Q3 2021 Arbutus Biopharma Corp Earnings Call
Ladies and gentlemen, thank you for standing by and welcome to the a Buddhist pharmaceutical.
Biopharma Corporation 2021 third quarter financial results Conference call at this time, all participants are in listen only mode.
After the speaker's presentation, there will be a question and answer session to ask a question. During the session you will need to press star one on your telephone keypad.
Please be advised that today's conference is being recorded.
If you require further assistance. Please press star Zero I Wonder I'd like to turn the conference over to at least have kept rally Vice President of Investor Relations. Please go ahead.
Thank you Angie good morning, everyone and thank you for joining our beautiful third quarter financial and business update call joining.
Joining me today from the our beauty executive team are Bill Collier, President and Chief Executive Officer, David Hastings, Chief Financial Officer, Dr. Goffstown P. T L 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 L. One 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.
<unk> P. T O 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.
<unk> 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.
Thank you Lisa and thank you everybody for joining US today, we really appreciate your interest in Arbutus Biopharma.
This morning, we issued our third quarter financial and business update press release, which highlights the significant progress. We've achieved this year towards our goal, which is to develop a proprietary portfolio of products with different mechanisms of action.
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 to suppress HBV DNA three boost the host immune system.
And intend to accomplish this with our RNA therapeutic 17, all in all.
Oral capsid inhibitor 836.
All PD L. One program, where we recently commenced R&D, 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 seven to nine.
Peter.
As you know seventy-nine is specifically designed to the juice, all hepatitis b viral antigens, including hepatitis B surface antigen.
We're seeing this activity in our ongoing phase one a one b clinical trial.
In fact, the data to date has shown that a b 17 on 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, some two nine continues to show a favorable safety and Tolerability profile.
Also too in addition to reporting significant drops in S. Antigen. Some 17 million patients have shown increased HBV specific immune responses.
Which further supports our rationale for combination therapy to include an immuno modulator agent.
Now next week a F. L. D. We will report additional data from additional cohorts of patients in this clinical trial.
Poster presentation.
And in that presentation. Among other things, we will show that seven to nine repeat dosing remains generally safe and well tolerated.
We will show the robust mean declines in surface onto Joe more sustained with repeat dosing of seven to nine 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 the S antigen suppression to levels below 100 international units per ml.
Which is a clinically relevant threshold, which could inform when to stop therapies.
Is maintained in some subjects up to 20 weeks following the last dose of seven to nine.
As we continue to involve more data with seven two now and we continue to believe that the drug has the potential to be a cornerstone agent and future HBV combination regimens.
Our strategy is to evaluate 17 nine in combination with our own.
Novel agents and with other approved or investigational agents with complementary mechanisms of action to set.
<unk> for future trials.
No we've made great progress in advancing seventy-nine in clinical trials of all of them.
This quarter, we initially initiated and dosed. The first patient you know one phase Iia randomized open label proof of concept clinical trial to evaluate 17 nine in combination with ongoing standard of care in nuc therapy and.
Short courses of Peg interferon in 40 patients with chronic HBV infection.
Based on clinical data from our Phase one program. 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 two a triple combination trial with assembly biosciences lead HBV core inhibitor.
Nucleoside analog.
Assembly is conducting this trial unexpected to see data in 2022.
Also activities to initiate a separate phase two clinical trials with <unk> and vacs attack ongoing.
We expect that the arm that will include seven to nine and the <unk> clinical trial will commence this quarter.
The vaccine clinical trial will initiate in early 2022.
Both trials are designed to evaluate the triple combination of seven to nine a nucleoside analog and either the intl's pullbacks detects proprietary agent.
Now I'd like to move on to the second arm of our approach that's to suppress HBV DNA with a next generation oral capsid inhibitor 836.
Now 836 is specifically designed to completely block viral replication and infected cells by preventing the assembly of functional viral capsid.
Preclinical data suggests that 836 may have the potential for increased efficacy and an enhance resistance profile compared to previous capsid inhibitors.
Preliminary data from healthy volunteers and HBV patients in a phase one a one b clinical trial is on track to report out by the end of this year.
These data may support the initiation of a phase II 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 all excuse me our oral PD L. One 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 oral combination treatment for hepatitis b patients.
And to achieve that we're 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 or internal research program to identify new Antivirals small molecules to treat COVID-19, and future coronavirus outbreaks continues to make progress.
So as you can see despite the challenging impacts of the pandemic. The team at Arbutus has been relentless in our 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 the share.
Holder 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 Corona viruses.
So with that I'll turn the call over to Mike Sofia for an update on our PD Lone program.
Yeah.
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.
Key to that is to boost reawaken the immune system.
Given this we have nominated for R&D, enabling studies and oral.
<unk> PDL, one 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 a PD one PD lone immune checkpoint axis.
<unk> target perspective immune reawakening in the context of HBV.
It is well established that the immune system HBV chronically infected individuals whose power on to the recognition of the virus or infected cells.
It is also believed that highly functional HBV specific T cells are required for long curve HBV viral control setting a functional cure.
However, the HBV specific T cells become punctually, defective and greatly reduced and their frequency.
HBV infection.
Immune checkpoints, such as PD, one PDL one play an important role in the <unk>.
<unk> and maintenance of immune tolerance and in T cell activation.
It is well established that the PD, one PDL, one signaling pathways and immune cells.
A critical role in the human immune response, the borne pathogens.
So the initial immune response to a pathogen and an increased expression of PD, one and it's finding the PDL one leads to down regulation of the immune response.
In cancer biology, the Upregulation of the PD, one PDL one axis has been linked to immune tolerance resulted in the development of several important immune therapies.
Similarly, the PD one PDL, one axis has been implicated as having a role in HBV specific immune tolerance.
It has been shown that HBV specific T cells in the blood and liver from chronically infected HBV patients.
Correct.
PD, one levels and this levels correlate with S antigen alone.
PD L. One has been shown to be up regulated from viral hepatitis and PD. One has been shown to be up regulated on HBV specific T cell and S antigen specific T cells.
Ex vivo studies, using HBV patient blood and liver samples as demonstrated that HBV specific T cell responses are improved with checkpoint blockade.
Yeah.
It has been our long standing strategy to combine agents that reduce the HBV specific immune tolerance antigen S antigen agent.
Is inspecting further reawaken the immune system.
Therefore, we hypothesize that one approach to reawaken HBV specific T cell is to block the PD, one PD lone protein protein interaction.
And hopefully break HBV specific immune tolerance.
Support for this approach was observed in preclinical animal model studies.
Checkpoint blockade in combination with other direct acting antiviral.
But both DNA clearance and sustained viral suppression.
Our research efforts.
Identified a class of small molecule oral checkpoint inhibitors that we believe will allow for control checkpoint blockade enable oral dosing and mitigate systemic safety that you've seen with checkpoint antibody therapies.
From this class of small molecule PDL one 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 Lone Biowaste EC 50 was less than 29 are more competitive with external compounds.
With respect to immune restoration. This lead agent displayed primary human T cell activation in a preclinical model and restoration of T cell activity from chronic hepatitis b patient samples in vitro.
The in vivo efficacy favorable pharmacokinetic and anti tumor efficacy in preclinical tumor models.
From a selectivity standpoint agent binds the PD lone with minimal binding to off target in vitro. The agent has an acceptable safety profile based on Progresso ball in vitro safety pharmacology and in vivo mouse Tolerability studies.
<unk> molecule PD, one inhibitor possesses in vitro intrinsic activity and functional activity both in wholesale systems in animal models that are equivalent to known PDL one antibodies.
Based on this preclinical work. This compound is now in IND, enabling studies.
Excited by the advancements that we've made to identify this lead compound, which we believe is an acceptable safety profile and functional activity play a key role in a combination approach to finding a cure for HBV.
I'll now turn to Dave Hastings for a brief financial update.
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 of $151 9 million as of September 32021.
Compared to $123 3 million.
31 2020.
Our cash used 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 use 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.
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.
Absolutely if you will.
To ask an audio question. Please press star one on your telephone keypad again, Thats star one to ask an audio question.
Your first question comes from the line of Roy Buchanan with JMP Securities. Please proceed with your question.
Hi, great. Thanks for taking the questions I wanted to start on a B 836, Bill you mentioned.
The phase one results I think coming at the end of this year you think can support they started the combo.
Phase two I'm just wondering if you give a little more details 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.
Kind of what would that look like thanks.
Thank you very much ROI great question I think we've.
She'd been saying for quite some time that it's always been our aim to have our own.
<unk> combination so kind of logically.
In our minds it makes sense to look at our $836 seven to nine and a nuc.
[noise] combination Ah trial.
And.
Well clearly share more details on that as the mixture 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.
Okay, Great and then another 836 question I'm not sure I'm, probably not going to tell me what the chemistry is but I mean on the slides. It says it's a unique chemistry, just maybe you can confirm it's not a <unk>.
Hey, P 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.
Mike do you want to take that one yes.
This is Mike, yes, I can confirm that it's neither of those.
Okay, great. Thanks, 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 you know I mean is there any reason if a functional cure is found that it wouldn't be you know price, let's say similarly to the appetite.
See carriers that were developed.
Just give us maybe your thoughts around that thanks.
Yeah right. Thank you.
Yeah.
I think as you said in your question, maybe a tad early to get into pricing specifics, but I mean theres obviously.
Benchmarks are existing therapy, you've got benchmarks across other viral diseases.
And you know 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 he's kind of relevant here because.
You too.
Whatever the price is ultimately going to be.
Without too much worry about economics too.
Third party or a partner or rolled 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.
Okay, Great I'll hop back in queue. Thanks.
Your next question comes from the line of Brian Kearney with Baird. Please proceed with your question.
Hi, This is Luke on for Brian We were just hoping you could maybe talk a little about the upcoming reef one data that J&J is presenting at <unk> next week in terms of the implications that has for the field and given the kinetics of response, what do you think the of the stopping criteria at 48 weeks do you think that's sufficient time.
Ryan.
Yes. So thank you look for that question.
Let me make a couple of comments and then maybe <unk> can be available for any additional comments I think.
We've seen the abstract as have many other people I think it may still be a little early for us to come in.
On the competitor data until we see the full presentation in here.
Jensen I have to say.
I would maybe just add a.
A couple of additional points.
Our development strategy is around.
This three pronged approach that we've talked about which would include <unk>.
Therapeutic a capsid inhibitor and immunotherapy.
The data that you've just referred to the reef data includes an RNA only therapeutic <unk>.
Our capsid inhibitor and a nuc.
And so you know.
It may be that this further supports our strategy that in immunotherapy is needed in the treatment regimen to show continued improvement.
I think the second point to make.
Early stage.
Is that it appears that the contribution of the capsid inhibitor in the J&J study.
May have been insufficient and we need to understand that more.
But all capsid inhibitor as you you've heard on previous calls 836 unique and its differentiated from other capsid inhibitors.
In preclinical data.
We've shown that therapeutically relevant doses of <unk> hundred six has increased potency.
And engages the second mechanism of action. So I think there is some differences when you look from caps at the capsid.
And I think beyond that we really just have to wait for the presentation next week.
Hey.
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 guest on any any additional comments you want to make.
Yes. Thanks.
No I think you covered it very well.
In regards to the stopping rule I think it was referenced in the question.
I think it's just one approach the stopping rule as a comp aside.
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 are still based on that criteria. After the presentation.
Great. Thank you.
You do have a follow up question from the line of Roy Buchanan with JMP Securities. Please proceed with your question.
Great. Thanks, So I'll start with the easy one for Dave I guess any ATM you since I think the update was the October eight.
Prospectus with the last one is you guys have used it since then.
Yes, I mean, we will update.
Everybody.
During our fourth quarter update.
Early March on that ROI so okay.
We will comment on that at that point.
Great, Okay and then.
A couple of maybe more complicated ones, but and early again, but you know.
Bill you your response to the pricing question.
What are you guys thinking in terms of partnering I mean, it sounds like you wanted to retain.
As much ownership as possible, but if he you know presumably you go to regions like Europe, and China are you also thinking youre going to retain ownership there or will you likely partner.
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 on him Hello underneath in arbutus umbrella.
It gives us more flexibility.
On pricing I think the.
The question that you referred to now which is around you know how do we access different markets around the world.
Again at this early stage.
I would say is that we are we remain open to different strategic approaches.
And head of BD.
Regular contact with lots of different people.
My My General approach is if we feel that a partnership he's going to be the right way to access the market or.
Enable us to meet the needs 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 Q.
Remain within the El beaches umbrella and potentially we partner for different geographies, but we have not.
Clearly not talked about that and I'm, giving you a hypothetical answer to your question Yep Yep still early got it that's helpful. Thanks.
And then another another early one but.
The regulatory path, what do you guys envision.
The phase III and initial approvals looking like.
It's potentially 17 not gonna be approved.
As monotherapy.
Or are you going to go for approvals of the combinations, how do you envision that playing out I guess.
Yeah, so right.
Right now.
What we're really focused on these.
Four different phase Iia proof of concept studies.
And so I think it's really important to underline this.
When it comes to our strategy of reduced suppressed and boost you can do that with different combinations of agents homeaway.
Homeaway clearly testing out that hypothesis in these four phase III studies.
So I think again great question Roy.
But I would like to see a seven to nine as a cornerstone agent performs in all of these studies.
And then to move into phase two b phase III accordingly, but thank you.
You can determine that as we've set up these different proof of concept combinations. We are really looking for the combination to move forward.
To get to us a functional cure.
Don't you want to add.
No no. Thank you I think you've covered it well okay.
Okay, great. Thank you guys. Thanks for taking my questions. Thank you everyone.
Your next question comes from the line of Ed Arce with H C. Wainwright <unk> Company. Please proceed with your question.
Great Hi, everyone. Thanks for taking my question just one for me.
An 836.
Honestly.
Data coming up here at the end of the year on your.
Phase one study.
This word.
As you've mentioned allow for.
Our phase two presumably next year or two to.
Put together your initial combination studies.
Wondering if.
You could talk a little bit about.
Data.
What you're expecting in particular.
Given that <unk> hundred six as you mentioned is a unique.
Capsid inhibitor and <unk>.
Utilizes a novel binding site.
Within the core protein dimer dimer interface.
I wondered if there was anything that youre looking from.
That data there.
Help support the differential profile that you.
You expect thanks.
Yes. Thank you Ed So maybe Mike Sofia first and then and then guests on as it relates to the clinical data.
Yes, thanks for the question.
So youre right <unk> hundred six is what we call our next generation agent.
It differentiates itself significantly from earlier generation agents because of the high intrinsic potency it has but also.
As we have commented on many times.
The ability to engage the second mechanism right. So.
Inhibition of the replenishment of the pool of CCC DNA, we believe will be a therapeutically relevant dose and I think one of the problems with the.
Our first generation agents is that the.
Yeah.
<unk>.
The activity at the second mechanism was sufficiently.
Less than the first mechanism activity.
Relevant doses that they could given 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.
No response against production 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, let's see.
In fact that sector mechanism is.
Is playing an important role in accounts in space.
So so we have a molecule that we're very excited about liver exposure.
So I think overall, we're anxious to see the data to see how this translates.
This is Tom.
No I think that that's that's basically where.
We're going to be looking at depth and speed of both HBV DNA.
Freshman and then Theres a little bit about.
A wildcard that we may be able to in.
Irrigation, which is.
The activity of the compound against where system variance we're not.
Selectively enrolling patients with resistance, but we know that there was there is out there and if we buy a chance and Roes on myself.
We may be able to also.
And the early read.
The activity of these new.
Generation didn't keep dragging this variance, but thats a little bit.
Something that we cannot control.
Right.
Fantastic great. Thank you.
Thank you Ed.
Your next question comes from the line of Kian Nicky with Chardan.
Please proceed with your question.
Yes Kate.
Some questions for Mike on the PD one.
First.
Mike can you point us to any.
Preclinical data that you've published on your oral checkpoint.
Checkpoint inhibitor.
Sure.
Well, we haven't published any specific preclinical data on the molecule that we nominated right Ken.
10 point, you to a major communication paper.
We published looking at the very unique mechanism of how the small molecule works relative to relative to.
Let's say in <unk>.
Antibody right.
So that I can point out to you. We recently published that I think it was.
Towards the middle end of last year came out.
And also in that paper, we showed a small the small molecule that we used.
Which was an earlier generation agent does have that.
Sort of an anti tumor effect. So we were using an anti tumor model because that was the most readily available model at the time, we have now subsequently developed.
In HBV model that we're looking at molecules in an animal model. So.
So you can see in that in that work that we do.
Small molecules do have very unique characteristics both mechanistically.
Function very competitively with with antibodies.
Yeah.
Okay.
Back with you to get that.
So then just kind of moving on then to I guess the safety profile.
Again relative to an antibody you should have some advantages there, but how do we how do we then think about it.
Safety as you move into combo therapies.
<unk> therapies and what would you.
Be on high alert to look for there in terms of safety.
Well as you know.
And sort of the oncology setting.
And antibody based checkpoint blockade does have some adverse events associated with that right and then one of the things we wanted to do with 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.
With an antibody you have a very long action occurring right.
So you have one dose.
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 give to get the response plus you can if there's any issue we can actually remove dropped because.
Okay washout.
Alright, okay.
So that's one thing the other thing is we we have.
We always do is look at liver targeting and so we have drugs that have high liver centric.
Richter so so these molecules.
Much reduced systemic exposure therefore allows us to two <unk>.
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 where ought to see that in the clinic, but.
I think I think we're pretty excited about.
Yeah.
The overall profile of these molecules and the potential.
Yes, I guess, I guess, where I'm going with that mic is.
With.
Well certainly the Destabilizer you know there were some tax issues.
Oral compound.
So again, when we get to a point, where you're combining these and your eventual oral solution.
How should we think about any synergistic toxic issues we might be.
Sure.
Sure. So so obviously.
Each of these molecules work by different mechanism of action.
They arent different chemical entities themselves, so they'll have different characteristics.
We clearly in all our preclinical.
In non clinical studies are very careful in ensuring that we don't have any drug drug interaction issues.
Associated with that now now we can't predict exactly what's going to happen clinically.
We do do combination studies in preclinical models.
To assess the compatibility of these molecules.
From from agonists or antagonistic standpoint, we get some sense of of <unk>.
Safety.
<unk>.
Read on the combination when we do combination studies in vivo so.
No 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 performs safely, but really the clinical setting is going to be.
The total.
No the theory.
Okay, well thanks for that.
Your next question comes from the line of collect each quarry with Jefferies. Please proceed with your question.
Yes, Thank you and good morning, I guess, a single question for me here I guess, there's ongoing debate as to what the appropriate stopping criteria should be for many of these combination therapies.
I was.
For the new component can you opine on and discuss a little bit more about that and what you think the stopping criteria should be and I guess related to that with 7090 <unk> demonstrated the ability to increase HBV specific immune responses could that potentially be added on that component.
What could be a stopping criteria for your combination studies.
Yes, Thank you <unk> I'm going to hand that one over to guests Don.
Yes, hi.
So yeah, great question, I mean look I think as I was trying to say.
I think.
Groups will come up with different stoping criteria there is no.
Single as far as I know unified stopping criteria unusually stopping criteria our combo site.
Endpoints. It doesn't just factor for example, a concentration of S antigen.
Can do.
Founded in Platts for example, HBV DNA and the aot criteria.
I think we will know whether we.
Which is the most appropriate.
The stopping criteria once we see what happens to the patients after they stop all therapy.
And for example.
When should this 100 and then we see that there is a high relapse, but when she was at 10.
As part of the composite endpoint and there is less way less than one can conclude obviously that tends to rather than the hundreds, but we're not there yet we don't have that data.
I think it will be.
I mean for lack of a better.
Tom I think it would be try on there I think.
We'll have to try different things.
There is no even.
<unk> consensus on how the stock has done their care today with no clear up these people use different things, but that's we've repeated a number of locations. For example, 100 IU per ml in patients who have been for many years.
As a criteria.
Especially in Asia.
No.
You're right about the.
What we observe.
Three of the five patients that we were able to measure in a cohort of our ongoing seven to 9001 study.
The challenge there.
Immune reconstitution would be at criteria is something that cannot be measured really quickly to make that decision. As you know these T cell assays are very labor intensive.
Why are the collection of peripheral blood mononuclear cells.
And they cannot be just run like a viral load.
The way in the Sunrise way, so I think.
Good idea.
I hope that we can find maybe some surrogate.
Indicators are deeper reconstitution.
Perhaps something in line with our measurement of soluble cytokine storm.
If youre on gamma.
It comes to mind that can be more readily and rapidly.
In the clinical lab found the right way.
That would be the challenge I ambition.
Clothing T thought were closed the deal with T cell immune reconstitution to HBV as part of the criteria.
Got it. Thank you that's very helpful. Thank you.
Ladies and gentlemen, we have reached the allotted time for questions I would now like to turn the floor back to management for any additional or closing remarks.
Well, thank you Andrea and thank you everyone for your questions. We really appreciate you joining us this morning, and obviously Youll continued interest in the company.
Look forward to keeping you up to date as we continue to move forward to secure achievement of the milestones that we've shared with you today.
And those obviously include the announcement of additional data from the seven to nine phase <unk> clinical trial at <unk>.
And the initial data from 836 phase <unk> trial by the end of the year. So we look forward to being in touch and operator that concludes our call. Thank you.
Thank you for participating in today's conference call. You May now disconnect your lines at this time.
Yeah.
Okay.
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Ladies and gentlemen, thank you for standing by and welcome to the <unk> pharmaceutical.
Biopharma Corporation 2021 third quarter financial results Conference call at this time, all participants are in listen only mode.
After the speaker's presentation, there will be a question and answer session to ask a question. During the session you will need to press star one on your telephone keypad.
Please be advised that today's conference is being recorded.
If you require further assistance. Please press star zero I want I'd like to hand, the conference over to at least temporarily Vice President of Investor Relations. Please go ahead.
Thank you Angie good morning, everyone and thank you for joining our beautiful third quarter financial and business update call joining.
Joining me today from New York beautifully executive team are Bill Collier, President and Chief Executive Officer, David Hastings, Chief Financial Officer, Dr. Goffstown P. T O 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 L. One 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.
<unk> P. T O 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.
<unk> 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.
Yeah, Lisa and thank you everybody for joining us today, we really appreciate your interest in <unk>.
As biopharma.
This morning, we issued our third quarter financial and business update press release, which highlights the significant progress. We've achieved this year towards our goal, which is to develop a proprietary portfolio of products with different mechanisms of action.
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.
G suppressed HBV DNA.
Really boost the host immune system.
And intend to accomplish this with our RNA therapeutic seventy-nine oral capsid inhibitor 836.
And our oral PD, one program, where we recently commenced.
You're doing 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 compounds southern Chino in the.
Therapeutic.
As you know seventy-nine 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 <unk> clinical trial.
In fact data to date has shown that a b seventy-nine 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, 79 continues to show a favorable safety and Tolerability profile.
Also too in addition to reporting significant drops in S. Antigen. Some 17 million patients have shown increased HBV specific immune responses.
Which further supports our rationale for combination therapy to include an immuno modulator free agent.
Now next week I E. L. D. We will report additional data from additional cohorts of patients in this clinical trial.
Poster presentation.
And in that presentation. Among other things, we will show that 17 on repeat dosing.
<unk> is generally safe and well tolerated.
We'll show the robust mean declines in surface antigen was sustained with repeat dosing of seven to nine 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're also show the S antigen suppression to levels below 100 international units per ml.
Which is a clinically relevant threshold, which could inform winter stopped therapies.
Is maintained in some subjects up to 20 weeks following the last dose of seven to nine.
As we continue to unveil more data with seven two now and we continue to believe that the drug has the potential to be a cornerstone agent and future HBV combination regimens.
Our strategy is to evaluate 17 nine in combination with our own novel agents and with other approved or investigational agents with complementary mechanisms of action.
The foundation for future trials.
Now we've made great progress in advancing seven to nine in clinical trials the volatile.
This quarter, we initially initiated and dosed the first patient in our own phase two a randomized open label proof of concept clinical trial.
Evaluate 17 nine in combination with ongoing standard of care in Nuc therapy, and short courses of peg interferon in 40 patients with chronic HBV infection.
Based on clinical data from our Phase one program. 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 17 line is being evaluated in an ongoing phase two a triple combination trial with assembly Biosciences lead HBV core inhibitor and a nucleoside analog.
Assembly is conducting this trial unexpected to see data in 2022.
Also activities to initiate a separate phase two clinical trials with NTS and vacs attack ongoing.
We expect that the arm that will include 17 on in the <unk> clinical trial will commence this quarter.
The <unk> clinical trial will initiate in early 2022.
Both trials are designed to evaluate the triple combination of seven to nine a nucleoside analog and either the Ngls <unk> proprietary agent.
I'd now like to move on to the second arm of our approach that's to suppress HBV DNA with a next generation oral capsid inhibitor 836.
Now 836 is specifically designed to completely block viral replication and infected cells by preventing the assembly of functional viral capsid.
Preclinical data suggests that 836 may have the potential for increased efficacy and an enhance resistance profile compared to previous capsid inhibitors.
Preliminary data from healthy volunteers and HBV patients in a phase one a one b clinical trial is on track to report out by the end of this year.
And these data may support the initiation of the 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 all excuse me our oral PD L. One 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 oral combination treatment for hepatitis b patients.
And to achieve that we're 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 our 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 share.
Holder value.
I really am very grateful for the team's commitment and dedication to funding a cure for hepatitis b and for the treatment of Corona viruses.
So with that I'll turn the call over to Mike Sofia for an update on our PD Lone program.
<unk>.
Yeah, 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.
Key to that is to boost reawaken the immune system.
Immune response, the farm pathogens. After the initial immune response to a pathogen and increase expression of PD, one and it's finding to PDL one leads to downregulation of the immune response.
And cancer biology, the Upregulation of the PD, one PDL one axis has been linked to immune tolerance, resulting in the development of several important immune therapies.
Similarly to PD, one PDL, one axis has been implicated as having a role in hvv's specific immune calls.
It has been shown that HVV specific T cells in the blood and liver from chronically infected HVV patients expressed IPD one levels and this level correlates with antigen lobe.
PDL wrong has been shown to be Upregulated gone viral hepatitis MPD. One has been shown b upregulated on HBV specific T cells and S antigen specific b cells.
Ex vivo studies, using HBV patient blood and deliver samples as demonstrated that HBV specific T M b cell responses or improve with checkpoint blockade.
It has been a long standing strategy to combined agents that reduce the HVV specific immune tall rising antigen S antigen with agent spectrum further reawaken the immune system.
Therefore, we hypothesize that one approach to reawaken HBV specific T cell as to block the PD, one PDL one protein protein interaction.
And hopefully break HVV specific immune tolerance.
Support for this approach was observed in preclinical animal models studies with.
Where checkpoint blockade in combination with other direct acting in a viral but to both DNA clearance and sustained borrow suppression.
Our research efforts have identified a class a small molecule oral checkpoint inhibitors that we believe will allow for control checkpoint blockade enable oral dosing and mitigate systemic safety issue scene with checkpoint antibiotic therapies.
From this class a small molecule PDL one inhibitors, we nominated 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 star.
Starting with in vitro potency.
The <unk> bio assay easy 50 was less than 20, Nanomolar just competitive with external compounds.
With respect to immune restoration. This lead agent display primary humour T cell activation and a preclinical model and restoration of T cell activity for chronic hepatitis b patient samples in vitro.
The in vivo efficacy bearable, pharmacokinetic and anti tumor efficacy and a preclinical tumor model.
From a selectivity standpoint is you're buying the PDL along with minimal binding to off target in vitro. The agent has an acceptable safety profile based on progressive or in vitro safety pharmacology, an in vivo mouth Tolerability studies.
The small molecule PDL, one inhibitor possesses in vitro intrinsic activity and functional activity. Both in wholesale systems in animal models that are equivalent to known PDL one antibiotics.
Based on this preclinical work. This compound is now an indie enabling studies <unk>.
I'm excited by advancements that we've made to identify this lead compounds, which we believe is an acceptable safety profile and functional activity play a key role in our combination approach to finding a cure for HBV.
I will now turn to Dave Hastings for a brief financial update.
Thanks, Mike and good morning, everybody.
As I've mentioned in the past are key financial metrics cash in financial runway.
Our cash cash equivalents in investments is $151.9 million as of September 30th 2021 that compares to $123.3 million as of December 31, 2020.
Our cash use from operations for the nine months ended September 30th 2021 was 47 9 million.
Which was offset by 75 $4 million of net proceeds from the issuance of common shares.
Under our 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.
Thanks, So much day, then team Mike as well, so operator, maybe now's the time to open up the lines for the Q&A session.
Absolutely if you would like to ask an audio question. Please press star one on your telephone keypad again, that's star one to ask an audio question.
First question comes from the line as Roy Buchanan with JMP Securities. Please proceed with your question.
Alright, great. Thanks for taking the questions I wanted to start on.
Three six Bill you mentioned.
The phase one results I think coming at the end of this year you think can support that started the combo.
Phase two I'm just wondering if you give a little more details maybe what that phase two would look like would you start with an initial.
836, plus a nuke only to do dos finding or would you go straight to a triple combination with your proprietary compounds.
Just kind of what would that look like thanks.
Yes. Thank you very much Roy Great question I think we've.
I should have been saying for quite some time that it's always been our aim to have our own.
Internal combinations, so kind of logically.
Online that makes sense to look at 836729 and a new.
Combination.
Trial.
And.
Little cliche and more details on that 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.
Okay, Great and then another 806 question I'm not sure probably not going to tell me what the chemistry is but.
On the slides it says it's a unique chemistry, maybe you can confirm it is not a H P or SBA and I can try to say their names if you want but.
I think.
Thank you guys know what those are so.
Is that possible you could confirm that.
Mike.
Yes.
Yes, I can confirm that it's neither of those.
Okay, great. Thanks.
And then I had a question it's kind of early it's really early but I wanted to get you guys thinking about potential.
Potential pricing for a functional care you know I mean is there any reason.
If a functional curious found that it wouldn't be priced let's say similarly today hepatitis C carriers that were developed.
Just give us your maybe your thoughts around that thanks.
Yeah Roy Thank you.
I think as you said in your question may be a tad early to get into pricing specifics, but I mean, there's obviously.
Benchmarks are existing therapy <unk> go benchmarks across other viral diseases.
And I think beyond that is very difficult for us to say.
I will add.
One of our strategies as I've mentioned to have all the components of the functional Q.
Within our own proprietor umbrella.
Is kind of irrelevant here because.
Hi, Aussie to set whatever the price is ultimately going to be.
Without too much worry about economics to a third party or a partner or rolled and so on and so forth. So.
One of the underpinnings of our strategy.
Find our own internal combo is not unrelated to your question.
Okay, Great I'll hop back in queue. Thanks. Thank you.
Your next question comes from the line of Bryant's Corny with Bird. Please proceed with your question.
Hi, this is low carbon on for Brian. We were just hoping you could maybe talk a little about the upcoming refund data that J&J is presenting it so the next week.
Terms of the implications it has for the field and given the kinetics of response, what do you think the of the stopping criteria at 48 weeks do you think that's sufficient timeframe.
Yeah. So thank you look for that question let.
Let me make a couple of comments and then maybe guest on can be available for any additional comments I think.
We've seen the abstract as have many other people I think it may still be a little early for us to come in.
Holton competitor data until we see the full presentation in here.
Johnson I'd have to say I.
I will maybe just add.
A additional points.
All development strategy is around.
This three pronged approach that we've talked about.
Which would include.
He therapeutic captured inhibitor.
Immunotherapy.
The day that you just referred to the reef data includes an orange alley therapeutic.
Ah captured inhibitor and a nuke.
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.
Early stage.
Is that it.
Is that the contribution of the captured inhibitor in the J&J study.
May have been insufficient and we need to understand that more.
But all caps at inhibitor is you've you've heard on previous calls 836 in ache and it's differentiated from other captured inhibitors.
And in preclinical data.
We've shown that therapeutically relevant doses <unk> hundred six has increased potency.
And engages the second mechanism of action. So I think there is some differences when you look from caps it to cabinet.
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 homes not just your question, but some of the questions that we have as well so with that guest on any any additional comments you want to make.
Yeah. Thanks.
I think you cover it very well.
Regards to stop it <unk> I think it was referenced in the question.
I think it's just one approach the smoking ruins of Champa side and.
<unk> point that they use which appears reasonable.
I think there may be different ones are going to be used in the field. So we'll look forward to see what happens to patients when they are still based on that criteria. After the presentation.
Great. Thank you.
You do have a follow up question from the line of variety cannon with JMP Securities. Please proceed with your question.
Thanks, So I'll start with the easy one for Dave I guess.
<unk> I think the update with the October 8th.
Prospectus was the last one of you guys who used it since then.
Yes, we will update.
Everybody.
During our fourth quarter update.
Early March on that Roy so okay.
We'll comment on that at that point.
Great, Okay and then.
Couple, maybe more complicated ones, but I'm, an early again, but.
Hi.
Your response to the pricing question, but.
What are you guys thinking in terms of partnering it sounds like you want to retain.
As much ownership as possible but.
<unk> go to regions like Europe, and China are you also thinking you're going to retain ownership there or will you likely partner.
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 and.
Underneath and Lbj's umbrella it.
It gives us more flexibility on pricing.
Thank thee.
The question that your research you know, which is around how do we access different markets around the world.
Again at this early stage.
Well I would say is that we are we remain open to different strategic approaches.
<unk>.
Head of B DS in regular contact with with lots of different people.
My 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 needs 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 Lpga's umbrella and potentially we.
For different geographies, but we have not.
Okay talked about that and I'm, giving you a hypothetical answer to your question, Yes, Yes, it's still early got it that's helpful. Thanks and then.
Another another early one but.
Now the regulatory path what are you guys envision.
The phase three an initial approvals looking like.
It's potentially 17 not going to be approved.
As mono therapy, with a nuke or or are you gonna go for approvals of the combinations, how do you envision that playing out I guess.
[noise] yeah. So.
Right now.
What we're really focused on all these.
Four different phase two a proof of concept studies.
So I think it's really important to underline this.
When it comes to a strategy of reduced suppressed and boost you can do that with different combinations of agents.
Clearly testing out the hypothesis in these full face to a studies.
So.
Again, great question Roy.
But I would like to see how seven to nine at a cornerstone agent performs and all of these studies.
Then to move into phase to be faced three accordingly.
Think.
You can determine that as we've set up these different proof of concept combinations. We are really looking for the combination to move forward.
To get to us a functional Q.
<unk> do you want to add.
No no. Thank you I think you covered it well.
Okay.
Okay, great. Thank you guys. Thanks for taking my questions. Thank you really.
Your next question comes on the line of at Orange.
H T Wainwright through company. Please proceed with your question.
Great how everyone. Thanks for taking my question just one for me.
836, obviously.
Data coming up here at the end of the year on your things one study and and this word as you have mentioned allow for.
Let's face to presumably next year or two to really put together your initial combination studies.
I'm wondering if you could talk a little bit about the data what you were expecting in particular.
Given that.
Three six as you mentioned this is a unique capsid inhibitor and utilizes a novel binding site.
Within the core protein Zheimer dimer interface.
I wondered if there was anything that you're looking from that data that.
Help support the differential profile that.
You expect thanks.
Oh, yes. Thank you so it may be months to see a first and then and then guest on as it relates to the clinical data.
Yeah. Thanks for the question.
So you're right now a pretty six is what we call our next generation agent right in.
Differentiated cell itself significantly from earlier generations because of the high intrinsic potency at hand, but also.
As we've commented on many times the.
Ability to engage this second mechanism right. So that he can replace inhibition of the replenishment of the pools CCC DNA. We believe we will be therapeutically relevant dose and I think one of the problems with.
The first generation agents is that the.
E.
The activity at the second mechanism was sufficiently.
Less than the first mechanism activity.
And relevant does that they could give you the clinic just couldn't bouquets that so when you do engage that second mechanism clearly we believe we're going to have a fairly robust.
Response against production on RMA 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.
In fact that second mechanism.
Is playing an important moment carpeted space.
So so we have a molecule we're very excited about my liver exposure.
So I think overall, we're we're anxious to see the data to see how this translates.
The phone.
No I think that's that's basically it we're going to be looking at depth and speed of both HV.
Pardon the pressure and then there's a little bit about.
<unk> card that we may be able to interrogate which is.
Of the activity of the compound where system variance we're not.
Selectively enrolling patients with resistance, but we know that there was there is out there and we by chance and rolls on myself.
We may be able to also.
I nearly right.
The activity of this new generation I didn't keep dragons and variance, but that's a little bit.
Something that we cannot control.
Alright.
Fantastic. Thank you.
Thank you it.
Your next question comes from the line of Kiana K with charting.
Please proceed with your question.
Yes, K kind of Chardan some questions for Mike on the P. D. One.
Uhm first.
Mike can you point us to any.
Preclude data that you've published on your aural checkpoint inhibitor.
Well, we haven't published any specific preclinical data on the molecule that we nominated great icon to to a major communication paper that we published looking at the very unique mechanism of how the small molecule works relative to relative too.
Let's say.
An antibody right.
So.
No I can point that too we recently published that I think it was.
The.
Towards the middle of the end of last year came out.
And also in that paper, we show the small small molecule that we used.
Which was an earlier generation agent does have that.
Sort of anti tumor effect with so we were using anti tumor model because it was the most readily available model at the time, we've now subsequently developed.
HVV model that we're looking at molecules in animal models. So so you can see in that in that work that these.
These these small molecules do our very unique characteristics, both mechanistically and no function.
Very competitively with with antibiotics.
Okay.
I'll circle back with you to get that and so then just kind of moving on them too.
I guess the safety profile.
Again relative to an antibody you should have some advantages there, but how do we how do we then think about it the safety as you move in two combo therapies and what would you.
Be on high alert to look for their in terms of safety.
Whereas you know.
In the oncology setting.
An antibody based took one blockade does have some adverse events associated with that right and one of the things we wanted to do with 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.
With their body you have a very long action occurring right.
So you had 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.
And.
Essentially.
Just does enough of what we need to give to get the response plus you. If there's any issue we can actually remove drop because the PK washout.
Alright.
So so that's one thing the other thing is we we have.
We always do is look at Liberty targeting and so we have drugs that have high liver centric character. So so these molecules have.
Much reduce systemic exposure therefore allows us to to.
Target HBV versus having sort of that systemic.
Immune activation that we see with the typical antibody so I think.
Those characteristics of these molecules, we believe will support a better safety profile now where I can see that in the clinic, but.
I think we're pretty excited about.
You know the overall profile these molecules and the potential.
Yeah, I guess, I guess, where I'm going with that Mike is.
With the certainly the Destabilizer there was some tax 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.
Sure. So so obviously.
Each of these molecules work by different mechanism of action.
They are like different chemical entities vanilla themselves, so they'll have different characteristics.
We clearly in all our preclinical.
A non clinical studies are very careful ensuring that we don't have any drug drug interaction issues.
Associated with that now now we can't predict exactly what's going to happen clinically.
We do do combination studies in preclinical models to.
To assess the compatibility of these molecules.
From from agonists are antagonistic standpoint, we get some sense of of.
Safety.
Read on the combination when we do combination studies in vivo so.
No.
No I think we are 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 total of.
The theory.
Okay, well thanks for that.
Your next question comes from the line of collect each carry with Jeffries. Please proceed with your question.
Yes, Thank you and good morning, I guess, a single question in front of me here I guess, there's ongoing debate as to what the appropriate stop ringing criteria should be for many of these combination therapies.
I was or for.
For the new component can you opine on discuss a little bit more about that than what you think the suffering criteria should be and I guess related to that with 17 90 demonstrated the ability to increase hte specific immune responses could that potentially be added on as a component.
What could be a stopping criteria for your combination studies.
Yeah. Thank you collect J I'm going to hand that one over to guest.
Yes, hi.
So yeah great question.
I think.
Trying to say I think different groups will will come up with different scoping criteria. There is no.
Single as far as I know unified spoken criteria unusually stopping criteria our combos site.
You know and points it.
Doesn't just factor for example, a concentration of antigen.
Can do include pissed founded in blasts for example, HBV DNA another allt criteria.
I think we will know whether which is the most appropriate.
Hoping for a day or once we see what happens to the patients after they stop all therapy.
And for example.
When truth is 100, and then we see that there is a higher relapse, but when she was 10.
As part of the combo site endpoint and there's less way less than one can conclude obviously that is better than 100, but we're not there yet we don't have that data.
So I think it will be.
For lack of a better.
I think it would be try on there I think we'll have to try different things.
There is no even stray.
Straight consensus on how the subsequent to repair today with with no clear up as some people use different things, but that's we've repeated a number of locations. For example, 100 per mil in patients who have been for many years on milk therapy.
Is that criteria Go's thing, especially in Asia.
No you're right about the.
What we observe.
Three of the five patients that we were able to measuring cohort E Y where I'm going seven to 9001 study.
The challenge there.
Can you recall institution would be at criteria is something that cannot be measured really quickly to make a decision as you know this piece of assay a very labor intensive.
The collection of her for a blood more of a nuclear ourselves and they cannot be just run like a viral load uncoordinated way in the Sunrise way. So I think is a very good idea Michael.
I hope that we can find maybe some surrogate.
Indicate or the peace of our constitution.
Perhaps something lined with a measurement of sorry, both cytokinin interfering.
Interferon gamma comes to mind that can be more readily.
Italy run in the clinic a lot in a standardized way and that will be the challenge I ambition of including T. Start we're closed the deal. So we're confusion to hav as as part of the criteria.
Got it. Thank you that's very helpful. Thank you.
Ladies and gentlemen, we faced the a lot of time for questions I wasn't I'd like to turn to fly back to management for any additional are closing remarks.
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 with you today.
And those obviously include the announcement of additional data from the 729 phase one a one b clinical trial at Aas LD.
And the initial data from 836 phase one a one b trial by the end of the year. So we look forward to being in touch an operator that concludes our call. Thank you.
Thank you for participating in today's conference call. You May now disconnect your lines at this time.