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 Gleizer, 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 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, Doctor.
John McCutcheson to provide opening remarks, and then we will host a Q and A session. Joining John for the Q and A portion of the call will be our Chief Medical Officer, Doctor. Louisa Spam our Chief Scientific Officer, Doctor. 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 will now hand the call over to our CEO, Doctor.
John McCutcheson.
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 C 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 bevicorvya solely in cyanide and curative 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 4th generation core inhibitor, our 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 believed and I still do that we will cure this disease as we did hepatitis C. Of the approximately 270,000,000 hepatitis C patients worldwide, only 5,000,000 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 of therapy.
We need 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 development. In Phase II trials, BAVCORVA 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 bevicoirvir as well as our next generation more potent Chlor inhibitor candidates. We believe the combination of these potent direct antiviral mechanisms that is Cor Plus Nuc that suppresses viral replication 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 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, Beijing, 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. So after significant internal and external discussions and analyses, including discussions and agreement with our partner Beijing for the China territory, we have concluded that rather than proceeding with the Phase 3 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 needs of 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 bevacorvir as well as additional potential combination studies and study arm, 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 3 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 3 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 discovery program.
All 4 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 durative combination regimen. However, we do not plan on bringing all 4 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 2nd component of our strategy, advancing proven concept triple and potentially quad combination studies with nukes and our core inhibitors. The initial step in this approach include vevicorovir combined with a nuke serving as the antiviral backbone of these planned triple combination studies, 2 of which we expect to initiate in the first half of this year. As previously noted, the combination of bevacorvira and ANUCE has already demonstrated potent antiviral activity at 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 bevicorvir 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, it is a drug that has shown the highest rates of S loss in combination with ANUCE in previous controlled studies. The other combination trial with vevicorvii we anticipate initiating shortly is being conducted in collaboration with Arbutus, combining their RNAi therapeutic candidate, AB-seven twenty nine, with bevicorvira and Nuc in a Phase 2 trial 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 3 drug combinations versus each of the 2 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. And new backbone together with 1 or potentially 2 other mechanisms.
So please stay tuned here also. In parallel with the vericulovir combination studies I've just described, we are actively advancing our pipeline of more potent generation core inhibitors. The most advanced, 2,158, has been shown to be 10 fold more potent than beviporvir against the formation of new cccDNA in in vitro lab studies. In Phase 1b, 2,158 demonstrated potent antiviral activity and a Our Phase 2 trial of 2,158 combined with ANUCE is ongoing and treatment naive E antigen positive subjects, and we hope to report interim data later this year. Initially, we will be evaluating the changes in DNA, pre genomic RNA and other HBV related viral antigens and comparing that to our prior data 8 in the lab has translated to improved clinical efficacy on treatment, we'll also be able to incorporate modified subbing criteria for the purpose of evaluating off treatment response.
Additionally, we also have 3,733, which recently completed initial Phase Ia evaluation in healthy subjects. And as I mentioned earlier, we are very excited with our progress towards nomination of a 4th 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 panjunativic 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 4 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. So again, stay tuned there, please. The 4th generation core inhibitor actually leads me into the 3rd 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 Dor Pharmaceuticals.
Dor's discovery platform targets different phases of the hep B virus replication cycle distinct from viral assembly and that has 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 had been to develop therapies that target cccDNA to either degrade, disrupt, prevent transcription or silence this reservoir. So 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 purity 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 this group, of course. While it would be premature to disclose those 2 specific targets, we can tell you that we have 2 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 of 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 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 cyanide 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 and curative therapy approach for these patients. With that, we are now happy to take your questions. As a reminder, Louisa, Bill, Tom and Jason are all here with me. So operator, would you open the question and answer session line, please?
Thank 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.
Hey, good afternoon guys. Thanks for taking the question. Thanks I guess, maybe you can just dig a little bit deeper into kind of the thoughts on not pursuing the chronic indication for vebacorovir and really going full bore into targeting sort of acute curative therapy. I mean, 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 nucorovir pegolitin interferon Phase 2 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. And then I'll ask Louise to comment on the triple combination therapy initiation with interferon in terms of is it safety or efficacy and what the plan is. So 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 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 Nucs that haven't been seen with Nucs alone before with our 1st generation compound. And then we'll be looking at 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 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.
Yes. John, so yes, just to respond to that, and yes, 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 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 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's we're hoping we'll be able to advance and nominate that candidate soon, but that has a very attractive profile. So Louisa, the second part of Brian's question, is this just a safety study with interferon or what is it?
Yes. So we are happy to start our first triple combination study with NRTI core inhibitor, veviporvir 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 think about this question, we haven't reached the criteria there, but we're going to be looking at the on treatment response and anticipate incorporating a lot of life stopping criteria and we'll share more details about that when we have more information.
Great. Thank you very much.
And 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 158 study in the context of the triple combo data as as some of the stopping criteria comments you've made. Are there any specific data points that you're looking at internally there that gives you will give you more confidence on a potential, maybe 12 week regimen with the 2nd gen core inhibitor? Thanks.
Thanks, Raj. I'll ask Louisa to answer the question first, and I might chime in a bit afterwards.
Thank you. So as John mentioned, our current Phase 2 study with 2,158, we'll be evaluating 2,158 and Entekavira treatment naive e antigen positive individual. 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 2 study 202 in a similar population. We are going to be doing cross study on treatment comparisons of spiral parameters including tgRNA, 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 2,158 is better than DVR.
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'll share it while we can.
So thanks, Louise. Look, we'll look, we can look at 12 weeks. We can look at 24 weeks. The half life of lifespan of CCC DNA is, we believe, somewhere in that range. So if this is more potent against the prevention and formation of new cccDNA, we'll be hoping to look for those differences.
And we have the study conducted for now in the same population as 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 talked a little bit about in terms of the triple. We've initiated and we said we're going to initiate both of these 2 of our first combination studies now, so we wouldn't be getting data to compare them with to compare this experiment with 2 drugs with 2,158 until the following year.
So that would be another component here as well. So look, we'll see how deep as well. So that's the approach on the core inhibitors. But I do believe, and I think this gets back to Brian Corning'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 well as prevent the formation of new cccDNA.
So thank you, Raj.
And 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 kind of that 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? 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-one to PD L1, etcetera, DLR? Maybe just ease this a bit. Thank you.
Thanks, Mike. Congratulations on the birth of your son. I will ask Louise to talk first about the combinations what we're doing with the SI and RNA and duration. In terms of other triples, let me just say that checkpoint inhibitors would be 1. 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. But duration of siRNA in the Arbutus collaboration, Louisa?
Yes. So as John mentioned, we're going to be again looking at the triple combinations compared to the 2 double combinations. And 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 want to share more about the dosing and the duration at that time.
Thanks, Louisa. 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, 2 populations, safety database, etcetera. 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. So it would have been a China only territory plan. So we had these extensive discussions with Beijing 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.
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 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. So that's what transpired, Mike, without getting into all the details. I hope
that answers your questions. That makes sense. Thanks, Tron. And my son says he looks forward to your data.
Okay. Good.
And 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 verbicovir fail? You achieved prolonged undetectable virus and the 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 can only get to undetectable, can't you?
So, I'm trying to understand what failure mechanism a more potent TOR inhibitor is going to fix? And then if that's your prevailing assumption, then why send any more money on vermicovir?
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 is the virologist as well. And then I'll circle back on the why spend more money on bevicorps here. 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? Yes.
I'd be happy to, John. Yes. 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 formation and release of new virus, they don't all have similar activity against formation of new cccDNA.
And looking at the potency of evicorvir 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 why having a compound that's 10 fold more potent with 2,158, 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 sevacorviere. So that's part of our strategy is answering that question in the clinic. And then I think the second part is, as John talked about, 2nd out of 3 is looking at combinations, which we've also discussed and the value of bevacorvir and pushing down antiviral replication further during the combinations.
So that's so thank you, Bill. So Jeff, it's about the second miss, and it's not just the antiviral potency. I think Bill 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 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 question, Jeff, is with some enhanced potency according to what Bill's being able to show me in the lab, in the clinic, we can switch vevicorphia 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.
Yes, in
the right direction, but thank you.
Thank you, Jeff.
And our next question comes from Salim Syed from Mizuho. Please go ahead.
Great. Thanks for the question guys. So John, just one from you or maybe Bill. When I'm looking at Slide 16 in FIDEC, you guys have the VBR and 2,158 in 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 CCC and DNA 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 2,158, do you think you'll be able to get CCC complete CCC DNA inhibition? Does it fall on the bottom part of this curve?
Bill, do you want to address the curve? You're on Slide 16. Yeah. Thanks, Celine.
Yes. So this will certainly give us if you're looking at Slide 16, this gives us a 20 fold above what we could achieve with bevacorovir, which we certainly believe is worth exploring. And this will this should be enough potency to start to in terms of additional potency compared to bevacorvira. And 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 3rd compound and then the 4th compound, we're targeting an even greater level of potency so that we could inhibit maximize that inhibition on that second mechanism of action.
Okay. Thanks so much.
Does that help, Salim?
Yes. I think it helps. Thank you.
Our next question comes from Nicole Gromino from Truist. Please go ahead.
Hi, good evening guys and thanks for taking my question. So as you were saying earlier, you're all in on finite charters therapy. What data helped you with this decision and with BeiGene as well? And did SEDI-two eleven play a key role in this decision? And 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 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 forward a chronic suppressive therapy. We had data in house and in house, in hand from Study 211 based upon DNA and RNA that allowed us to have to be able to cure anybody or lead to an SVR upon cessation of therapy. So as I said and as I 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, Beijing, about what to do in China as well. So it was those discussions, but it wasn't the failure to obtain an SBR of a significant percentage in Study 211 that changed that decision making process. So again, I'll just say, the chronic suppressive therapy was our 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 are best off and our company is best off and our patients are best off if we put those resources into final curative therapies and that will also expand our runway. So 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. 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 Doctor. John McCutcheon 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. 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.
Thank you, ladies and gentlemen. This concludes today's conference. Thank you for participating. You may now disconnect.