Good afternoon, and welcome to 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. Good afternoon, and thank you for joining us as we discuss 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 interim data, the timing of clinical trials, trial results, and therapeutic potential of our research and development programs. 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'll now hand the call over to our CEO, Dr. John McHutchison. Thanks, Lauren, 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've decided going forward to focus our efforts with vebicorvir solely in finite and curative combinations 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 4th-generation core inhibitor, our work on cccDNA disruptors, and other preclinical programs focused on novel hepatitis B virus targets. 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 believed, 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. We need finite and curative combination therapies. 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 development. In phase II trials, vebicorvir plus NUC 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, as well as our next -generation, more potent core inhibitor candidates. We believe the combination of these potent direct antiviral mechanisms, that is core plus NUC, that suppresses viral replications to levels that could not be previously achieved, will form the backbone for combination therapies that remain central to our finite and curative strategies. We know that finite and curative therapies are 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 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 pursuing a global chronic suppressive therapy program. FDA feedback, however, has been different from that of the Chinese NMPA, and we do not see a clear path forward in the U.S. for this approach, given FDA's view that the vast majority of these patients are in large part served by the current standard of care. Our 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 treating physicians need or want for their patients. 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 and 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, and expansion of the breadth 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. The 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 4th-generation compound in the first half of this year, which I'll speak more about shortly in discussing our new research and discovery program. All four core inhibitors have different scaffolds and present a unique opportunity to more deeply suppress viral replication and hence be an integral component of the drive towards finite and curative combination regimens. 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 or potentially quad combination studies with NUCs and our core inhibitors. The initial step in this approach includes vebicorvir combined with a NUC 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 a NUC has already demonstrated potent antiviral activity and a favorable safety profile in phase II studies, so it's 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 II trial evaluating vebicorvir plus NUC in combination with interferon in treatment-naive hepatitis B antigen-positive subjects. In addition to its antiviral effect, interferon has many pleiotropic immunological effects that are beneficial in augmenting both specific and non-specific hepatitis B-related immunity. Notably, it is the drug that has shown the highest rates of HBsAg loss in combination with a NUC in previous controlled studies. The other combination trial with vebicorvir we anticipate initiating shortly is being conducted in collaboration with Arbutus, combining their RNAi therapeutic candidate AB-729 with vebicorvir and NUC in a phase II trial enrolling virologically- suppressed e- antigen negative subjects. RNAi 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 will be evaluating the safety and on-treatment response of the three drug combinations versus each of the two drugs in combination with NUC. 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 NUC 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, ABI-H2158, has been shown to be 10-fold more potent than vebicorvir against the formation of new cccDNA in vitro lab studies. In phase I-B, 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 NUC, is ongoing in treatment-naive e-antigen positive subjects, and we hope to report interim data later this year. Initially, we'll be evaluating the changes in DNA, pre-genomic RNA, and other HBV-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 improved 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 initial phase I-A evaluation in healthy subjects. As I mentioned earlier, we are very excited with our progress towards nomination of a fourth core inhibitor candidate during the first half of this year. In our 4th-generation core inhibitor, we are aiming for a compound with a potential best-in-class profile. This will include greater potency, that is single-digit nanomolar potency against cccDNA formation and also antiviral potency. Of course, it will have pan-genotypic hepatitis B activity, a 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 4th-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 our most promising candidates into latter stages, as I've outlined. Again, stay tuned there, please. The 4th-generation core inhibitor actually leads me into 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 option rights to core protein cccDNA disruptors arising through a research collaboration with Door Pharmaceuticals. Door's discovery platform targets different phases of the hep B virus replication cycle, distinct from viral assembly, and that have the potential to interfere with viral nucleic acid, including cccDNA transcription within the nucleus of the cell, where the mini chromosome resides. This could prove a strong complementary 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 either degrade, disrupt, prevent transcription, or silence this reservoir. We are 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, has 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, hepatitis B remains a critical and exciting field of research, focusing on a 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 the 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. Operator, would you open the question-and-answer session line, please? Thank you. If you have a question, please press star then one on your touch-tone phone. If you wish to be removed from the queue, please press the pound sign or the hash key. If you're using a speaker phone, you may need to pick up the handset first before pressing the numbers. Once again, if you have a question, please press star then one on your touch-tone phone. 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. Hey, good afternoon, guys. Thanks for taking the question. Thanks for the update. I guess maybe you could just dig a little bit deeper into kind of the thoughts on not pursuing the chronic indication for vebicorvir and really going full bore into targeting sort of acute curative therapy. Is there any new data that's been generated sort of in the space that kind of gives you confidence in a pathway to achieve here, particularly with core inhibitors? Maybe the second question, on the NUC 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 there'll be durability of treatment here that would eventually lead to maybe some sort of stopping criteria as well? Thanks. Hey, Brian, it's John. Thanks for the question. I'll start with the first part, and then I'll hand it over to Bill in terms of that as well. Then I'll ask Luisa to comment on the triple combination therapy initiation with interferon in terms of is it safety or efficacy and what the plan is. To answer your question, is there new data that give us greater confidence that a core inhibitor-based program is going to provide us curative regimens? It's clear to all of us that you must inhibit all evidence of viral replication to even before you can cure anybody. I think that's the premise, and we've seen levels of viral suppression with the core inhibitor NUC that haven't been seen with NUCs alone before, with our 1st-generation compound. Then we'll be looking at the more potent compounds, which have been designed to be more potent against cccDNA. We don't have new data in the clinic today, but the premise is there from a virologic 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 or the field has that sways us to think that a stronger antiviral backbone will get us towards a cure? John, just to respond to that, thanks, Brian. 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. 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 2nd-generation compounds. 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 4th-generation compound as well, that we've talked about, that we're hoping we'll be able to advance and nominate that candidate soon. That has a very attractive profile. Luisa, the second part of Brian's question, is this just a safety study with interferon, or what is it? Yes. We are happy to start our first triple combination study with N rtI core inhibitor, vebicorvir, and interferon just last week. 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 a high level last fall, and 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 modified stopping criteria, and we'll share more details about that when we have more information. Great. Thank you very much. Our next question comes from Raju Prasad from William Blair. Please go ahead. Thanks for taking the question. I want to kind of discuss a little bit about how we should be looking at the potential interim data readout from the ABI-H2158 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 will give you more confidence on a potential maybe 12-week regimen with the 2nd-gen core inhibitor? Thanks. Thanks, Raj. I'll ask Luisa to answer the question first, then I might chime in a bit afterwards. Thank you. As John mentioned, our current phase II study with ABI-H2158 will be evaluating ABI-H2158 and entecavir in treatment-naïve e-antigen positive individuals. We chose this population because of the dynamic range afforded and the ability to assess the impact of the 2nd-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-treatment comparisons of viral parameters, including pgRNA, e -antigen, and core-related antigen. To your point, we've started internal discussions about what statistically and clinically would be meaningful and give us confidence that ABI-H2158 is better than VBR. 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'll share it when we can. Thanks, Luisa. Raj, look, we could look at 12 weeks, we could look at 24 weeks. The half-life of lifespan of cccDNA is, we believe, somewhere in that range. If this is more potent against the prevention of formation of new cccDNA, we'll be hoping to look for those differences. We have the study conducted for now in the same population as we did with vebicorvir. That will be the approach. 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. Then in terms of the triple, you talked a little bit about in terms of the triple. We've initiated, and we've said we're going to initiate both of these, two of our first triple combination studies now. We wouldn't be getting data to compare this experiment with two drugs with ABI-H2158 until the following year. That would be another component here as well. Look, we'll see how deep we can drive it down. We'll see about modified stopping rules. We'll see how it compares with vebicorvir. We'll take a scientific approach, and we'll work it out. We have ABI-H3733, and hopefully we'll be able to accelerate our 4th-generation compound as well. That's the approach on the core inhibitors. 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 new cccDNA. Thank you, Raj. Our next question comes from Michael Yee from Jefferies. Please go ahead. 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 said this is going to take too long, or maybe there's just a market opportunity thing? Maybe just shed some more light on what happened there and what BeiGene says. 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? What other types of combos could be possible, PD-1 to PD-L1, et cetera, TLR? Maybe just tease us a bit. Thank you. Thanks, Mike. Congratulations on the birth of your son. I will ask Luisa to 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 fourth mechanism of action. Duration of siRNA in the Arbutus collaboration, Luisa? Yes. As John mentioned, we're going to be, again, looking at the triple combinations compared to the two double combinations. We are targeting initially evaluation of safety and efficacy in 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. 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. Two populations, safety database, et cetera. 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 NUC therapy, with a very, very small niche population that are only partially virologically suppressed. Therefore, our global trial and our global plans wouldn't have been a global trial or plan. It would've been a China-only territory plan. We had these extensive discussions with BeiGene, and we came to the conclusions that we've made to you today, that we're not going to move forward with a chronic suppressive therapy, even one that's based alone in China. We should put those valuable resources 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. 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? I think to summarize for you, over a period of many, many, many months, we listened to many constituents here, and I think we made the right decision, and that we're doing what we should be doing, what's best for the patients. It's 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. That's what transpired, Mike, without getting into all the details. I hope that helps. That makes sense. Thanks, John, and my son says he'll explode your data. Okay. Good. Our next question comes from Geoffrey Porges from SVB Leerink. Thank you very much. John, I have a fairly fundamental question, which is why did vebicorvir fail? You achieved prolonged undetectable virus, and the virus came back. What's your prevailing explanation for why it's failed that you're trying to fix with more potency? Because going down the side of a mountain faster doesn't necessarily make a big difference. You can only get to undetectable, can't you? I'm trying to understand what failure mechanism a more potent core inhibitor is going to fix. If that's your prevailing assumption, then why spend any more money on vebicorvir? Thank you, Geoff. I think you've asked me this one before. I'll start again, then I'll hand it over to Bill, who's the virologist as well. Then I'll circle back on the why spend more money on vebicorvir. We've had the discussion before, and it's not just about inhibiting what we can detect, it's about inhibiting new cccDNA formation. Bill, perhaps you could add on a little bit more. Would you mind? Yeah, be happy to, John. Yeah. Thanks, Geoff. This comes back to, and I think also touches on some of the earlier questions, the differences in our compounds. 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. 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. That's why having a compound that's 10-fold more potent with 2158, we believe we'll be able to address that mechanism. I believe we haven't hit the threshold we need to hit in the clinic with vebicorvir. That's part of our strategy, is answering that question in the clinic. I think the second part is John talked about second out of three is looking at combinations, which we've also discussed and the value of vebicorvir in pushing down antiviral replication further during the combinations. Thank you, Bill. Geoff, 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. We're looking at other mechanisms as well, and we've talked about initiating our first two triples. As I said to you today, I'm quite eager to do more of that. We're sort of postured toward that today as well, and it might even involve an additional mechanism. I've said stay tuned. That's all I've said today. Look, the second part of your question, Geoff, is why spend more money on vebicorvir? If I have a compound that's as safe with some enhanced potency according to what Bill's been able to show me in the lab, in the clinic, we can switch vebicorvir out. 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. 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. That is the plan. I hope that helps and addresses your question. It's, yeah, in the right direction, but thank you. Thank you, Geoff. Our next question comes from Salim Syed from Mizuho. Please go ahead. Great. Thanks for the question, guys. 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 in the cccDNA formation chart. I'm just curious where the 300 mg you think falls on this curve. Do you think that is? Because you never got full cccDNA inhibition with vebicorvir, right? Even though it sounded like initially that for some reason we would be able to achieve finite therapy with VBR. I'm just curious here with the 300 mg 2158, do you think you'll be able to get complete cccDNA inhibition? Does it fall on the bottom part of this curve? Bill, do you want to address the curve? Yeah. You're on slide 16. Yeah. Yeah. Thanks, Salim. This will certainly give us, if you're looking at slide 16, this gives us a 20-fold above what we could achieve with vebicorvir, which we certainly believe is worth exploring. This should be enough potency to start to inhibit that reservoir. Whether the kinetics of it, we'll have to determine that in the clinic. Certainly believe that this is over an order of magnitude in terms of additional potency compared to vebicorvir. How that will play out over time, we believe this is something that needs to be tested, and we'll answer that question. Also, that's why with our third compound and then the fourth compound, why we're targeting an even greater level of potency so that we could maximize that inhibition on that second mechanism of action. Okay. Thanks so much. That helps, Salim? Yeah. I think it helps. Thank you. Our next question comes from Nicole Germino from Truist. Please go ahead. Hi. Good evening, guys, thanks for taking my question. As you were saying earlier, you're all in on finite curative therapy. What data helped you with this decision and with BeiGene as well? Did Study 211 play a key role in this decision? Can you elaborate a little bit more on the modified stopping criteria after the results from 211? 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 will look at some of the analysis of that data. 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 forward a chronic suppressive therapy. We had data in-hand from Study 211 based upon DNA and RNA that allowed us to have approvable endpoints for a better chronic suppressive therapy. 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. It was, as I said, and as I've responded to others today, we spent 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. 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 chronic suppressive therapy trial, which is not really what we had envisioned we would be doing. We had extensive discussions with our partner, BeiGene, about what to do in China as well. 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. Again, I'll just say the chronic suppressive therapy was our in-parallel strategy where we were trying to do these other things. 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 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 expand our runway. That's what we've decided to do, and I think that's the best thing. It's the smartest decision. It's 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 that's answered both of your questions. Yes, that's helpful. Thank you so much. We have no further questions at this time. I will now turn the call back to Dr. John McHutchison for closing remarks. 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. 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 teams, the resources, and the collaborators necessary to try and accomplish these goals. With that, we look forward to providing you updates in the future on our clinical development and our research programs as they mature. Thank you all for joining us again today, and this concludes our call. Thank you, ladies and gentlemen. This concludes today's conference. Thank you for participating. You may now disconnect.