Q3 2023 Vir Biotechnology Inc Earnings Call
Hello, and welcome to their Biotechnologies third quarter 2023 financial results and business update call. As a reminder, this conference call is being recorded at this time all participants are in a listen only mode. After the speaker's presentation. There will be a question and answer session I will now turn the call over to <unk>.
Sasha <unk> Ellis Executive Vice President Chief Corporate Affairs Officer, you May begin Mr. Minneapolis.
Thank you and good afternoon.
With me today are Dr. Marianne de backer, Chief Executive Officer, Dr. Phil Kang, Chief Medical Officer, and suddenly Chief Financial Officer.
Before we begin I would like to remind everyone that some of the statements. We're making today are forward looking statements under the securities laws.
These forward looking statements involve substantial risks and uncertainties that can cause our clinical development programs future.
Your results performance or achievements to differ significantly from those expressed or implied by such forward looking statements.
These risks and uncertainties and risks associated with our business are described in the Companys reports filed with the Securities and Exchange Commission, including forms 10-K, 10-Q and 8-K.
I will now turn the call over to our CEO, Dr. Mary Anne de backer.
Thank you good afternoon and welcome.
And the partners CEO.
I'm pleased to welcome you all here today.
Since the last time, we spoke you have made some impressive progress on driving our scientific platform, our pipeline and our clinical trials forward.
All this positive momentum is encouraging as we seek to serve all the patients who are waiting.
Specialty dose with unmet medical needs in multiple infectious disease area and beyond.
Let me first call your attention to the updates we are most looking forward to at E. <unk> deliver meeting in Boston later this month.
Our phase III data Readouts from two of our most advanced program chronic hepatitis b and chronic hepatitis Delta.
As a reminder, this includes initial data from part D. After March trial, where we are looking at combinations of our monoclonal antibody for a 34 34 and are assai our need for your two 280, 424, and 48 weeks with and without <unk> interferon Alpha.
We also look forward to sharing initial data from our ongoing solstice trial, which is evaluating our antibody fewer 34 34 alone. Our psionic you two to one even though or the combination of these can be a viable chronic therapy for <unk>.
<unk>, who are co infected with hepatitis Delta virus.
Thanks to the approximately 50 million in new BARDA funding, we have had positive momentum on the development of your 7% to nine.
Investigational next generation COVID-19, monoclonal antibody with a distinct combination of potency breadth and file in this capability.
This funding includes $40 million in project Nextgen, non diluted funding, which will support the development of your 7% to nine through phase one.
We expect the phase one trial to initiate in 2024, and we will be exploring a partnership for the development of this antibody post phase one.
The BARDA funding also supports alternatives monoclonal antibody delivery technologies, such as our EMEA delivered monoclonal antibodies, which have the potential to revolutionize the field of antibody therapeutics with the ultimate benefit of enabling greater patient access and ease.
Okay.
This funding is another testament to Pierce World class antibody platform and our ability to discover rare raw and highly potent monoclonal antibodies with the hope of generating powerful new medicines.
Switching gears to one of our newest clinical program in September the first participant was dosed in a phase one trial evaluating fear 13, 88, an investigational novel T cell vaccine for the prevention of HIV.
This trial is especially meaningful because it brings us and our supporters, which includes depend on Melinda Gates Foundation, the National Institute of allergy and infectious diseases and the HIV vaccine trials network, one step closer in our share pursuit of developing an HIV vaccine.
We are hopeful that our unique approach will help close the long standing public health gap in HIV prevention, and we look forward to sharing initial data from this trial in the second half 2024.
Finally, I want to give you a glimpse into some of the transformative strategic decisions fear has made to drive future growth and increased patient impact.
As you know our founding mission wasn't world without infectious disease, and we are now embarking on a broader vision powering the immune system to transform lives.
<unk> always seen ourself of anemia.
Monology company first and are now ready to expand into new areas with growth by applying our deep immunology expertise beyond infectious disease with the first applications in autoimmune diseases and immuno oncology.
This is made possible by our platform that has already created monoclonal antibody with enhanced selectivity and potency using AI based protein engineering.
We have some existing in house immuno oncology experience and we are already advancing in house antibody for tumor immunotherapy, we documented selectivity and potency under the leadership of Dr. Allen Korman, Senior Vice president of immune targeting here and fear.
Prior to joining here I don't know that the discovery of three approved drugs for oncology.
We are also embarking on a novel agnostic way to identify T cell receptors specific for tumor antigens and.
An effort led by our National Academy of Sciences Hematologist, Dr. Antonio answer that yeah.
We look forward to keeping you updated on this in 2024.
We believe all of this is we didn't reach thanks to our strong balance sheet, which allows us to take a chronic hepatitis b and chronic hepatitis delta programs through development inflection points as well as invest in our core antibody platform and to evaluate complementary external opportune.
Cities.
Meanwhile, we will continue to be judicious in our spend and investments to ensure that we maximize the deployment of the $1 7 billion in cash and investments.
Finally, I want to highlight that next week, we will be welcoming our new Chief Scientific officer talk to Jennifer town.
Jennifer brings more than two decades of R&D experience and a proven track record of successfully developing breakthrough medicines and bringing multiple investigational new drug application for innovative therapeutics for it.
This includes bringing 16 drug candidates from preclinical research to IMD and early clinical development.
Her scientific and external innovation leadership experience combined with her deep immunology expertise will be critical to delivering on our strategy to go beyond infectious disease.
I want to thank Phil pen for expanding his responsibilities as interim head of research.
We will continue to lead clinical research development and medical Affairs, as Chief Medical officer to bring our late stage portfolio to fruition.
As a top priority at fear.
With that I'll now turn the call over to Phil to provide an update on the progress we are making in our preclinical and clinical programs.
Thank you Mary Anne.
As Maryann mentioned, we're looking forward to sharing it is all the data from our phase two March chronic hepatitis B trial, and our phase two solstice chronic hepatitis Delta trial.
First I want to talk about chronic hepatitis b and our goal which is to achieve a functional cure defined as life won't control over four hours after a finite duration of treatment.
So that would be welcomed by the 300 million people living with chronic hepatitis b.
The only treatment available to achieve a functional cure is arduous and result in a functional cure when was three 7% of the time, we are aiming to flip the bar much higher with the goal of achieving a 30% or better functional cure it.
A partnership is that you cannot achieve a functional cure with only an anti viral or with any immuno modulator, which you really need both mechanisms of action, which is exactly what we are evaluating and our multiple ongoing clinical trials.
Our <unk> antibody beer 34, 34, and our SA RNA to Q&A and potentially act as both immuno.
Immuno March leaders and the Ebola virus.
We were $34 34 versus three mechanism stretch.
First it is a neutralizing antibody preventing viral entry of HBV and <unk>.
Second.
Enhanced optimization it removes viral particles.
Barbara particles from bloodstream.
Third it has a modified FC domain, which allows it to act as a potential direct immune activator capable in vitro stimulating dendritic cells to mature and create T cells against HBV or excuse me.
This is otherwise known as what maximal effect.
We were 2218 connect doesn't hamper our bottle by knocking down HBV RNA transcripts <unk> can also act as potential immuno modulator, because we believe the HBV protein hepatitis b surface antigen isn't immune tolerance and by knocking it down we can unleash the brake on the immune system severe.
<unk> is designed to act by analogy with the checkpoint inhibitor.
We have demonstrated that when viewed through 'twenty for peg interferon Alpha is given for 48 weeks about 30% of participants achieved hepatitis b surface antigen loss at the end of treatment and about 16% had sustained hepatitis b surface antigen loss 24 weeks after the end of treatment.
Although the number of participants treated to date is relatively small this is the first demonstration.
<unk> can have a potential impact on functional cure rates.
Okay.
In that same study identified that we may be able to predict who will have an off treatment response based on their endogenous anti <unk> antibody levels at the end of treatment.
There was also the first to demonstrate the additive impact of combining an SA RNA and a monoclonal antibody specifically veer too to aid with beer 34 34.
This combination resulted in the largest declines in hepatitis b surface antigen ever observed after just 12 weeks of combination therapy.
In part B of the <unk> study, we are evaluating geared to 'twenty. So severe 34 34 with them without peg interferon Alpha for 24 and 48 weeks.
To remind you after 24 weeks of your 220, plus peg interferon Alpha without your 34 34, we saw that 6% of patients achieved hepatitis b surface antigen loss at the end of treatment.
Thus for.
The fundamental questions are around the role of our fractional antibody we are 34 34.
First if we have 34 34 severe to 20, plus peg interferon alpha when we see an end of treatment response greater than 6%.
Second if we replace peg interferon Alpha with fear 34, 34, where we see an end of treatment response better than 6%.
Third if we give mir 34, 34 for 24 weeks or more will we see any signs of immune modulator activity suggestive of a maximal effect.
So that would strongly support the potential role of your 34 34 functional curative regimen.
Now, let's shift gears to chronic hepatitis Delta.
About 100000 people in the United States and potentially over 200000 and <unk> are currently estimated to have HBV HCV co infection.
This is likely to be an underestimate given the under diagnosis rates for chronic hepatitis Delta, we believe having a highly efficacious easy to use treatment for chronic hepatitis Delta will drive the desire to be diagnosed.
Delta is one of the most severe forms of viral hepatitis with four times greater risk of liver cancer, and two times greater risk of death compared to hepatitis B.
Notably, we don't yet have potent chronic viral suppressive therapy for adult and recognition of this urgent unmet medical need there are potentially accelerated path to approval.
Our antibody <unk> thousand 34, and our <unk> can also links with the hepatitis Delta lifecycle, because hepatitis Delta virus requires for hepatitis b surface antigen to be infectious, notably with the only currently available chronic treatment.
What percent of patients achieved undetectable HBV RNA after a full 48 weeks of therapy with 45% of patients receiving some benefit.
This regimen also requires lifelong daily subcutaneous injections.
We have challenged ourselves to develop chronic suppressive therapy that is better not just in terms of efficacy, but also in terms of convenience safety and Tolerability I'm excited to see if we can get there.
Data from our solstice trial will be shared as a late breaker oral presentation at <unk>.
Specifically, we will be evaluating the safety and antiviral efficacy of your 34 34 loans were $2 one eight alone and the combination of the two together in a small cohort of participants.
Looking ahead to what we believe will enter the clinic next is near $70 to nine our next generation investigational COVID-19, monoclonal antibody, which is being funded in part by part of.
This funding include the parallel research and development of next generation <unk>, such a circular RNA or self amplifying RNA that would actually include this antibody potentially allowing your own cells to make the year, 7% to nine this.
This would be the ultimate combination of RNA in antibody technology instead.
Instead of using RNA to encode a protein that your body then must develop an immune response against this is about RNA coded antibody that directly to furniture.
Finally, a quick look back as I know there remain questions about beyond 2042, our investigational prophylactic influenza a antibody.
Our ongoing post hoc analyses have yielded the following two important insights first near 2480, <unk> ability to reduce cases of symptomatic flu improved to 57% for the 200 milligram dose when the case definition includes fever that is how symptomatic illness is defined.
Second this relative risk reduction increases further to 65% when excluding the cases of flu that occurred within a few days of dosing.
Notably our next generation antibody Vir 2009 to 81 is not only more potent in vivo, but covers both flu and flu B <unk>.
Furthermore, because it inhibits the neuraminidase enzyme like all current through anti Virals. Its mechanism of action has been clinically validated and is derisked.
The IND submission for <unk> 2000, 1981 is anticipated in the second half of 2024.
In addition to Vir 2081, and <unk> 72 to nine we have two other preclinical candidates that we expect an IND filing for in the next 12 months to 24 months.
<unk> hundred 90 is an investigational monoclonal antibody against respiratory syncytial virus and human Metapneumovirus.
You may have heard the news of the incredible demand surrounding the currently available map for RSV.
If you can have a single monoclonal antibody that not only covers RSV, but also a second viruses human metapneumovirus that also causes significant morbidity and mortality in infants.
We also have an investigational novel therapeutic vaccine candidate for control of high grade squamous epithelium, precancerous lesions and HPV cancers that is called Vir $19 49.
Our talented researchers here at <unk> have been very busy executing and I'm excited to hand over the reins to Jennifer town as Chief Scientific Officer. She will no doubt further bolster our innovation mindset.
I will now turn the call over to Chief Financial Officer somebody.
Thank you Phil we're pleased to share our financial results for the third quarter of 2023.
Total revenues were $2 6 million compared to $374 6 million for the same period a year ago.
The primary reason for the decline is lower collaboration revenues from such roadmap compared to a year ago.
We continue to expect collaboration revenues to be at minimal levels and potentially make a negative contribution to our top line due to the ongoing required investments to support the marketing authorization for <unk>.
App, which our partner GSK leads the efforts.
Turning to operating expenses.
R&D expenses in the third quarter of 2023 were $148 $3 million compared to $114 $2 million in the same period in 2022.
In the third quarter of 2023, we recorded an expense of $21 9 million for the cancellation of phase III manufacturing activities for <unk> 'twenty for <unk>, our investigational flu monoclonal antibody.
With this expense recorded costs related to mirror 2482 are now largely behind us.
Other drivers of year over year growth worthy investments in our ongoing phase III studies in hepatitis B and hepatitis Delta.
SG&A expenses in the third quarter of 2023 were $41 1 million compared to $43 2 million for.
For the same period in 2022.
The decline was primarily driven by lower consulting expenses and stock based compensation.
For the third quarter of 2023, we reported a consolidated net loss of $163 4 million.
<unk> to a net income of $175 3 million for the same period in 2022.
Turning to the balance sheet, we ended the third quarter of 2023 with cash and investments of $1 $74 billion.
Compared to $1 9 billion.
The end of the second quarter of 2023.
During the third quarter, we made a payment of $67 million to our collaborator GSK for excess the turbine that supply manufacturing capacity, which were originally recorded as a liability in 2022.
With this recent payment the liability that GSK is effectively paid off.
Excluding the payment to GSK, our cash utilization during the third quarter was approximately $94 million.
In closing I would like to add that we are taking measures to optimize our cost structure and capital allocation.
You can expect us to continue to be strong stewards of capital and having a disciplined approach to capital allocation and expense management I will now turn the call back this option.
Thank you sung we will now start the Q&A session. Please limit questions to two per person. So that we are able to get to all of our covering analysts.
Operator, please open up the lines.
Our first question will come from the line of Gena Wang with Barclays. Please go ahead.
Thank you for taking my questions I have two questions. One is a big picture question.
So maryann.
You mentioned that you wanted to I guess expense strategic focus altra.
Auto immune diseases, and immuno oncology could you share with us your key rationale.
For selecting.
St lead indications and my second question is small few regarding the E. S O D upbeat.
If I hear you correctly, you mentioned that Youre looking for.
In general for HBV over 30% functional cure so for this particular March part B data.
Given we know that.
Shimon complete the treatment so what will be the initial bar you'll be looking for so that we can see.
After six months of treatment that could be above 30%.
Thank you very much Gina appreciate those questions maybe first on the Big picture one as you mentioned so as you know our ambition here is to book become an integrated commercial company and of course, it products that address significant unmet patient need.
And ever since Q as filed with US we have 13 ourselves of immunology company. So what we have been doing at theories always aiming.
Aiming to bolster the immune system.
<unk> ability to fight disease and in the first seven years clearly that was focused entirely on me.
Addressing unmet need in infectious disease. However, as you well know we have both a very powerful T cell antibody platform and we have a T cell platform and you really want to build on those tools to make an impact.
In a much broader area, we can use exactly the same types of technologies and platforms to also for example helps that the balance of the immune system to fight cancer what to address.
Diseases, where the immune system really has gone.
<unk> such as in autoimmune disease.
And we are not starting here from scratch, we already had a small team focused on immune targeting an oncology under the leadership of Alan Corpsman, who as mentioned in my introductory comments is first and for discover free.
<unk> blockbuster Sweeney and immuno oncology some of those being euro for Arnold Evo, while he was at BMS and that's also mentioned in my prepared comments.
Also have here the royalty known Immunologists Antonio answer that.
So it's really working again on a novel agnostic way to identify T cell receptors specific to vary.
Specific tumor antigens. So we have a lot here to build on and mostly we want to make sure that all of that great knowledge platform technology that we have also using AI and machine learning for example to in house the interaction of antibodies with south of the immune system. That's been do not just limit.
It ourselves to exploring that in infectious disease, but also explore it in other areas of significant unmet patient need.
Now turning to your second question as to the a S. L. D updates I would just maybe start with reminding everyone, where we come from and our novel <unk> failed to provide a little bit more color on what we will be reading out at <unk>. So just for everyone to remind ourselves so.
In hepatitis B, we started by testing the hypothesis, whether combining an anti viral and an immuno mother Nader would be able to exert significant effect in chronic hepatitis b patients.
He started off initially by looking at if the wood apps to interferon Alpha work functional cure rates. After 48 weeks of treatment only 3% to 7%. If you would add to interferon Alpha <unk> could you actually increase the functional cure rate and.
As Phil.
Phil mentioned it in his prepared comments I mean, we have thus far shown a 16% sustained at Sanchez S antigen loss with that combination and that's really the highest antigen loss that has thus far been reported for a regimen in this field.
We then want to go all in and also the question could be potentially replace interferon alpha with our antibody 34, 34 or what would it look like if we would replace them.
Or what would it look like if we added them.
34, 34, our antibody to that regimen. So in large part a we started.
Answering that initial question.
And again only bits shorts regiments short treatments five in 12 weeks in part a of the much trial, we could see that combining <unk> and our antibody.
Really delivering additive effects.
<unk> $2 seven lakh decline in S antigen <unk>.
There were no safety signals seen to date.
So that gave us a lot of confidence to look forward to our part b.
<unk>, where we actually are exploring the same combination with or without back interferon, but now for longer.
Treatment durations, 24% and 48 weeks and perhaps with that intro I want to ask Phil to provide a little bit more color. What is there to expect that are at a S.
Okay.
Thank you Mary Anne and thank you Gena for the question. So maybe I'll put a put a couple of statements in context, first which is that predicting off treatment rates from on treatment response rates is still very much in its infancy. As you know from our previous presentation at <unk>, we were the first to.
Right that if you had a endogenous anti Hbf's response, you were more likely to have an off treatment response and that was one of the first times. There was any hint of a predictor of off treatment response from entrepreneurs response so.
So I can just say generally that of course in answer to your question is.
One is looking for a greater than 30% off treatment response than the Entre men response should be out there or higher and that would be the clinical bar to progressive regimen for and that's true for all for all the regiment that we're looking at but to be specific on <unk> I think what's really important to think about is that with <unk>.
Maryann statement, we've proven that <unk> could have a role in a functional cure. The next question is can 34 34 have a role in a functional cure and that's why I in my prepared remarks, I talked about the fact that when you have <unk> plus interferon for 24 weeks, you will see only 6% of patient probably end of treatment.
And the first question we need to answer is if we add 34 34 or replace peg interferon, where we move beyond that and therefore really honing in on the role of 34 34 that it can have either in achieving another treatment response and then hopefully.
Later on and off treatment response, so the answer to your question is is that predicting an off human response from an entre in response is still in its infancy, you would need at least a 30% rate.
What we're focused on for ESOP is with $34 34 get us closer to that answer.
Yeah.
Our next question will come from the line of Paul Choi with Goldman Sachs. Please go ahead.
Hi, Thank you and good afternoon, everyone I want to maybe follow up on <unk> question. A question regarding the expansion into autoimmune and immuno oncology Maryann could you maybe.
Sketch for us how youre thinking about the metrics that youre going to share with the street in terms of.
How to further allocate capital and sort of again.
The street might be able to keep score on your progress and expansion into these two areas.
Second.
Regarding RSV I was wondering I realize it's still relatively early stage, but given the commercial success at Pfizer in Santa Fe are saying with their products can you maybe again sketch out how you envision clinical development of <unk> hundred 90 over the next couple of years. Thank you.
Yes.
Yes.
Thank you Paul maybe we'll start with the RSV.
Phil do you want to give a bit more color on why we stopped it program.
Yes definitely Paul so thank you for that question, so with our <unk> hundred 90 antibody, which is both covering both <unk>.
In human Metapneumovirus. The answer is that we believe we can bring it forward in the next 12 to 24 months and the path is relatively straightforward and has really been blazed by others were in the infant population what youre trying to demonstrate is prevention of lower risk or <unk>, which were attractive friction medically attended.
Respiratory tract infection or lower respiratory tract infection, and we believe that there is a relatively straightforward path to do so after you obtain phase one PK data beyond that as you know this is a partnered program with GSK and we are working closely with our collaborator to determine the fastest and most robust path forward. So thats, what I can say about the.
<unk> hundred 90 at this time.
Thank you Phil and then Paul on your first question I first want to clarify that the efforts. We are doing in these new areas are at discovery stage and so.
Maybe also ask a sort of provide a little bit more background on how we are allocating capital.
Yes, Thanks, Mary Anne and thanks, Paul for any questions. So so Paul in terms of the metrics as Maryann said.
The efforts in autoimmune and oncology discovery.
That's not an expensive part.
Or it doesn't require a large investment of your <unk>.
Capital allocation here will still largely be directed toward our mid stage programs in hepatitis B and hepatitis Delta.
Those will be ongoing.
For the foreseeable future.
A majority of our capital allocation will be directly there.
No.
Wanted to add something here.
We have in the past year to date, our capital allocation has been heavily directed towards a couple of items, obviously of the phase III study and the related phase III manufacturing activities.
So the liability to GSK related to natural gas supply and manufacturing.
As you probably saw from the press release, we did take a write down for those manufacturing activity. So those costs the food costs are behind us now.
On the liability that just hit the button when.
When you pay down so again, the capital going forward largely largely be director Jeremy clinical stage programs.
Yeah, so that would just add.
In addition to capital allocation to predominantly our clinical stage programs and of course, we continue to explore if there are external innovation opportunities that could help us accelerate our programs or complement what together with young kids.
Thank you Paul.
Your next question comes from the line of Eric Joseph with Jpmorgan. Please go ahead.
Hi, there it's still there.
Right.
Couple of ones from us.
Following up on that last question. So we think that opportunity do you see that.
Something maybe more than new immuno oncology side all the.
Historical mineralogy side of the business.
And I'll put in myeloma.
Okay.
I'm very sorry, Eric if he could not understand you've heard as well.
Alright, sorry can you hear me now.
Could you try again.
Yeah. So the question was just following on from the previous question about.
There's some comp metrics opportunity I know you were looking at potentially I'm glad you could be more in the immuno oncology space or in the historical faced embryology.
Okay. Thank you for that question Eric Yes. So that's as mentioned we are looking at external innovation really from the perspective of.
How can we accelerate once they are already doing I I really do believe that we have world class expertise in our platform 71 of course stay at.
At the forefront in our fields and so we're looking at anything that could help us of stadia, Tennessee leapfrog. So that's got them.
Both he and infectious diseases or beyond.
Alright, Thanks, Tim just one quick one about the HBV program.
Forward to the off treatment follow up Dan you've now got into into Q4.
Would you expect patients.
The off the nuc by that point, we'll still on nukes.
Thanks.
Thank you for the question. This is <unk> so <unk>.
24 weeks post treatment.
Will.
It's actually somewhat of a mixed bag, but they will you can continue to expect that they will still be on nukes and usually what happens is once they've demonstrated that they have.
<unk> surface antigen for at least six months off treatment their nuclear stopped and then you follow them for another period of time to make sure that they don't relapse further I will say, though that as you know the nukes are usually only suppressed HBV DNA and therefore surface antigen loss, which is a protein would be unexpected.
It should be impacted by the nucleoside reverse transcriptase inhibitor. So although of course, it's not a perfect match I think thats what were looking forward to and what we're guiding to is the post treatment data.
All of our drugs, but still on the nucleoside reverse transcriptase inhibitor.
Great. Thank you. Thank you. Thank you.
Okay.
Thanks Jack.
Your next question comes from the line of Patrick <unk> with H C. Wainwright. Please go ahead.
Thanks. Good afternoon first I'm wondering if you can discuss the bar for regulatory approval in H D D or hepatitis Delta and what you would need to see in solstice to give confidence that this program is on track and secondly, what would be the next steps for the Delta program specifically.
Would you, possibly be able to move directly into a phase III program. After a socialist readout based on all of the data that's been generated across HBV and H D D.
Yes, thank you for that question.
So I mean, that's you know the goal of therapy in Dallas last chronic suppression as well as a reduction of liver inflammation. That's also how the bar is set on the regulatory side.
Phil do you want to add any more color to what he wanted to seen solstice, yes definitely maryanne. So so exactly as Maryann said the regulatory bar is two log decline in HBV RNA and the normalization of ALP.
That was one of the bonds that were set early on to allow for and incentivize drug development and I think that that's one of the bars, one should look at but I think another part of look at is undetected ability and of HBV RNA that is another marker that is totally associated with.
With the clinical benefit.
So we're looking at both of those bars I do want to remind you that for <unk>, we're going to be having a small cohort of patients treated for a relatively short period of time and I think that we will have to just wait to see what that data looks like to be able to know what the next steps are going to be but as I've mentioned in my prepared remarks, the regulatory path.
Halfway can be accelerated.
If warranted given the unmet need in this space.
Yep.
Thank you very much.
Thank you Bob for your next question comes from the line of Atlanta release with Leerink Partners. Please go ahead.
Hi, Good afternoon. This is Nick <unk> on for <unk>. Thanks for taking my question, maybe first could.
Could you remind us what the status is of the next generation 291 antibody against flu, a and B I guess could you talk a little bit about how this antibody is differentiated from 2482 aside from this will be targeting aspect as well but.
Then secondly could you discuss some of the learnings, which you might apply from your experience developing too quick to move to the development of 291.
Thanks.
Yes. Thank you for that question Nick.
Yes, so I will start and then I'll ask Phil to provide a bit more.
So first of all as you rightly pointed out one of the major differences between 248 to $29 81, our next generation <unk> antibody is the fact that it covers both <unk> and <unk>. It's also the different mechanism of action is to not many days inhibitor and that as you know.
Mechanism of action that has been proven to work before we have also seen in vitro. That's the antibody is more potent than 2482, so just a lot of differentiating.
Bonus here for our next generation antibody that we feel are very relevant.
And as it relates to our learnings from 2482 S.
Joe pointed out in his prepared remarks.
Some learnings that we already have based on initial data analysis I mean, obviously, we have seen that's for the to the clinical trials. It does make a difference but you include fever in your primary endpoint. It also is really important.
How much time elapsed between.
Some of them being dosed on someone being infected. So these are of course very important learnings for us and we are of course, continuing to analyze the data and cluster as much learnings as we can for our next steps and maybe you can talk a little bit more about all the data analysis that is ongoing.
And we're planning to learn more about by beginning of next year definitely Marianne so.
Nick the one of the critical questions that always exists regardless of the space and especially as true for infectious disease is how does your in vitro or in vivo results.
Translate into the clinic and so one of the critical questions. In addition to all the lessons that Marianne pointed out is how do we calibrate dose between in vivo findings and clinical efficacy. So one of the advantages of having really been the first.
Company to ever run a prophylactic outpatient flu trial as we now will end soon we'll have the data that really calibrates PK PD as I mentioned in my as I May have mentioned previously which allows us to really understand the dosing concentration that is necessary and translate in vitro.
And in vivo filings to people and so that will be a very useful part of our 2000 1981 development. In addition to what Marion mentioned about clinical endpoints and timing is really trying to calibrate that bridge that gap and using $2092 82 to help inform 2091, and we're already planning a series of studies.
To make sure that that gap is as small as possible.
Okay helpful. Thanks, Phil So thinking about this future trial design would you consider using the who and CDC and who <unk> CDC endpoints.
Your primary.
Future trials in flu shot should we think about that since they both feature fever.
Yes, so I think we maybe even a little bit more advanced beyond that we are basically certainly recognizing that fever is an important or temperature. If you would now they do have a slightly different temperature between the CDC and the <unk> 37, eight versus 38 degrees Celsius.
So we are looking into that as well as any other symptoms that are well covered by 2042 and post hoc analysis. So we're going to put all that together to decide but certainly FIFA will be a part of what we consider moving forward.
Thank you.
Your next question will come from the line of <unk> <unk> with TD Cowen. Please go ahead.
Hi, good afternoon, and thanks for taking our questions we.
We have one on the solstice trial with data E. S. L D.
Approximately how many patients worth of data should we expect and are each treatment group pretty balanced and.
What efficacy measures do you expect to report in addition to the primary endpoint.
Thank you ever.
I will just say that obviously just still be the very first time that we show them.
Really very initial data also from our solstice trial So F.
Phil mentioned in his prepared remarks. This is still a small number of participants in each of the arms, but we will see some initial data on of course to do a one eight alone 34 34 loan and then the combination.
Anything to add there Phil.
No I don't think maybe I'll just clarify a couple of things that essentially we are going to be looking at as maryann pointed out the monotherapy and the combination therapy and the way in which the study is designed as we enrolled a very small number of patients in both monotherapy arms and then if they.
It showed signs of anti viral activity or didn't show signs of Orange Factbook antiviral activity, they would or would not roll into a competition or treatment to be able to really understand how the two drugs work together or don't work together. So that's going to be the design of the trial and we look forward to sharing data and MLB.
Thank you had some spending on talent.
How important is getting.
Getting H T V to undetectable levels granted that the regulatory bars, the two log decline.
So I think that the answer to your question is certainly getting to undetected book is a higher bar than a two log decline I think that there is good clinical data, suggesting that on detectability correlates well with clinical outcomes and I think that as I mentioned before.
In other words, the current therapy, it's about 12%. So I would I would say that that 12% of course happens after a full four weeks of therapy and the question is can we meet or do better than that given the fact that we have been following our patients for a much shorter period of time. So I think we'll just have to wait and see what <unk> has to say and let the science speak.
Thank you very much.
Thank you Ed.
Your next question comes from the line of Joseph Stringer with Needham <unk> Company. Please go ahead.
Hi, Thanks for taking our question just a quick one on the HIV program.
Phase one readout what type of data do you plan to announce on that the second half of next year and what would give you confidence, but what would you need to see to proceed to next steps in that program.
Okay.
Yes. Thank you for that question Joey.
So do you want to.
Hey, Kevin. Thank you definitely so as you noted it is a phase one study is an immunogenicity study in healthy volunteers. So the primary endpoint is obviously safety plus immunogenicity and so the answer is as we expect to have.
Understanding of one is the insert which is obviously, an HIV insert immunogenic and we Mount <unk> T cell responses or sorry, rather CD eight T cell responses against the cassette then the next question is is if we do what type of T cells are we creating are we creating what we're calling effective.
Emory T cells, which are really T cells that are very special that reside in the newco. So they're ready to fight they don't need to be they don't need to multiply before they can have impact and then third if possible to understand what type of HLA restriction they have and whether for example, they will be restricted by MHC E which.
As something that would be a very unique immune response, which might be harder for the virus to overcome so all of those are things. We are looking for in our immunologic Readouts. We are planning initial data from those immunologic Readouts next year.
Right and then maybe just to add to that.
The HCN fee based vaccine or what we call the T cell.
That form I mean learning dose data initial data for HIV, but also really be.
Helpful in guiding us for our next IND.
<unk> T cell vaccine that is focused on.
On the HPV.
Thank you for taking my question.
Thank you Joe I will now turn the conference back over to Dr. Marianne tobacco for closing remarks.
Okay.
Hey, Thank you operator, and thank you all again for your time and attention today to close I just want to leave you with these couple of takeaways.
First we continued to make progress on our clinical programs and you can expect new data from our ongoing phase two clinic, hepatitis B and chronic hepatitis Delta clinical trial to be presented on November 13th.
Second we are expanding our strategic focus beyond infectious disease.
Two auto immune diseases and immuno oncology.
We also pioneering the discovery of RMA delivered monoclonal antibodies are thanks to the help of new funding from BARDA.
And lastly, the $1 7 billion in cash and investments that we have available supports the advancement of our hepatitis B and <unk> clinical trials and our core antibody platform. Yes. Additionally, Additionally, it enables us to evaluate complementary external opportunities that's trying to.
Our existing platform and pipeline.
Thank you again all of you for joining US today, we really appreciate your time and your interest in <unk>.
Operator, you may end the call.
Thank you all for joining this does conclude today's meeting you may now disconnect.
Okay.