Assembly Biosciences，Inc.（ASMB）首席執行官就乙肝計劃更新電話

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Assembly Biosciences, Inc. (ASMB) CEO on Hepatitis B Program Update Call Transcript
Feb. 28, 2021 4:57 PM ETAssembly Biosciences, Inc. (ASMB)

    Q4: 2021-02-25 Earnings Summary

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Assembly Biosciences, Inc. (NASDAQ:ASMB) Hepatitis B Program Update Conference Call February 25, 2021 5:00 PM ET

Company Participants

Lauren Glaser - Senior Vice President of Investor Relations and Corporate Affairs

John McHutchison - President and Chief Executive Officer

Bill Delaney - Chief Scientific Officer

Luisa Stamm - Chief Medical Officer

Conference Call Participants

Brian Skorney - Baird

Raju Prasad - William Blair

Michael Yee - Jefferies

Geoffrey Porges - SVB Leerink

Salim Syed - Mizuho

Nicole Germino - Truist

Operator

Good afternoon and welcome to the Assembly Biosciences conference call. At this time all participants are in a listen-only mode. After the prepared remarks, we will conduct a question-and-answer session. As a reminder, this conference call is being recorded.

I would now like to turn the call over to Lauren Glaser, Senior Vice President of Investor Relations and Corporate Affairs for Assembly.

Lauren Glaser

Good afternoon, and thank you for joining us as we discussed the Hepatitis B program update that we announced today. This press release is available in the news and events section of our corporate website at www.assemblybio.com. Our corporate presentation is also available in the same section of our website as a reference, though we will not be referring to it specifically on this call. Please note that a replay of today's call and audio webcast also will be available from our website. In a moment, I will turn the call over to our Chief Executive Officer and President Dr. John McHutchison to provide opening remarks and then we will host a Q&A session. Joining John for the Q&A portion of the call will be our Chief Medical Officer, Dr. Luisa Stamm; our Chief Scientific Officer, Dr. Bill Delaney; our Chief Financial Officer, Tom Russo; and our Chief Legal and Business Officer, Jason Okazaki.

Before we begin, I want to remind you that we will be making forward-looking statements including statements regarding our future research and development plans, evaluation of intern data, the timing of clinical trials, trial results and therapeutic potential of our research and development program. These statements are subject to the Safe Harbor protections provided under the Private Securities Litigation Reform Act of 1995. They involve certain assumptions, risks and uncertainties that are beyond our control and actual results may differ materially from those forward-looking statements. A description of these risks can be found in our latest SEC disclosure documents and press releases. Assembly does not undertake any obligation to update any forward-looking statements made during this call.

I will now hand the call over to our CEO, Dr. John McHutchison.

John McHutchison

Thanks Lauren. And thank you to everyone for joining us today. As I've shared with you since I joined the company in 2019, our vision and ultimate goal has been and continues to be curing patients with Hepatitis B and freeing them from the burden of a lifetime chronic treatment. In order to advance and accelerate our progress towards that goal, we have decided going forward to focus our efforts with vebicorvir solely in Sinai's incurred in combination for Hepatitis B, rather than continuing to pursue a chronic suppressive therapy indication in parallel. This afternoon, we would like to provide more background on that decision, as well as an update on our overall Hepatitis B strategy. And our expanding research pipeline, which includes work on our fourth-generation core inhibitor. Work on cccDNA disruptors and other preclinical programs focused on novel Hepatitis B virus targets. And of course, we're happy to answer any questions you may have as Lauren said.

The greatest unmet medical need for Hepatitis B patients is a finite and curative therapy and solving for that has always been the ambition of this company and the team with you on the call today. I remember saying to you when I joined Assembly about 18 months ago that I believe and I still do that we will cure this disease as we did Hepatitis C. Of the approximately 270 million Hepatitis B patients worldwide, only 5 million or so are currently being treated. While those treatments are safe for most patients they are also lifelong. In order to truly change outcomes for patients with Hepatitis B infection and treat a far greater proportion of these patients, it's clear that we need to more than just a chronic viral suppressive type approach to therapy. With a finite and curative combination therapies and based upon our work so far, we are confident and I am confident that core inhibitors will be a central part of this.

As you know, our pipeline includes the most advanced and potentially best in class core inhibitor candidates in developed. In Phase II trials, vebicorvir plus Nuke therapy demonstrates deeper viral suppression with a favorable safety profile, which was an important step for the Hepatitis B field. A step that we plan to build upon through continued development of vebicorvir vial, as well as our next generation more potent core inhibitor candidates. We believe the combination of these potent direct antiviral mechanisms that is called plus new that suppresses viral replication to levels that could not be previously achieved. Perform the backbone for combination therapies that remain central to our finite and curative strategies. We know that finite and curative therapy is still a way off particularly in light of the Study 211 results we shared with you in the fall.

However, we've always viewed the pursuit of cure as a longer-term endeavor. And it was that insight that drove us to evaluate in parallel near-term opportunities to bring a more effective chronic suppressive therapy to patients who do not currently achieve adequate or complete viral suppression with the standard of care therapy. As you recall, last year, we completed our interactions and received regulatory go ahead in China, to commence two Phase III registrational studies to evaluate vebicorvir as a common chronic suppressive therapy in different populations. China obviously has a large Hepatitis B prevalence and its regulatory agencies are therefore eager to consider new treatment options. As we plan for those studies with our partner BeiGene, we met with experts around the world and then also initiated discussions with the FDA, with the intention of issuing a global chronic suppressive therapy program.

FDA feedback, however, has been different from that as the Chinese and in PA and we do not see a clear path forward in the US for this approach, given FDAs view that the vast majority of these patients are in large part served by the current standard of care. And discussions with hepatitis experts have also indicated that this type of approach of an add on to suppressive therapy is less of a need and less valued in terms of what training physicians need or want for their patients. So after significant internal and external discussions and analyses, including discussions and agreement with our partner BeiGene for the China territory, we have concluded that rather than proceeding with the Phase III suppressive therapy studies, we should go all in and focus our efforts on finite and curative therapies. We believe this represents the greatest unmet medical need for the Hepatitis B patients that we serve, that has the potential to create the greatest value for our organizations as well.

With the decision to not pursue chronic suppressive therapy, we can now concentrate our resources on finite and curative therapies, including initiation of the planned triple combinations with vebicorvir, as well as additional potential combination studies and study arms, advancement of more potent next generation core inhibitors, an expansion of the breadths and depth of our research and discovery program. Redirecting the resources previously reserved for those registrational studies, and other related activities will allow us to advance all of these initiatives faster, while simultaneously extending our cash runway into 2023. I know I've already provided a lot of information and updates to you. So in light of all this, let me review for you the three key components of our Hepatitis B strategy, and how our current and future pipeline will drive our progress.

First component centers on advancing our portfolio of leading core inhibitors to select the best molecule to bring forward as part of finite and curative combination strategy. We have three potent core inhibitors in the clinic. And we are planning on selecting a fourth-generation compound in the first half of this year, which I'll speak more about shortly in discussing our new research discovery program. All four core inhibitors have different scaffolds and present a unique opportunity to more deeply suppress viral replication, and hence been an integral component of the drive towards finite and curative combination regimen. However, we do not plan on bringing all four core inhibitors forward in sequential and similar fashions, but rather, we will execute on our concise data driven development plans to select the optimal core inhibitor that we'll be then able to use in latter stage finite and curative combination studies.

This leads me to the second component of our strategy, advancing proof of concept triple and potentially quad combination studies with Nukes and our core inhibitors. The initial step in this approach includes vebicorvir combined with a Nuke, serving as the antiviral backbone of these planned triple combination studies, two of which we expect to initiate in the first half of this year. As previously noted, the combination of vebicorvir and Nuke has already demonstrated potent antiviral activity and a favorable safety profile in Phase II study, so its ideally situated now for those proof-of-concept studies. As the other core inhibitors progress, and if they show a differentiated efficacy and safety profile, we'll be able to bring them forward into this part of the strategy.

Earlier today we announced the initiation of a Phase two trial evaluating vebicorvir plus Nuke in combination with interferon in treatment naive Hepatitis B antigen, positive subject. In addition to its antiviral effects, interferon has many pleiotropic immunological effects that are beneficial in augmenting both specific and nonspecific Hepatitis B related immunity. Notably, this is a drug that has shown the highest rates of F loss in combination with a Nuke in previous controlled studies. The other combination trial with vebicorvir we anticipate initiating shortly is being conducted in collaboration with our Arbutus combining their RNAi therapeutic candidate AB-729, with vebicorvir and Nuke in a Phase II trial enrolling virologically-suppressed entities E antigen negative subject. RNAi AI has been shown to inhibit viral antigen production, and its effects on surface antigen also offer the potential to restore the immune response to Hepatitis B.

In both triple combination studies, we'll be evaluating the safety and on treatment response of the three-drug combination, versus each of the two drugs in combination with Nuke. If the data suggests in each of these trials, enhanced on treatment efficacy parameters, we then have the option to incorporate modified stopping criteria to assess off treatment response. We also continue to explore additional combination studies to evaluate the core inhibitor vebicorvir for now, and Nuke backbone together with one or potentially two other mechanisms. So please stay tuned here also. In parallel with the vebicorvir combination studies I've just described, we are actively advancing our pipeline of more potent next generation core inhibitors. The most advanced 2158 has been shown to be tenfold more potent than vebicorvir against the formation of new cccDNA in, in vitro lab studies. In Phase Ib, 2158 demonstrated potent antiviral activity, and a favorable safety profile when dosed once daily for 14 days.

Our Phase II trial of 2158 combined with a Nuke is ongoing in treatment naive E antigen positive subjects and we hope to report interim data later this year. Additionally, we'll be evaluating the changes in DNA, pre-genomic RNA and other HPV related viral antigens, and comparing that to our prior data in the same population that were treated with vebicorvir. If these data suggest that the increased potency observed with 2158 in the lab has translated to improve clinical efficacy on treatment, we'll also be able to incorporate modified stopping criteria for the purpose of evaluating off treatment response. Additionally, we also have 3733, which recently completed an initial Phase Ia evaluation in healthy subjects.

And as I mentioned earlier, we are very excited with our progress towards nomination for fourth core inhibitor candidate during the first half of this year. In our fourth-generation core inhibitor we are aiming for compounds with a potential best in class profile. This will include greater potency, that is single digit nanomolar potency again cccDNA formation and also antiviral potency. Of course, it will have pan-genotypic Hepatitis B activity, the clean preclinical safety profile, high solubility, once daily single pill dosing, and the potential to be co-formulated with other therapeutics in a fixed dose combination regimen. Once we nominate our fourth-generation core inhibitor, we will proceed as quickly as possible to develop all four of these compounds as I've described them today with a data driven approach to ultimately advance only on most promising candidates into latter stages as I've outlined, so again, stay tuned there please.

The fourth-generation core inhibitor actually leads me to the third and final component of our strategy, which is expanding the breadth and depth of our research engine beyond the core inhibitor mechanism. In 2020, we made significant strides in expanding our pipeline of research programs, both internally and externally. As we announced also back in November, we obtained options rights to core protein cccDNA disruptors arriving through a research collaboration with Door Pharmaceutical. Door's discovery platform targets different phases of the HB virus replication cycle distinct from viral assembly, and they have the potential to interfere with viral nucleic acids, including cccDNA transcription within the nucleus of the cell with a mini chromosome reside. This could prove a strong complimentary mechanism of action to our core inhibitor pipeline. For over a decade, the holy grail of the Hepatitis B cure field has been to develop therapies that target cccDNA to able to grade, disrupt, prevent transcription, or silence this reservoir. So we're very excited about this novel small molecule approach.

At the same time, our internal research team has worked very hard on unique Hepatitis B targets that we believe are also differentiated in the space and have the potential to accelerate our progress towards those finite and curative therapies for Hepatitis B. These research programs have coalesced from the decades of experience that our CSO, Bill Delaney had dedicated to pioneering Hepatitis B virus biology and virology, as well as the contributions of his group, of course. While it would be premature to disclose those two specific targets, we can tell you that we have two novel differentiated projects underway, and we will keep you apprised of this work as it progresses.

The emergence of our early-stage pipeline is further evidence to me that we now have precisely the right people in place to pursue our vision. Many of us have spent a large part of our careers in virology and Hepatitis B remains a critical and exciting field of research focusing on very pervasive difficult to cure viral disease. Our world class team has extensive Hepatitis B experience, a very strong track record executing in viral hepatitis, and is committed to advancing the field of HBV research towards this goal of finite and curative therapies for patients with the disease. We are all excited to develop our leading core inhibitor portfolio and accelerate our novel discovery programs to drive us closer to that finite and curative therapy approach for these patients.

With that, we are now happy to take your questions. As a reminder, Luisa, Bill, Tom and Jason are all here with me. So operator, would you open the question-and-answer session line please?

Question-and-Answer Session

Operator

Thank you. [Operator Instructions] And our first question comes from Salim Syed from Mizuho. Please go ahead. Salim you might be on mute. Our next question comes from Brian Skorney from Baird. Please go ahead.

Brian Skorney

Hey, good afternoon, guys. Thanks for taking the question. Thanks for the update. I guess maybe you can just dig a little bit deeper into kind of the thoughts on not pursuing the chronic indication for the quarter of year and really going full bore into targeting sort of acute therapy? I mean is there any new data that's been generated sort of in the space that kind of gives you confidence and a pathway to achieve here, particularly with core inhibitors? And then maybe the second question on the Nuke, vebicorvir pegylated-interferon Phase II triple combo study, just thoughts on is this primarily just kind of a safety of a triple combination study? Or do you think they'll be durability of treatment here that would eventually lead to maybe some sort of stopping criteria as well? Thanks.

John McHutchison

Hey, Brian, it's John. Thanks for the question. I'll start with the first. And then I'll hand it over to Bill in terms of that as well. And then I'll ask Luisa to comment on the triple combination therapy initiation was interferon in terms of is it safety or efficacy and what the plan is? So to answer your question, it's a new data that give us greater confidence that - a corridor curative regimens. It's clear to all of us that you must inhibit all evidence of viral replication even before you can cure anybody. So I think that's the premise. And we've seen levels of viral suppression with the core inhibitor Nuke that haven't been seen with epsilon before without first generation compound. And then we'll be looking at the more potent compounds which have been designed to be more potent against cccDNA. So we don't have new data in the clinic today. But the premise is there from a virological perspective. Bill, do you want to add anything to that, in terms of what Brian's asked here? He's asking, really, is there any new data that we have on the field test that sways as to think that a stronger antiviral backbone will get us towards a cure?

Bill Delaney

Yeah. John, so yeah, just to respond to that. And yeah, thanks, Brian. So I mean, I think greater potency, particularly against the second mechanism of core inhibitors, is really what we're driving after the ability to inhibit the formation of new cccDNA. So while we don't have new data. Just looking at the data that we have, in terms of the potency of the molecules that we have, the exposure that they achieve in the clinic, we're confident we'll reach a much higher level of inhibition with that second mechanism with our second-generation compounds.

John McHutchison

We have a slide, Brian, in our new corporate slide deck that's on our website that looks at the potency of the compounds and what we're hoping to achieve with the fourth-generation compound as well, that we've talked about. We're hoping we'll be able to advance and nominate that candidate soon, but that has a very attractive profile. So Luisa the second part of Brian's question, is this just the safety study with interferon or what is it?

Luisa Stamm

Yes, so we are happy to start our first triple combination study with an RTI core inhibitor vebicorvir and interferon just last week and the primary objectives are safety and efficacy. Initially, we'll be looking at on treatment efficacy, looking at the different viral parameters, DNA, pgRNA, and antigens with the dual combinations compared to the triple combination. Based on what we see there, we anticipate that we'll incorporate modified stopping criteria and be able to evaluate off treatment efficacy. What those modified stopping criteria are at this time is undetermined. We continue to analyze the data from study 211, the results of which we shared at high level last fall and I think about this question. We haven't reached a criteria there, but we're going to be looking at the on treatment response, and anticipate incorporating modify stopping criteria. And we'll share more details about that when we have more information.

Brian Skorney

Great, thank you very much.

Operator

And our next question comes from Raju Prasad from William Blair. Please go ahead.

Raju Prasad

Thanks for taking the question. Want to kind of discuss a little bit about how we should be looking at the potential interim data readout from the 2158 study in the context of the triple combo data as well as some of the stopping criteria comments you've made? Are there any specific data points that you're looking at internally there that that gives you - that will give you more confidence on a potential maybe 12-week regimen with the second gen core inhibitor? Thanks.

John McHutchison

Thanks Raj. I'll ask Louisa to answer the question first, and I might chime in a bit afterwards.

Luisa Stamm

Thank you. So as John mentioned, our current Phase II study with 2158, we'll be evaluating 2158 in effect of your end treatment naive A-antigen positive individual. We chose this population because of the dynamic range afforded and the ability to assess the impact of the second-generation core inhibitor on cccDNA and compare it to the prior results with VBR Phase II study 202 in a similar population. We are going to be doing cross study on treated comparisons of viral parameters including pgRNA, E antigen and correlated antigen. And to your point, we've started internal discussions about what statistically and clinically would be meaningful and give us confidence that 2158 is better than VBR. And as mentioned, we hope to have some interim data by the end of this year and that would be the earliest point at which we could be making this assessment. When we have more information about this we will be share it while we can.

John McHutchison

So thanks Luisa. Raj, we can look at 12 weeks, we can look at 24 weeks since the half-life of - lifespan of cccDNA is we believe somewhere in that range. So if this is more potent against the prevention of formation of new cccDNA, we'll be hoping to look for those differences. And we have a study conducted for now in the same population, as we did with vebicorvir. So that will be the approach. So again, it's going to be driven by the data. We have to see the safety. There's 80 patients in that study. It gives us a fairly good feeling. We know where we're going. And then in terms of the triple, you touched - talk a little bit about in terms of the triple, no, we've initiated and we said, we're going to initiate both of these two of our first triple combination studies now that we wouldn't be getting data to compare them with - to compare this experiment with two drugs with 2158 until the following year, so that would be another component here as well.

So look, we'll see how deep we can drive it down. We'll see if that multiplies stopping rules. We'll see how it compares with vebicorvir. We'll take a scientific approach and we'll work it out. And then we have 3733 and hopefully, we'll be able to accelerate our fourth-generation compound, as well. So that's the approach on the core inhibitors. But I do believe, and I think this gets back to Brian Skorney's question as well. You must inhibit all evidence of viral replication and shut the spigot off. And that's what we're trying to do, as well as prevent the formation of cccDNA. So thank you, Raj.

Operator

And our next question comes from Michael Yee from Jefferies. Please go ahead.

Michael Yee

Hi, guys. Good afternoon. Thanks for the call. Two questions, one is in relation to the chronic suppressive treatment strategy. I'm not sure if I caught it. But was there any incremental information from FDA or even China FDA that kind of that this is going to take too long or maybe there's just a market opportunity thing? Maybe just to shed some more light on what happened there and what BeiGene says. And then the second question is in regards to combination studies, can you comment how long the RNAi combo would be? And what kind of information you get out of that that would be good data? And what other types of combos could be possible, PD-1 to PD-L1 et cetera, TLR, maybe just a bit. Thank you.

John McHutchison

Thanks Mike. Congratulations on the birth of your son. I will absolutely talk first about the combinations, what we're doing with the siRNA and duration. In terms of other triples, let me just say that checkpoint inhibitors would be one. There are some other possibilities out there that we're considering and discussing as well. We could also look at quad arms as well in future studies and in other studies, we could add in a support mechanism of action, but duration of siRNA in the Arbutus collaboration Luisa?

Luisa Stamm

Yes. So as John mentioned, we're going to be again, looking at the triple combinations compared to the two double combinations. And we are targeting initially evaluation of safety and efficacy and virologically suppressed patients. As was mentioned, we're going to be starting the study in the first half of this year, and we'll share more details about the dosing and the duration at that time.

John McHutchison

Thanks Luisa. Mike, the first question about - a bit delving into the chronic suppressive therapy why the change in the strategy, what transpired? Look, the interactions with the Chinese regulatory body was a go ahead to populations, safety database, et cetera, so that was tied down. The FDA doesn't see it the same way. And they feel that most of these patients are currently served appropriately and adequately by standard of care new therapy with a very, very small niche population that are only partially virologically suppressed. So therefore, our global trial and our global plans wouldn't have been a global trial or plan if it would have been a china only territory plan. So we have these extensive discussions with BeiGene. And we came to the conclusion, so we've made to you today that we're not going to move forward with the chronic suppressive therapy, even one that's based alone in China.

We should put those valuable results into trying to cure patients, which is going to be more of a balanced approach. And it's going to take longer, we understand that. So it did become a discussion about well, it's a much smaller population, it's a niche population, it's going to take longer, is that really what we should be doing? So I think, to summarize for you, we listened to - over a period of many, many, many months, we listened to many constituents here. And I think we made the right decision, and we're doing what we shouldn't be doing, what's best for the patients, and certainly best for us, our company, our shareholders and our collaborators that we focus on cure, which is actually as I said, why I came to the company anyway. So that's what transpired, Mike, without getting into all the details. I hope that makes sense.

Michael Yee

That makes sense. Thanks John. And my son says you explored your data.

John McHutchison

Okay. Good.

Operator

And our next question comes from Geoffrey Porges from SVB Leerink.

Geoffrey Porges

Thank you very much. John, I have a fairly fundamental question which is, why did vebicorvir fail? You achieved for long, undetectable virus and virus came back? So what's your prevailing explanation for why it failed that you're trying to fit with more potency, because going down the side of a mountain faster doesn't necessarily make a big difference. So I mean you're trying to get to undetectable currently. So I'm trying to understand what failure mechanism are more potent for inhibitor is going to fit? And then if that's your prevailing assumption, then why spend any more money on vebicorvir?

John McHutchison

Thank you, Jeff. I think you've asked me this one before. So I'll start again, then I'll hand it over to Bill who's the virologist as well. And then I'll circle back on the why spend more money on vebicorvir. So we've had the discussion before. And it's not just about inhibiting what we can detect. It's about inhibiting new cccDNA formation. So Bill, perhaps you could add on a little bit more, would you mind?

Bill Delaney

Yeah, be the happy to John. Thanks Jeff. So this comes back to and I think, also touches on some of the earlier questions, the differences in our compounds. And while they're all potent antivirals and can interfere with the formation and release of new virus, they don't all have similar activity against formation of new cccDNA. And looking at the potency of vebicorvir for that second activity and the plasma concentrations it achieves and the protein binding for that compound, it isn't where it needs to be to really address that mechanism. And that's, that's why having a compound that's 10 more - tenfold more potent with 2158 we believe we'll be able to address that mechanism. And I think that's - I believe we haven't hit the threshold we need to hit in the clinic with vebicorvir. So that's part of our strategy answering that question in clinic. And then I think the second part as John talked about - second out of three is looking at combinations, which we've also discussed and the value of vebicorvir and pushing down anti-viral replication further during the combinations.

John McHutchison

So that's - thank you, Bill. So Jeff, it's about the second mechanism not just the antiviral potency, I think Bill's articulated that better than I can articulate it, as he usually does, in terms of formation of cccDNA. And then we're looking at other mechanisms as well, we've started our - and we've talked about initiating our first two triples. And as I've said to you today, I'm quite eager to do more of that. And we're sort of postured toward that today as well. And it might even involve an additional mechanism, so I've said, stay tuned. That's all I've said today.

The second part of your questions Jeff is why spend more money on vebicorvir? If I have a compound that assays with some enhanced potency according to what Bill's being able to show me in the lab, in the clinic, we can switch vebicorvir out. And that is what I've tried to say indirectly today. And we will do that by looking at our subsequent core inhibitors, when we have enough safety data and we can assume they're more potent against this mechanism of cccDNA formation. And I'd be very happy to do that and accelerate them and to switch them out into double combinations, triple combinations, and do all of those things that we need to do. So that is the plan. So I hope that helps and addresses your question.

Geoffrey Porges

Yeah, in the right direction, but thank you.

John McHutchison

Thank you, Jeff.

Operator

And our next question comes from Salim Syed from Mizuho. Please go ahead.

Salim Syed

Great, thanks for the question, guys. So John just one from me or maybe Bill, when I'm looking at Slide 16 in the deck, you guys have the VBR and 2158 and the cccDNA formation chart. I'm just curious where the 300 milligram sort of you think falls on this curve? Do you think that is - because you never got full cccDNA is inhibition with VBR, right? Even though it sounded like initially that for some reason, we would be able to achieve finite therapy with VBR. So I'm just curious here with the 300 milligram 2158, do you think you'll be able to get complete cccDNA inhibition? Does it fall on the bottom part of this curve?

John McHutchison

Bill, do you want to address the curve? You're on Slide 16. Yeah.

Bill Delaney

Thanks Salim. So this will certainly give us - if you're looking at Slide 16 this gives us a 20-fold multiple of what we could achieve with vebicorvir, which we certainly believe is worth exploring, and this will - this should be enough potency to start to inhibit that reservoir, and whether - the kinetics of it, we'll have to determine that in the clinic, but certainly believe that this is over an order of magnitude in terms of additional potency compared to vebicorvir. And how that will play out over time, we believe this is something that needs to be tested and will answer that question. Also that's why with our third compound, and then the fourth compound, while we're targeting an even greater level of potency, so that we could inhibit - maximize that inhibition on that second mechanism of action.

Salim Syed

Okay, thanks so much.

John McHutchison

Does that help Salim?

Salim Syed

Yeah, I think it helps. Thank you.

Operator

Our next question comes from Nicole Germino from Truist. Please go ahead.

Nicole Germino

Hi, good evening, guys. And thanks for taking my question. Two, as you were saying earlier your own on finite curative therapy. What data helped you with this decision and with BeiGene as well? And did that 211 play a key role in the decision? And can you elaborate a little bit more on the modified stopping criteria after the results from 211?

John McHutchison

Thanks Nicole. It's John. I'll start. We haven't talked about the modified stopping criteria. We have a scientific presentation coming up at a meeting that would look at some of the analysis of that data. But for right now, we haven't publicly talked about modified stopping criteria, if that's okay, for now. Study 211 did not play a part in the decision to not take for the chronic suppressive therapy. We had data in house in hand from study 211, based upon DNA and RNA that allowed us to have a provable endpoint for a better chronic suppressive therapy. So it wasn't the failure of our first experiment or our first trial, to be able to cure anybody or lead to an SVR upon cessation of therapy.

So with that as I said, and as I've responded to others today, we spend a lot of time as you always do when you're gathering information from regulators, you're gathering information from KOLs. You're doing all of that work to try and determine what you should do as well as planning your clinical trial. And we had a divergence of opinions between what we could do in China and what we could do with the FDA that meant that we would have ended up with a regional China only global suppressive - global chronic suppressive therapy trial, which is not really what we had envisioned we would be doing. And we had extensive discussions, with our partner BeiGene about what to do in China as well. So it was those discussions, but it wasn't the failure to obtain an SVR of a significant percentage in study 211 that changed that decision making process.

So again, I'll just say the chronic suppressive therapy was out in parallel strategy where we were trying to do these other things. Now that has changed because we can't do a global trial. And we don't want to do a regional trial. We've had extensive discussions. It's a very small population, and we think we should - we are best off and our company is best off. And our patients are best off if we put those resources into finite curative therapies. And that will also extend our runway. So that's what we've decided to do. And I think that's the best thing. It's the smartest decision in science. You gather data, you go down one path, you change your mind. That's what's happened here. It's a smart decision. It's not necessarily anything other than that. And that's what I would say to you today Nicole. I hope this answered both of your questions.

Nicole Germino

Yeah, that's helpful. Thank you so much.

Operator

We have no further questions at this time. I will now turn the call back to Dr. John McHutchison for closing remarks.

John McHutchison

Well, thank you, Jenny. We are excited about our singular focus on finite therapy and curative therapies moving forward. This is a longer-term effort. And progress will come incrementally over time, as I've said today and in the past also. But I believe it's the right thing to do scientifically and for the patients. And we believe it has the potential to create the greatest value for all the constituents moving forward. We are fortunate to have the programs, the team, the resources and the collaborators necessary to try and accomplish these goals. So with that, we look forward to providing you updates in the future on our clinical development and our research programs as they mature. So thank you all for joining us again today. And this concludes our call.

Operator

Thank you. Ladies and gentlemen, this concludes today's conference. Thank you for participating. You may now disconnect

StephenW

但是，我们一直将追求治愈视为长期努力。正是这种见识驱使我们评估近期并行的机会，以便为目前尚无法通过标准护理疗法实现充分或完全病毒抑制的患者提供更有效的慢性抑制疗法。您还记得，去年，我们在中国完成了业务往来并获得了监管机构的批准，开始了两项三期注册研究，以评估威比可韦在不同人群中作为一种常见的慢性抑制疗法。中国显然乙肝流行率很高，因此其监管机构急于考虑新的治疗选择。当我们与合作伙伴百济神州计划进行这些研究时，我们会见了世界各地的专家，然后还与FDA进行了讨论，目的是发布全球慢性抑制疗法计划。

但是，FDA的反馈意见与中国人和PA的反馈意见有所不同，而且鉴于FDA认为这些患者中的绝大部分在目前已得到服务，因此我们在美国并未看到这种方法的明确路径。护理标准。与肝炎专家的讨论也表明，这种添加抑制疗法的方法较少需要，并且在培训医师对患者的需求方面不那么有价值。因此，经过大量的内部和外部讨论和分析，包括与我们的合作伙伴百济神州在中国领土的讨论和达成的协议，我们得出的结论是，我们不应该继续进行III期抑制性治疗研究，而应该全力以赴并专注于有限的根治性疗法。我们认为，这代表了我们所服务的乙肝患者的最大未满足医疗需求，这也有可能为我们的组织创造最大价值。