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Arbutus Biopharma (NASDAQ:ABUS)
Q3 2021 Earnings Call
Nov 04, 2021, 8:45 a.m. ET

Contents:

  • Prepared Remarks
  • Questions and Answers
  • Call Participants

Prepared Remarks:


Operator

Ladies and gentlemen, thank you for standing by, and welcome to the Arbutus Pharmaceutical Biopharma Corporation 2021 third quarter financial results conference call. [Operator instructions] Please be advised that today's conference is being recorded. [Operator instructions] I would now like to hand the conference over to Lisa Caperelli, vice president of investor relations. Please go ahead.

Lisa Caperelli -- Vice President, Investor Relations

Thank you, Angie. Good morning, everyone, and thank you for joining Arbutus' third quarter financial and business update call. Joining me today from the Arbutus executive team are Bill Collier, president and chief executive officer; David Hastings, chief financial officer. Dr.

Gaston PGO, chief development officer; and Dr. Mike Sofia, chief scientific officer. Bill will begin with a review of recent accomplishments and clinical developments, followed by Mike Sofia, who will provide an update on our research efforts with an oral PD-L1 inhibitor. Dave Hastings will then provide a review of the company's third quarter financial results.

After our opening remarks, we will open the call up for Q&A. Gaston Picchio will be available to address clinical development-related questions at that time. Before we begin, we'd like to remind you that some of the statements made during the call today are forward-looking statements, which are subject to a number of risks and uncertainties that may cause our actual results to differ materially, including those described in our most recent annual report on 10-K, quarterly report on Form 10-Q and our other periodic reports filed with the SEC from time to time. I'll now turn the call over to Bill.

Bill?

Bill Collier -- President and Chief Executive Officer

Thank you, Lisa, and thank you, everybody, for joining us today. We really appreciate your interest in Arbutus Biopharma. Now, this morning, we issued our third quarter financial and business update press release, which highlights the significant progress we've achieved this year toward our goal, which is to develop a proprietary portfolio of products with different mechanisms of action, but when used in combination result in a functional cure for patients living with chronic hepatitis B. We're taking a three-pronged approach that's intended to: one, reduce HBV surface antigen; two, suppress HBV DNA; and three, boost the host immune system and intend to accomplish this with our RNAi therapeutic 729, our oral capsid inhibitor-836, and our oral PD-L1 program, where we recently commenced IND-enabling studies.

So I'd like to start by walking through the clinical advancements we've made with this approach, starting with reducing surface antigen with our lead compound 729, the RNAi therapeutic. As you know, 729 is specifically designed to reduce all hepatitis B viral antigens, including hepatitis B surface antigen. And we're seeing this activity in our ongoing phase 1a/1b clinical trial. In fact, data to date has shown that AB-729 consistently provides a mean 1.8 log reduction in hep B surface antigen which is sustained over time in patients with chronic HBV.

In addition, 729 continues to show a favorable safety and tolerability profile. Also, to -- in addition to reporting significant drops in S antigen, some 729 patients have shown increased HBV-specific immune responses, which further supports our rationale for combination therapy to include an immunomodulatory agent. Now, next week, at AASLD, we will report additional data from additional cohorts of patients in this clinical trial in a poster presentation. And in that presentation, among other things, we will show that 729 repeat dosing remains generally safe and well tolerated.

We'll show that robust mean declines in surface antigen were sustained with repeat dosing of 729 with no meaningful differences observed to date between 60-milligram or 90-milligram doses or dosing intervals, which included every four, eight or 12 weeks. And we'll also show that S-antigen suppression to levels below 100 international units per ml, which is a clinically relevant threshold, which could inform when stop therapies is maintained in some subjects up to 20 weeks following the last dose of 729. As we continue to unveil more data with 729, we continue to believe that the drug has the potential to be a cornerstone agent in future HBV combination regimens. Our strategy is to evaluate 729 in combination with our own novel agents and with other approved or investigational agents with complementary mechanisms of action to set foundation for future trials.

Now, we've made great progress in advancing 729 in clinical trial development. This quarter, we initiated and dosed the first patient in our own phase 2a randomized, open-label proof-of-concept clinical trial to evaluate 729 in combination with ongoing standard of care in new therapy and short courses of PEG interferon in 40 patients with chronic HBV infection. Based on clinical data from our phase oneprogram, we selected 60 milligrams every eight weeks as the dose and dosing schedule for this trial and other trials. We're currently in the process of opening sites, screening patients, and we will provide further updates on this trial when appropriate.

And then, from a collaboration standpoint, 729 is being evaluated in an ongoing phase 2a triple combination trial with Assembly Biosciences lead HBV core inhibitor and a nucleoside analog. Assembly is conducting this trial and expecting to see data in 2022. Also, activities to initiate separate phase 2a clinical trials with Antios and Vaccitech are ongoing. We expect that the arm that will include 729 in the Antios clinical trial will commence this quarter and that the Vaccitech clinical trial will initiate in early 2022.

Both trials are designed to evaluate a triple combination of 729, a nucleoside analog and either the Antios or Vaccitech's proprietary agent. I'd now like to move on to the second arm of our approach that's to suppress HBV DNA with our next-generation oral capsid inhibitor 836. Now, 836 is specifically designed to completely block viral replication in infected cells by preventing the assembly of functional viral capsids. Preclinical data suggests that 836 may have the potential for increased efficacy and an enhanced resistance profile compared to previous capsid inhibitors.

Preliminary data from healthy volunteers and HBV patients in our phase 1a/1b clinical trial is on track to report out by the end of this year. and these data may support the initiation of a phase two combination clinical trial with our own proprietary compounds. The third arm of our approach is to boost the immune system, which we hope to do with our oral PD-L1 program, for which we recently commenced IND-enabling studies. And after my prepared remarks, I'll turn the call over to Mike Sofia to provide more details about this exciting compound.

Now, ultimately, we strive to have a convenient, all oral combination treatment for hepatitis B patients. And to achieve that, we are progressing our research efforts with an oral RNA destabilizer program and look forward to providing updates on our lead optimization efforts in 2022. In addition to our efforts in HBV, our internal research program to identify new antiviral small molecules to treat COVID-19 and future coronavirus outbreaks continues to make progress. So as you can see, despite the challenging impact of the pandemic, the team at Arbutus has been relentless in their efforts to continue the advancement of our clinical and research programs to meet our corporate goals to address the needs of patients and to increase shareholder value.

I really am very grateful for the team's commitment and dedication to finding a cure for hepatitis B and for the treatment of coronaviruses. So with that, I'll turn the call over to Mike Sofia for an update on our PD-L1 program. Mike?

Mike Sofia -- Chief Scientific Officer

Thanks, Bill, and good morning, everybody. As Bill mentioned, we are focused on a three-pronged approach to developing a cure for chronic hepatitis B and key to that is to boost or reawaken the immune system. Given this, we have nominated for IND-enabling studies, an oral PD-L1 inhibitor that could potentially be an important part of a combination therapy for the treatment of HBV. Let me start with an overview of why we believe the PD-1/PD-L1 will an immune checkpoint access is a viable target for effecting immune reawakening in the context of HBV.

It is well established that the immune system in HBV chronically infected individuals is tolerized to the recognition of the virus or infected cells. It is also believed that highly functional HBV-specific T cells are required for long-term HBV viral control in the setting of functional cure. However, HBV-specific T cells become functionally defective and greatly reduced in their frequency during chronic HBV infection, immune checkpoints such as PD-1/PD-L1 play an important role in the induction and maintenance of a new tolerance and in T cell activation. It is well established that the PD-1/PD-L1 signaling pathway in immune cells plays a critical role in the human immune response to farm pathogens.

After the initial immune response to a pathogen an increased expression of PD-1 and its binding to PD-L1 leads to down regulation of the immune response. In cancer biology, the upregulation of the PD-1/PD-L1 axis has been linked to immune tolerance resulting in the development of several important immune therapies. Similarly, the PD-1/PD-L1 axis has been implicated as having a role in HBV-specific immune polymers. It has been shown that HBV-specific T cells in the blood and liver from chronically infected HBV patients express PD-1 levels.

And this level correlates with S-antigen load. PDL-1 has been shown to be upregulated dombiohepatitis, and PD-1 has been shown to be upregulated on HBV-specific T cells, and S-antigen specific B cells. Ex-vivo studies using HBV patient blood and liver samples, has demonstrated that HBV-specific T and B cell responses are improved with checkpoint blockade. It has been our long-standing strategy to combine agents that reduce the HBV-specific immune tolerizing antigen S antigen with agents that to further reawaken the immune system.

Therefore, we hypothesized that one approach to reawaken HBV-specific T cells is to block the PD-1/PD-L1 protein protein interaction and hopefully break HBV-specific immune tolerance. Support for this approach was observed in preclinical animal model studies where checkpoint blockade in combination with other direct acting no virus led to both DNA clearance and sustained viral suppression. Our resource efforts have identified a class of small molecule oral checkpoint inhibitors that we believe will allow for controlled checkpoint blockade enable oral dosing and mitigate systemic safety issues seen with checkpoint antibody therapies. From this class of small molecule PD-L1 inhibitors, we nominated a lead candidate based on in vitro potency, immune restoration, in vivo efficacy, selectivity and safety.

Let me provide a little more detail in each of these research parameters. Starting with in vitro potency. The PD-L1 bioassay EC50 was less than 20 nanomolar, which is competitive with external compounds. With respect to new restoration, this lead agent displayed primary human T cell activation in a preclinical model and restoration of T cell activity for chronic hepatitis B patient samples in vitro.

The in vivo efficacy showed favorable pharmacokinetic and antitumor efficacy in a preclinical tumor model. From a selectivity standpoint, the agent binds to PD-L1 with minimal binding to off-target in vitro, the agent has an acceptable safety profile based on progressible in vitro safety pharmacology and in vivo mouse tolerability studies. The small molecule PD-L1 inhibitor possesses in vitro intrinsic activity and functional activity both in wholesale systems in animal models that are equivalent to known PD-L1 antibodies. Based on this preclinical work, this compound is now in IND-enabling studies.

I'm excited by the advancements that we've made to identify this lead compound, which we believe as an acceptable safety profile and functional activity play a key role in our combination approach to finding a cure for HBV. I'll now turn to Dave Hastings for a brief financial update. Dave?

Dave Hastings -- Chief Financial Officer

Thanks, Mike, and good morning, everybody. As I've mentioned in the past, our key financial metric is cash and financial runway. Our cash, cash equivalents and investments was $151.9 million as of September 30, 2021 that compares to $123.3 million as of December 31, 2020. Our cash use from operations for the nine months ended September 30, 2021, was $47.9 million, which was offset by $75.4 million of net proceeds from the issuance of common shares under our ATM program.

For all of 2021, we expect our aggregate cash used to range from $70 million to $75 million. And therefore, we expect our current cash runway to be sufficient to fund operations into the second quarter of 2023. With that, I will now turn the call back to Bill. Bill?

Bill Collier -- President and Chief Executive Officer

Yeah. Thanks so much, Dave, and to you, Mike, as well. So operator, maybe now is the time to open up the lines for the Q&A session.

Questions & Answers:


Operator

[Operator Instructions] Your first question comes from the line of Roy Buchanan with JMP Securities. Please proceed with your question.

Roy Buchanan -- JMP Securities -- Analyst

Hi. Great thanks for taking the questions. I want to start on AB-836. Bill, you mentioned the phase one results.

I think coming at the end of this year, you think can support the start of the combo phase two. Just wondered if you could give a little more detail maybe what that phase two would look like. Would you start with an initial 836 plus a NUC only to do dose finding? Or would you go straight to a triple combination with your proprietary compounds? Just kind of what would that look like?

Bill Collier -- President and Chief Executive Officer

Yeah. Thank you very much, Roy. Great question. I think we've actually been saying for quite some time that it's always been our aim to have our own internal combinations.

So kind of logically in our mind, it makes sense to look at a 836/729 and a NUC combination trial. And we'll clearly share more details on that as next year evolves. I think the important point today is to to let everyone know that we're on track to deliver those 836 results by the end of the year.

Roy Buchanan -- JMP Securities -- Analyst

OK. Great. And then, another 836 question, I'm not sure, probably you're not going to tell me what the chemistry is, but on the slide, it says it's a unique chemistry. Maybe you can confirm it's not an HAP or SBA, and I can try to say their names, if you want.

But I think I think you guys know what those are. So is that possible you could confirm that?

Bill Collier -- President and Chief Executive Officer

Mike, do you want to take that one?

Mike Sofia -- Chief Scientific Officer

Yeah. This is Mike to say. Yes, I can confirm that it's neither of those.

Roy Buchanan -- JMP Securities -- Analyst

OK. Great. And then, I had a question, it's kind of early, it's really early, but I wanted to get your guys thinking about potential pricing for a functional cure. I mean, is there any reason as a functional cure has found that it wouldn't be priced, let's say, similarly to the hepatitis C cures that were developed.

Just give us maybe your thoughts around that.

Bill Collier -- President and Chief Executive Officer

Yeah, Roy, thank you. I think, as you said in your question, maybe a tad early to get into pricing specifics. But I mean, there's obviously benchmarks of existing therapy. You've got benchmarks across other viral diseases.

And I think beyond that, it's very difficult for us to say. I will add, though, that one of our strategies, as I've mentioned, to have all the components of the functional cure within our own proprietary umbrella, is kind of relevant here because it allows you to set whatever the price is ultimately going to be without too much worry about economies to a third party or partner or royalties and so on and so forth. So one of the underpinnings of our strategy to find our own internal combo is not unrelated to your question.

Roy Buchanan -- JMP Securities -- Analyst

OK. Great. I'll hop back in queue. Thanks.

Bill Collier -- President and Chief Executive Officer

Thank you.

Operator

Your next question comes from the line of Brian Skorney with Baird. Please proceed with your question.

Luke Herrmann -- Baird -- Analyst

Hi. This is Luke Herman on for Brian. We were just hoping you could maybe talk a little bit about the upcoming reform data that J&J is presenting at AASLD next week in terms of the implications it has for the field. And given the kinetics of response, what do you think of the stopping criteria at 48 weeks, do you think that's a sufficient time frame?

Bill Collier -- President and Chief Executive Officer

Yeah. So thank you, Luke, for that question. Let me make a couple of comments and then maybe Gaston can be available for any additional comments. I think we've seen the abstract as have many other people.

I think may still be a little early for us to come in on competitor data until we see the full presentation and hear what Janssen have to say. I would maybe just add a couple of additional points. Our development strategy is around this three-pronged approach that we've talked about, which would include an RNA therapeutic, a capsid inhibitor and immunotherapy. The data you just referred to, the RIF data, includes an RNAi therapeutic, a capsid inhibitor and a NUC.

And so, it may be that this further supports our strategy that an immunotherapy is needed in the treatment regimen to show continued improvement. I think a second point to make at this early stage is that it appears that the contribution of the capsid inhibitor in the J&J study may have been insufficient. And we clearly need to understand that more. But our capsid inhibitor, as you've heard on previous calls, 836 unique, and it's differentiated from other capsid inhibitors.

And in preclinical data, we've shown that therapeutically relevant doses 836 has increased potency and engages the second mechanism of action. So I think there is some differences when you look from capsid to capsid. And I think beyond that, we really just have to wait for the presentation next week and hear what the company say, and hopefully, that will help answer not just your question, but some of the questions that we have as well. So with that, Gaston, any additional comments you want to make?

Gaston Picchio -- Chief Development Officer

Yeah. Thanks, Bill. I think you covered very well. In regard to the stopping rule, I think it was referenced in the question.

I think it's just one approach to stopping rules, a composite endpoint that they use, which appears reasonable. I think there may be different ones that are going to be used in the field. So we look forward to see what happens to patients when they're still based on that criteria after the presentation.

Luke Herrmann -- Baird -- Analyst

Great. Thank you.

Operator

We do have a follow-up question from the line of Roy Buchanan with JMP Securities. Please proceed with your question.

Roy Buchanan -- JMP Securities -- Analyst

Great. Thanks. So I'll start with the easy one, one for Dave. I guess any ATM since -- I think the update was the October 8 prospectus was the last one.

Have you guys used it since then?

Dave Hastings -- Chief Financial Officer

Yeah. I mean, we'll update everybody during our fourth quarter update in early March on that, Roy. So we'll comment on that at that point.

Roy Buchanan -- JMP Securities -- Analyst

Great. OK. And then, a couple -- maybe more complicated ones, and early again. But Bill, your response to the pricing question, what are you guys thinking in terms of partnering.

I mean, it sounds like you want to retain as much ownership as possible. But if you -- presumably you go to regions like Europe and China, are you also thinking you're going to retain ownership there? Or will you likely partner?

Bill Collier -- President and Chief Executive Officer

Yeah. Thanks for the follow-up question, Roy. I mean, I think what I was trying to articulate is, if we have all of the individual components of a combination underneath in Arbutus umbrella, it gives us more flexibility on pricing. I think the question that you referred to now, which is around how we access different markets around the world.

Again, at this early stage, what I would say is that we are -- we remain open to different strategic approaches. And our Head of BD is in regular contact with lots of different people. And my general approach is if we feel that a partnership is going to be the right way to access the market or enable us to meet the need of patients then that's clearly going to be good for the medicine and good for shareholders as well. So it may be that the individual components of the cure remain within the Arbutus umbrella.

And potentially, we partner for different geographies, but we have -- we've clearly not talked about that, and I'm giving you a hypothetical answer to your question.

Roy Buchanan -- JMP Securities -- Analyst

Yeah, still early. Got it. That's helpful. And then, another early one, but the regulatory path, what do you guys envision the phase three and initial approvals looking like, is potentially 729 going to be approved as monotherapy with the NUC? Or are you going to go for approvals of the combinations? How do you envision that playing out, I guess?

Bill Collier -- President and Chief Executive Officer

Yeah. So right now, what we're really focused on are these four different phase 2a proof-of-concept studies. And so, I think it's really important to underline this, that when it comes to our strategy of reduced suppress and boost, you can do that with different combinations of agents. And we're clearly testing out that hypothesis in these four phase 2a studies.

So I think, again, great question, Roy. But I would like to see how 729 as a cornerstone agent performs in all of these studies and then to move into phase 2b, phase three accordingly. But I think you can determine that as we've set out these different proof-of-concept combinations, we are really looking for the combination to move forward, to get to a functional cure. Gaston, do you want to add?

Gaston Picchio -- Chief Development Officer

No, no. Thank you. I think you covered it well.

Bill Collier -- President and Chief Executive Officer

Thank you.

Roy Buchanan -- JMP Securities -- Analyst

OK, great. Thank you, guys. Thanks for taking my question.

Bill Collier -- President and Chief Executive Officer

Thank you, Roy.

Operator

Your next question comes from the line of Ed Arce with H.C. Wainwright & Company. Please proceed with your question.

Ed Arce -- H.C. Wainwright and Company -- Analyst

Great. Hi, everyone. Thanks for taking my question. Just one for me on 836.

Obviously, data coming up here at the end of the year on your phase one study, and this would, as you mentioned, allow for a phase two presumably next year to really put together your initial combination studies Wondering if you could talk a little bit about the data, what you're expecting in particular, given that A36, as you mentioned, is a unique capsid inhibitor and utilizes a novel binding site within the core protein dimer-dimer interface. I wondered if there's anything that you're looking from that data that could help support the differential profile that you expect?

Bill Collier -- President and Chief Executive Officer

Yeah. Thank you, Ed. So maybe Mike Sofia first and then Gaston as it relates to the clinical data. Mike?

Mike Sofia -- Chief Scientific Officer

Yeah. Thanks for the question. So you're right. 836 is what we call our next-generation agent, right? And it differentiates itself significantly from earlier generation agents because of the high intrinsic potency it had, but also, as we have commented on many times, the the ability to engage this second mechanism, right? So the inhibition of the replenishment of the pool of cccDNA, we believe will be a therapeutically relevant dose.

And I think one of the problems with the first-generation agents is that they -- the activity at the second mechanism was sufficiently less than the first mechanism activity puts that at relevant doses that they could give in the clinic, they just couldn't engage that. So when you do engage that second mechanism, clearly, we believe we're going to have a fairly robust response against reduction on RNA, as well as DNA, which is the primary mechanism. So I think we're looking forward to looking at that data. And looking at other biomarkers, HPV-related biomarkers to see back that second mechanism is playing an important role in the capsid space.

So we have a molecule that we're very excited about, has high liver exposure. So I think overall, we're anxious to see the data to see how this translates. Gaston?

Gaston Picchio -- Chief Development Officer

Yeah, I think that's basically it we're going to be looking at that speed of both HBV DNA and RNA expression. And then, there is a little bit of a wildcard that we may be able to interrogate, which is the activity of the compound against resistant variants. We are not selectively enrolling patients with resistance, but we know that there are resistant variants out there. And if we, by chance, enroll some of those, we may be able to also an early read out as the activity of this new generation [Inaudible] variance.

But that's a little bit something that we cannot control, really.

Ed Arce -- H.C. Wainwright and Company -- Analyst

Right. Fantastic. Great. Thank you.

Bill Collier -- President and Chief Executive Officer

Thank you, Ed.

Operator

Your next question comes from the line of Keay Nakae with Chardan. Please proceed with your question.

Keay Nakae -- Chardan Capital Markets -- Analyst

Yeah. Keay Nakae, Chardan. Some questions for Mike on the PD-1. First, Mike, can you point us to any preclin data that you've published on your oral checkpoint inhibitor?

Mike Sofia -- Chief Scientific Officer

Well, we haven't published any specific preclinical data on the molecule that we nominated, right? I can point you to a major communication paper that we published looking at the very unique mechanism of how the small molecule works relative to, let's say, an antibody, right? So that, I can point that to you. We recently published that. I think it was the -- toward the middle end of last year came out. And also, in that paper, we showed the small molecule that we used, which was an earlier generation agent who does have that sort of antitumor effect.

So we were using an antitumor model because that was the most readily available model at the time we've now subsequently developed an HBV model that we're looking at molecules in animal model. So you can see in that work that we -- these small molecules do have very unique characteristics, both mechanistically and function very competitively with antibodies.

Keay Nakae -- Chardan Capital Markets -- Analyst

OK. I'll circle back with you to get that. And so, then, just kind of moving on then to both, I guess, the safety profile again, relative to an antibody, you should have some advantages there. But how do we then think about it, the safety as you move into combo therapies? And what would you be on high alert to look for there in terms of safety?

Mike Sofia -- Chief Scientific Officer

Well, as you know, in sort of the oncology setting, antibody-based checkpoint blockade does have some adverse events associated with that, right? And one of the things we wanted to do was circumvent that. And the concept that we used was really the small molecule concept. And the reason why we believe that this is going to be a solution to the potential adverse events is with an antibody, you have a very long action occurring, right? So you give one dose and it's sort of onboard for weeks and weeks. With a small molecule, we can take advantage of PK/PD relationships and essentially just dose enough of what we need to get to get the response.

Plus, you can -- if there's any issue, we can actually remove drug because the PK wash-out of that. So that's one thing. The other thing is we have -- as we always do, is look at liver targeting, and so we have drugs that have high liver-centric characters. So these molecules have much reduced systemic exposure that, therefore, allows us to target HBV versus having sort of that systemic immune activation that we see with a typical antibody.

So I think those characteristics of these molecules, we believe will support a better safety profile. Now, we're at to see that in the clinic, but I think we're pretty excited about the overall profile of these molecules and the potential.

Keay Nakae -- Chardan Capital Markets -- Analyst

Yeah. I guess, where I'm going with that, Mike, is with the -- certainly the destabilizer, there were some tox issues, oral compound. So again, when we get to a point where you're combining these in your eventual all oral solution. How should we think about any synergistic toxic issues, we might be concerned about?

Mike Sofia -- Chief Scientific Officer

Sure. So obviously, each of these molecules work by a different mechanism of action. There are different chemical entities in and of themselves, so they'll have different characteristics. We clearly, in all our preclinical and nonclinical studies are very careful in ensuring that we don't have any drug-drug interaction issues associated with that.

Now, we can't predict exactly what's going to happen clinically, but we do combination studies in preclinical models to assess the compatibility of these molecules from agonist or antagonistic standpoint. We get some sense of safety read or on the combination when we do combination studies in vivo. So I think we're doing all the things that one needs to do to have a sense of confidence that these molecules will perform in the clinic and perform safely, but really the clinical setting is going to be the tell of the theory.

Keay Nakae -- Chardan Capital Markets -- Analyst

OK. Well, thanks for that.

Operator

Your next question comes from the line of Kelechi Chikere with Jefferies. Please proceed with your question.

Kelechi Chikere -- Jefferies -- Analyst

Yeah. Thank you and good morning. I guess, a single question for me here. I guess, on this going debate as to what the appropriate stopping criteria should be for many of these combination therapies.

How was -- for the new component, can you opine and discuss a little bit more about that and what you think stopping criteria should be? And I guess related to that, with the 729, you've demonstrated the ability to increase HB-specific immune responses, could that potentially be added on as a component of what could be a stopping criteria for your combination studies?

Bill Collier -- President and Chief Executive Officer

Yeah. Thank you, Kelechi. I'm going to hand that one over to Gaston.

Gaston Picchio -- Chief Development Officer

So yeah, great question. I mean, look, I think as I was just trying to say, I think different groups will come up with different stopping criteria. There is no single as far as I know, unified stopping criteria. And usually, stopping criteria are composite end points.

It doesn't just factor, for example, a concentration of S-antigen can do -- include S-antigen plus, for example, HBV DNA and ALT criteria. I think we will know whether which is the most appropriate stocking criteria once we see what happens to the patients after they stop, old therapy. And for example, if one chose 100, and then we see that there is a high relapse. But if one chooses 10 as part of the composite endpoint, and there is less relapse then one can conclude, obviously, that 10 is better than 100.

But we're not there yet. We don't have that data. So I think we'll be -- I mean, for lack of a better term, I think we'll be try on there. I think we'll have to try different things.

There is no even straight consensus on how to stop standard of care today with no therapy. So people use different things. But as we repeated the number of occasions, for example, 100 IU per ml in patients who have been for many years on NUC therapy is a criteria that's used in, especially in Asia. Now, you're right about what we've observed in three out of five patients that we were able to measure in cohort E of our ongoing 729-001 study.

The challenge there is immune constitution would be a criteria. It's something that cannot be measured really quickly to make that decision. As you know, these T cell assays are very labor-intensive requiring the collection of preferred blood mononuclear cells, and they cannot be just run like a viral load in an automated way and sandalized way. So I think it's a very good idea.

I hope that we can find maybe some surrogate indicators of T-cell reconstitution perhaps something in line with the measurement of soluble cytokines interferon gamma comes to mind that can be more readily and rapidly run in the clinical lab in a standardized way. But that will be the challenge ambition of including T cell constitution -- T cell immune reconditions to HBV as part of the criteria.

Kelechi Chikere -- Jefferies -- Analyst

Got it. Thank you. That's very helpful. Thank you.

Operator

Ladies and gentlemen, we've reached the allotted time for questions. I would now like to turn the floor back to management for any additional or closing remarks.

Bill Collier -- President and Chief Executive Officer

Well, thank you, Angie, and thank you, everyone, for your questions. We really appreciate you joining us this morning and obviously, your continued interest in the company. And look forward to keeping you up to date as we continue to move forward to secure achievement of the milestones that we've shared to you -- with you today. And those obviously include the announcement of additional data from the 729 phase 1a/1b clinical trial at AASLD and the initial data from our 836 phase 1a/1b trial by the end of the year.

So we look forward to being in touch. And operator, that concludes our call. Thank you.

Operator

[Operator signoff]

Duration: 45 minutes

Call participants:

Lisa Caperelli -- Vice President, Investor Relations

Bill Collier -- President and Chief Executive Officer

Mike Sofia -- Chief Scientific Officer

Dave Hastings -- Chief Financial Officer

Roy Buchanan -- JMP Securities -- Analyst

Luke Herrmann -- Baird -- Analyst

Gaston Picchio -- Chief Development Officer

Ed Arce -- H.C. Wainwright and Company -- Analyst

Keay Nakae -- Chardan Capital Markets -- Analyst

Kelechi Chikere -- Jefferies -- Analyst

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