented at this meeting. And for those of you, who obviously appreciate that we -- as a multinational company, we have the ability to do this conference call in both English as well as the Chinese. So for those of you, who are willing to listen for -- in the Chinese version, you welcome to join us later after this hour and then our Head of R&D, Dr. Chengdu, will present you in Chinese, the latest progress. So no worry, if you don't feel comfortable in asking questions at this English session, you can wait until the Chinese session. Or if you prefer to ask questions in Chinese, we can certainly answer your questions in Chinese. The executive team here are completely bilingual. So with that, I'm going to turn this to David. Please go ahead.

Thank you, Zhi, and I'm delighted to be able to walk you all through some of the data that we were able to share at the AASLD conference in Boston over the past few days. So as a reminder, Brii continues to have multiple clinical assets across a variety of therapeutic areas. Our Hepatitis B approach includes 3 clinical assets, all of which are now in Phase II development, BRII-179, a therapeutic vaccine for which we have global development rights in our collaboration with Vir has allowed us to focus on Greater China development for BRII-835, the siRNA approach and BRII-877 monoclonal antibody approach. Next slide. We continue to believe and believe also that the data from this most recent conference suggests the combination therapeutic approaches are likely going to be necessary for us to achieve functional cure in Hepatitis B. We're fortunate that we have access to multiple mechanisms of action for which we can look at a variety of clinical approaches and combination approaches. BRII-179 is an optimizer recommended vaccine containing S/Pre-S2 and Pre-S1 antigen and a [ viral-like ] protein has now been explored in 3 clinical studies. We'll share some immunologic data from one of the studies in further slides as well as some biologic efficacy data from another study. There have been over 180 subjects dosed. So we're starting to get a fairly good handle on the safety of BRII-179. BRII-877, of course, is a monoclonal antibody approach. We will also be sharing some evolving data from Vir with this compound as well as with BRII-835. Our -- at a very high level, our clinical development program is shown at the bottom, the BRII-835 plus BRII-179, we'll show some evolving immunology data, both T-cell and B-cell data from that program, BRII-179 plus pegylated interferon will show biologic efficacy data from a late breaker abstracts BRII-835 plus pegylated interferon is an ongoing study, where we continue to enroll to validate data that had previously been shown from the March study. And then lastly, a triple combination with the siRNA, the monoclonal antibody in pegylated interferon is data that Vir showed at this conference. Next slide. So the abstracts that we presented are shown here, 2 of which were late breaker acceptances as a posters in the last regular submission poster. I'll walk you through each of these. But just as a reminder, we'll be looking at immunologic data, both T-cell and B-cell efficacy data from BRII-179 combination with interferon and pharmacokinetic data from siRNA by looking at regional differences. Next slide. So first, we'll start with BRII-179 plus BRII-835. This is a study where safety and efficacy data has already previously been shared. We're going to focus on the immunologic data from this study. And as a reminder, we are looking at one arm with siRNA or BRII-835 alone and 2 arms with BRII-835 in combination with 9 doses of BRII-179 therapeutic vaccine. Next slide. So to the left, we'll focus on T-cell responses and to the right, we'll focus on antibody responses. It's important to note that most people believe to change -- attain functional cure, you likely need components from T-cell, humoral and antibody responses to establish a durable care. This data is important for us to help elucidate what type of immunologic coverage we have in the T-cell and the B-cell space, and we're learning more and more about each of these areas as we continue to look into our studies. Off to the left, we look at T-cell response by ELISpot and the top row is in a cohort A, BRII-835 alone and a combination of Cohort B and C in the bottom row, BRII-179 plus BRII-835. You can see to the left, minimal ELISpot response to have these specific antigens observed prior to dosing. And in the top column, some evolution of our primary S antigen response in the BRII-835 alone treated subjects. When 179 is introduced, we see a significant increase in the breadth and the strength of the T-cell response as noted by ELISpot, which increases over time and it's notable virtual reactions or broad spectrum of hepatitis B antigens. To the right, we have previously shown some antibody data for shorter-term vaccine dosing. But here, we can see evolution of the antibody response with significant strong anti-HBS responses elicited in some, but not all chronic HBV patients and the evolution of that response over continuous dosing. Similar kinetics were observed in patients receiving 4 or 9 doses of BRII-179 with or without BRII-835. We believe that it's important that there are some individuals, who are not able to fully elicit a response to BRII-179 suggesting those groups of individuals may be immunologically in confident to response and less likely to respond to functional cure. Next slide. So now we'll shift gears and look at the BRII-179 plus pegylated interferon study with a focus on biologic efficacy in correlating the antibody data that we just saw with outcomes. In this Phase II proof-of-concept study in China individuals with a heavy surface antigen less than 1,500 were initially treated with interferon across both owners. The initial phase of this study involved assessing the hepatitis B surface antigen response to interferon and individuals, who had a partial response with a heavy surface antigen between 100 and 0.05 were then eligible to be enrolled at Study Week 0 to either receive 7 doses of BRII-179 or interferon alone. In all cases, the interferon was then continued for further 6 months. So ultimately, all individuals received 1 year of interferon and 6 months of BRII-179 or placebo. The week-24 time point is the end of treatment time point and week 36, which is also shown here, gives us 12 weeks of off-treatment follow-up data. Next slide. Firstly, the BRII-179 plus pegylated interferon combination was generally safe and well tolerated. This is now our third study with BRII-179, and we did not identify any unique adverse events associated with BRII-179 during the conduct of the study. A fuller briefing of the safety is shown in the poster, which was presented at the conference. In the graph to the left, we're looking at hepatitis B surface antigen at the end of treatment week 24 time point and 12 weeks off of treatment week 36. The solid bars represent the intention to treat population and the dash bars represent the per protocol population. In this particular study, the per protocol population can be treated -- as treated population because this study was conducted during the COVID lockdowns, a number of individuals did not receive the full course of treatment and therefore, are more accurately represented in the per protocol population. In both groups, a delta favoring BRII-179 was seen with improved rates of HB surface [ seroclearance ] in the BRII-179 treated subjects. This difference was mained and/or increased following 12 weeks off of treatment as companies seen on the graph to the left. In the graph to the right, you're looking at hepatitis B surface antigen seroconversion defined as Hep B surface antibody greater than 10 I used per liter in combination with surface antigen loss. Here, we see strong correlation between antibody presence and use of BRII-179, linking that to surface antigen loss. And the next slide, we'll look at further details on the antibody response. So here, we're looking on the left side at different titers, greater than 10 on the left side and greater than 100 IUs per liter on the right side. BRII-179 leads to significantly higher anti-HBs levels than interferon alone treated subjects for both titers. Between 40% and 50% of individuals are able to generate greater than or equal to 10 IUs per liter and approximately 20% are able to generate 100 IUs per liter. In a multi-variant logistic regression within this study, we established that the presence of antibody titer greater than 10 or greater 100 was highly correlated and highly statistically significant with surface antigen loss. Next slide. So now we'll turn to the BRII-835 pharmacokinetic data. This study continues our collaboration with Vir and helps us establish the pharmacokinetic data with siRNA across regions inclusive of both APAC in the study on the left in China in the study to the right with a single and repeat dosing. Next slide. And here, we see similar PK profiles, whether or not individuals were enrolled in APAC or Mainland China across 2 different dosing cohorts and statistically comparable systemic exposures, demonstrating the PK characteristics of BRII-835 and participants with chronic HBV infection, some patients is similar to that reported from previous studies with healthy volunteers and Chinese ethnic background from Mainland China had no apparent impact on pharmacokinetic exposures. This data will help us bridge from ongoing studies around the globe, the additional studies, which will be conducted within China. Next slide. So our partners, Vir, also presented a number of data outputs from their programs, and we'll focus on the 2 at the bottom. This is looking at VIR-2218 and VIR-3434 sRNA plus monoclonal antibody with or without pegylated interferon for the treatment of chronic Hep B this is continuation of the March study Part B, which looked at various combinations of siRNA and monoclonal antibody. We'll also look at their data in chronic hepatitis D. Next slide. So firstly, we're looking at here the combination of VIR-2218 or -- and VIR-3434 and its effect on hepatitis D, whether in isolation or in combination. So you can see with the each monotherapy agent, whether it's with VIR-2218 or VIR-3434 modest effects, we're seeing in reduction from baseline and hepatitis D with a minimal number of individuals achieving below the quantitation of the level of quantitation or the limit of detection. However, when administered in combination, there was appeared to be optimal FD antiviral activity with a 100% of patients achieving HDV RNA less than limited quantitation and 80% lower than limited detection. ALT Safety was good in this study with one individual having a transient ALT rise in the VIR-2218 arm, but no individuals having ALT safety concerns in the combination. And lastly, we'll look at the follow-up from the MARCH study. MARCH study is a multi-cohort study looking at various durations and various combinations of VIR-2218, the siRNA with or without pegylated interferon and with or without monoclonal antibody combination. Previously reported or various combinations of siRNA at various durations with pegylated interferon, I won't discuss that data in detail. We have discussed previously the far right, which demonstrates that siRNA in combination with longer durations of pegylated interferon is able to achieve approximately 30% surface antigen loss rate. That's the data which prompted the additional follow-up study, which we're now conducting exploring the larger cohort of siRNA plus pegylated interferon in a controlled fashion. The new data shared by Vir at this study -- at this AASLD conference is highlighted in the purple and the blue columns were VIR-2218 plus VIR-3434 for 20 weeks as shown in the purple column and in combination with pegylated interferon in the blue column. In both instances, surface antigen lost was observed at end of treatment in approximately 15% of individuals. What's interesting here is that the dual combination without the presence of interferon is able to achieve surface antigen loss rate comparable to that without interferon, suggesting the possibility of further enhancement for pegylated interferon III regimen. That, of course, requires further validation in additional studies. Next slide. So now taking a step back again and just focusing on our overall hepatitis B care strategy. We continue to believe that this will be an iterative process, where multiple combinations are explored, and we feel that out of this conference has come a number of different important studies, which gives us confidence about our approach. We will be initially building on the Phase II results, which I've highlighted already, inclusive of BRII-835 combinations with interferon and now BRII-179 combinations with interferon to establish initial efficacy studies and confirmatory studies, validating surface antigen loss in those populations. We will then continue our collaboration with Vir and with others to optimize combinations for broader populations, targeting increased cure rates over time, 30% to 60% range and ultimately, to tackle all hepatitis B patients, giving them access to potential curative regimens. It's likely that additional agents will be needed. Next slide. We continue to release data across a multitude of combinations. Most of the data, which I have just talked about is already highlighted here, and we're working in close collaboration with Vir to ensure that we optimize collaborative potential, particularly with BRII-179 where we're now establishing a biological effects correlated with the antibody and T-cell production, which we've identified following the dosing of BRII-179. We'll continue to share data as it evolves, but we really look forward to your questions and the discussion around the data, which we've just shown.

Thank you, David. I think we're ready for questions. I will be trying my best to direct the questions. So let's open that up.

Okay. The first question is coming from Roanna from Leerink.

This is Rosa Chen on for Roanna Ruiz at Leerink Partners. Thank you so much for sharing your data. I'm going to ask the question in English if that's -- okay. Great. This is Rosa Chen on for Rane at Leerink Partners. Thanks so much for sharing and highlighting your recent data.

Maybe just lost the connection here. Roanna maybe we'll go to the next...

No, no, she's back. She's back.

Okay. Okay. Great. So in your Phase II interim study for BRII-179, it seems like there were 3 treatment emersion, a, is that led to discontinuation of BRII-179 and then also some grade 1 and 2AEs. So can you provide some additional details as to what these AEs were? And is there a way to mitigate this moving forward?

Okay. I'm going to turn this to David.

Yes. So the AEs that led to discontinuation were for proteinuria, pulmonary tuberculosis, pruritus and an issue with gastric emptying. So these were not necessarily felt to be related to study product, but nevertheless, led to discontinuation of dosing. And I don't believe we found a signal that was tightly associated with BRII-179 itself outside of ISRs, which were commonly reported with BRII-179 dosing, but there were no discontinuations due to ISRs. Most of the ISRs were considered mild or moderate.

Got it. That's helpful. And then a second one, the same study from weeks 24 to week 36 of treatment, we saw that antibodies titers continue to rise, but s-antigen loss slightly decreased or it was kind of flat from week 24 to week 36. So do you have any speculation as to, why? Since we typically expect the s-antigen to decrease with the treatment duration. And then you see the signal with the increased antibody titers, which is also positive.

Yes. So I can start and maybe others can comment. So I think -- this is probably the most critical finding from this study establishing the correlation between the antibody -- presence of antibody and surface antigen loss. So I think, while you're highlighting the persistence of the effect in the BRII-179 arm, what we think is actually most interesting here is that it's very likely, given the relatively lower surface antibody titers that are observed in the interferon arm that you may begin to see rebound. So the increasing delta that we're observing between week 24 and week 36 is essentially due to rebounding cases, where the surface antibody may not be high enough to hold. We're not necessarily expecting although we could see some additional surface antigen loss. But I think the most important finding is going to be seen whether or not we can maintain the durability of the response or whether or not there will be a rebound. And our hope is with the potent antibody levels we're seeing that we'll be able to maintain that response over time.

If I may add just that there are 9 -- there's 9 patients here converted in the BRII-179 group versus 1 in the peg interferon only group. There are 5 rebound between 24 weeks and 36 weeks as the 12 weeks follow-up. 4 of them have no antibody response. And one of them have a low antibody response. Now bear in mind, this is still a group level blinded data. So we don't know specifically which one. We can only tell from a rebound data, whether or not they have antibody response or not at the group level. So this is not at a patient level has not been unblinded, yeah, it's only unblinded at the group level.

Got it. Super helpful. And then one final big picture question. Do you plan to go forward with the Phase III using Peg-interferon and BRII-179? Or could you consider replacing Peg-interferon with a different mechanism that is also an immunomodulator and immunostimulant with maybe better tolerability? And like noteworthy that your partner of your present is pretty compelling data showing the same s-antigen clearance with Peg and without Peg. So is that something that you could consider adding VIR-3434, VIR-2179. What are your thoughts on that?

Yes. So these are indeed a big direction kind of question. We are very pleased with the versatility of BRII-179 because on one hand, we think we can use it to select patients to enrich patient and to identify patients who have a sufficient intrinsic antibody immunity. On the other hand, we have shown with the Peg combination that it does generate functional antibody that can directly contribute to the clearance of surface antigen and more importantly, sustaining that surface antigen clearance. There are obviously thought about if there's other agent can remove the surface antigen to undetectable level, whether or not the BRII-179 can be used as a booster to stimulate, seroconversions and as a way to sustain the clearance of surface energy. So there's a lot of ideas that we're looking at that. Obviously, I think our immediate focus is to move on into some studies that we will design and such that it will be definitively addressing some of this efficacy and safety end point. So we're in the process of engaging regulatory authority to determine, what are the top 2 or 3 study that like to move forward quickly. I think clearly, the goal here is to design the study to definitively address the efficacy and safety end point.

We also have an off-line question here on the competitive landscape. How to interpret the rationale behind the GSK deal, what's the difference between Brii's sRNA and J&J's? And if you can comment on that? And if Brii has any [ Hp B, BD ] plan? And what's the strategy here?

So it's our general practice that we do not comment on our competitors program unless it's already been published. So I think from the published results, that we do know that in the [ J&J sRNA ] program, there's 2 sRNAs that are targeting different site on the BioGenome. I believe one of them is at the DR1. The other one is in the overrating frame of the gene. Our sRNA is a single trigger so-called single trigger sRNA that targeting DR2 region. So that's one difference that I can share with you. I think from the clinical data perspective from our published data, I think all the SMA and seems to produce the same reduction of surface antigens. They all seems to be plateaued at around 2 logs and maybe a little bit more than 2 logs. I think at the very beginning, it was a little bit confusing that people who were seeing a different log drop, and that's because the dosing regimen was very different. Some was given on a very short a few doses others are given multiple doses and for longer duration of time. But it's fair from all the study we have seen so far, pretty much for all the sRNAs, it seems to relate some [indiscernible] between to 2.0 to 2.5. I think that's -- I don't think from a clinical perspective, there is no difference between the 2 sRNA program. And we cannot really comment on why they do the deal. I think clearly, this is something that may be better addressed by us being GSK directly the question. So I think that's hopefully answer your questions.

Okay. Thank you, Zhi. We will go next to David Guo.

May I ask something that is not really science related, but about the PreHevbri vaccines? Are there any updates from the discussion with [ CDE ] and other regulatory and any updates on that, please?

I would direct this question to [ Chung ] our Head of R&D in China.

For the -- just for the PreHevbri, we submitted pre-IND and we already had some discussion with Citi. So we're waiting for the normal meeting schedule in probably the early next year. I'll answer your questions. And then this will -- let us know what is required to continue to work on PreHevbri to bring to the China market.

Okay. Great. And do you have any expectations like the process ongoing, what kind of steps we may need to go through?

No, not really. So that's why we're waiting for the meeting scheduled, but we did submit our clinical study design. So we're hoping to get some feedback on this study. So do we have a clear path forward what you do with the PreHevbri registration.

And we also have another question on next steps. On BRII-179 new combination trials. If we can have an update on that and if there is any sequence of prioritization of launching BRII-179 in APAC and globally?

Yes. So as I mentioned earlier on, we are considering multiple combination. One of the study, we hope to start. And I think we are following regulatory document. We believe this is a subsidy of an ongoing study, where we are calling back all the previous patients that have been exposed to BRII-179 that we know their antibody response and their antibody phenotype. So we believe this group of people will be important for us to bring them back for a curative treatment in which we can and then determine whether or not how the antibody response guided curative treatment is an option for further improving the functional cure. So that study we can start before the end of the year. And then hopefully, we can share this information after we complete the study. And then we obviously consider a couple of other studies, where we've been in active discussion with regulatory authority to make sure that we can align on the study designs. And then obviously, you know this is, it will take some time. But we are very excited about some of these programs we should be able to embark on next year. I think this is something that we're very excited about it. We hope to design the study to definitively, as I mentioned early on, address the efficacy as well as the safety endpoint. So providing a very clear level of functional cure rate that we can anticipate. So clearly, we have multiple POC study, as I mentioned to you at the beginning of the call that Vir -- together with Vir, we are absolutely working on 5 or 6 different combination and data continue to reading out. And then from those readout, then we can design on the definitive study as a next step. So for those of you, who before us for a while that it's -- right now, I think the time is here not for us to transition all our combination studies, treatment options into late stage. So all of them will be designed to definitively answer the question with the right regimen potentially in the right patient population. So that's all I can see. I'm sorry that I'm a little bit vague, because I can't really say too much without getting alignment with the regulators. So that has to go first. I think somebody asked the question early on, with BRII-179 because we're holding the global rights. So that does give us the opportunity to talk about studies globally, either in partner with our -- in partnership with our partners or new partners. And that's what we are trying to do. So clearly, we're not going to start the BRII-179 program just in Greater China, and we're going to expand that study globally. So more to come, but I can't really comment in detail without having alignment on discussion with the regulators.

Thank you, Zhi. Okay. I think that concludes today's Q&A session. Now I will hand it over back to Zhi for some final remarks. Zhi, please go ahead.

Well, thank you very much for joining us. I know there's a lot of data to digest and I really appreciate all the support you have given us in the past. I think we, as a company, have gained a lot of insight through our own studies as well as our partner studies. I can categorically make the following comment. Hopefully, you agree. Compared to a few years ago, it's no longer a challenge for us to dramatically reduce the surface, the energy level and even to clear those service antigens. I think we have the tools available to do that, and that including our program as well as our competitors' program. So that's one thing that's very, very important that we have gained significant insight over the last 5 years. The second insight that we have gained and we've learned in the past 5 years was in order to sustain the clearance of surface energy, you must have immunologic control. In this case, we have, again, significant knowledge with the enzyme related to the antibody response, multiple study have shown that we're -- if you have a strong antibody response, then you have a much better chance to sustain the clear of surface antigen. And these are coming from a study that is done with sRNA as well as with Pegylated interferon. So antibody response is very important. At the same time, we also know through our own study that were a broader T-cell response is also important. In fact, in some of the study patients that we have seen in the BRII-179 process BRII-835. And those patients who have achieved loss of services antigen, they have very robust antibody response as well as T-cell response. So we're very pleased to have a therapeutic vaccine BRII-179 that allows us to broadly activate the T-cell response and then more specifically, activate a strong antibody response in a significant proportion of our patients. So we do believe that having both T-cell response and B cell response are very important. However, given the variability and the challenge of doing T-cell response analysis, and it's not always easy to correlate with the T-cell response because it's very broad, it's variable. With the antibody response, however, it's very easy to measure, and it's very specific. So we believe the -- we have learned in the last 5 years having a strong antibody response is highly correlative to the sustained clearance of surface antigen. So that's the second thing we learned. The last thing we learn is the challenge of curing HBV mostly because the [indiscernible] of the HBV patient not only with regard to the service antigen level at the baseline. Also, there are intrinsic immunities. There's really not a very good way of telling through biomarker research in terms of who has a stronger or more robust or more sufficient intrinsic immunity with regard to T-cell as well as B-cell, who does not. And we believe these -- the 3 study we have completed on the process of completing has gave us a lot of insight for a very unique opportunity to allow us to very safely select patient, who have strong intrinsic immunity that most likely will respond. And then at the same time, allow us to spare others, who probably does not have sufficient immunity to be treated at this point. It's not to say they will not be treated in the future. Obviously, it requires additional tools that has yet to become available. So these are the 3 things that I can share with you and that we continue to follow the landscape very closely. And at the same time, and invest in the direction that I just highlighted to you. Number one is to enrich patients to identify patients, who are most likely to respond. Number 2 is to clear the service antigen to the highest level we can with sRNA a combination of sRNA and neutralizing antibody. And lastly is to generate robust antibody response. And with this -- with T-cell response together to sustain the clearance of surface antigen. So these are the direction that we have just lay out. I think it's becoming clear now compared to a few years -- a couple of years ago that in terms of where we're going. So I want to thank you all for your patience and for appreciation of the work that we have done so far. And I really hope in the next 12 to 18 months, we're going to have some really exciting data to share with you. And so stay connected, and I appreciate all your support. So at this point, I'm going to draw close to the call. And I just remind you that we have a Chinese Conference Investor Call that's coming up in about 13 minutes. I look forward to communicate with the latest results in Chinese with you. Thank you very much.

Thank you, all of you for joining today's call. Good Bye.