Q4 2020 Genocea Biosciences Inc Earnings Call

February 11, 2021

[music].

Good morning, and welcome to you know Shack fourth quarter 2020 conference call. At this time all participants are in a listen only mode. Following the formal remarks, we will begin the call up for your questions. Please be advised that the call is being recorded at the company's request at this time.

I'd like to turn the call over to Dan Ferry of like site Advisors. Please proceed.

Thank you operator, and good morning, everyone.

Earlier today, we used.

The press release that outlines the topics we plan to discuss today.

This release is available at you know should I com under the investors tab.

Joining the call today chip Clark President and CEO.

Who will provide a brief corporate update and the company's chief financial officer to answer them all.

Will review the financial results.

After the prepared remarks, we will open up the call for Q&A.

Chip Diantha.

Tom Davis, Genocea, as Chief Medical Officer, and Jessica <unk>, <unk>, Chief Scientific Officer.

We'll then be available to answer your questions.

Before we begin I would like to remind everyone that statements made during this conference call.

Relating to Genocea is expected future performance.

Future business prospects or future events or plans may include forward looking statements as defined under the private Securities Litigation Reform Act of 1995.

All such forward looking statements are intended to be subject to the safe Harbor protection provided by the Reform Act actual outcomes and results could differ materially from those forecasts due to the impact of many factors beyond the control of Genocea.

<unk> expressly disclaims any duty to provide updates to its forward looking statements, whether as a result of new information future events or otherwise.

Participants are directed to the risk factors set forth in Genocea is 2019 annual report on form 10-K.

And other periodic reports filed with Securities Exchange Securities and Exchange Commission.

It is now my pleasure to pass the call over to chip.

Okay.

Thanks, Dan and thank you all for joining us today.

We're pleased to provide updates on several important efforts.

I'll start with our two clinical programs Gen nine and Gen 11.

As a reminder, Gen 11 is genocea is neo antigen targeted peripheral T cell therapy or <unk> therapy.

Which we're testing initially in checkpoint inhibitor refractory patients.

Our tightened study is a phase one two study evaluating safety biomarkers of activity and clinical efficacy in patients with a range of tumor types across two dosing cohorts, one with a single channel 11 dose.

And the other with Gen 11 administered as multiple low doses.

We have initiated two clinical sites and have begun accruing patients.

We will provide updates throughout the year and expect to report initial efficacy data from a patient subset.

The fourth quarter of this year or the first quarter on 2022.

Next let me update you on Gen nine our adjuvant and peptide neo antigen vaccine.

In November we presented expanded clinical and Immunogenicity findings for the ongoing phase <unk> trial.

The 2020 society for immunotherapy of cancer or <unk> annual meeting.

We were pleased to find evidence.

Excuse me Gen nine clinical activity on top of checkpoint inhibitor responses.

Among the nine CPI sensitive patients dosed with Gen nine.

Three patients experienced a novel reduction in tumor volume and achieved independent resist responses post to gen nine dosing, including two Prs and one CR.

Five additional CPI sensitive patients have shown disease control post vaccination for up to 11 months.

Within the CPI resistant population five of seven patients appear to have stabilized the disease lasting up to seven months.

And these results could become even more compelling with additional follow up.

Gen nine elicited strong.

Anti tumor before and CDA T cell responses.

We look forward to providing additional clinical and immunogenicity data from these patients in Q2.

Now, let me move on to some other news.

A few weeks ago, we announced a milestone publication in cancer discovery.

Which shares preclinical and clinical research confirming that Atlas is the only antigen selection platform able to identify the tumor surface presented antigens that induce T cell responses, whether they are neo antigens of anti tumor T cell responses or uniquely.

Uniquely to Atlas inhibitory antigens, which we call inhibits pro tumor CVA and CD four T cell responses.

We also demonstrated in the <unk> mouse melanoma model.

Net including an Atlas identified <unk> inhibitor <unk> in an otherwise protective cancer vaccine can completely abrogate such protection and.

And showed that inhibits <unk> mediated suppression of antitumor T cell responses cannot be overcome by checkpoint inhibitor therapy.

Finally, bringing it back to part a of the Gen. <unk> clinical trial, we showed that by selecting the right antigens with Atlas.

We were able to elicit T cell responses to 99% of the vaccine antigens.

Collectively.

These findings further validate our unique Atlas platform and highlight the potential importance not just of targeting the right Neo antigens, but also of identifying and excluding inhibitor <unk>.

Okay.

Answer immunotherapy targets to maximize patient clinical efficacy benefits.

As part of our efforts to investigate inhibits <unk> further.

We are excited to report our research collaboration with Dr. <unk> Laboratory at the University of Minnesota.

Leading group in cancer immunotherapy and T cell engineering methods.

Together, we will also develop T cell receptors targeting proprietary shared neo antigens identified the Atlas.

Now like everyone, we've been deeply affected by the global pandemic.

We believe we may be able to help enable our next generation Covid vaccine.

With the potential to protect universally against Sars Covid two.

And so we're pleased to unveil our ongoing effort to identify novel T cell antigens on the virus.

As part of this effort, we have initiated a collaboration with Dr. Robert Finberg share.

Share of the department of Medicine at the University of Massachusetts.

To identify conserved antigens of protective T cell responses to Sars Covid two.

Pairing atlas's antigen selection capabilities with Dr. <unk> expertise may lead to a better understanding around the role of T cells and inhibitor <unk> and the severity and duration of Sars Covid two symptoms.

In addition to this operational progress we recently strengthened our executive leadership team.

Pointing Dr. Raymond Stapleton.

<unk> executive Vice President of pharmaceutical Sciences and manufacturing.

Ray brings 20 plus years of industry experience, leading technical quality control and manufacturing operations at commercial and clinical stage biopharmaceutical companies.

I have no doubt that his leadership and expertise will prove essential to our plans to scale and commercialize our cancer Immunotherapies.

We are pleased that our progress on multiple fronts, not only this quarter, but throughout a very challenging 2020.

We believe this momentum has set us up well for success in 2021.

I'm now going to pass the call over to Diantha to summarize our financials from this quarter before opening the call up to questions.

But.

Thank you chip and good morning, everyone. We ended the quarter with $79 8 million of cash and cash equivalents compared with $40 1 million at December 31, 2019.

Our operating results for the quarter ended December 31, 2020 Orange balance.

R&D expenses were $7 8 million compared to $6 8 million for the same period in 2019.

G&A expenses were $3 9 million compared to $3 million.

Jim Carrey in 2019.

And our net loss was $15 million compared to $9 4 million same period in 2019.

<unk> operating plan extended cash runway to the end of 2010.

With that let's now open the call up for questions operator.

At this time.

Thanks, Brett sorry, and then the numbers.

Your question has been answered.

Can you share thoughts on the queue.

Yes.

For a moment.

On.

First question from Hawaii.

Okay.

Yeah.

Right.

Yeah.

Great. Thank you very much and congratulations on the update this morning.

Wanted to ask a question first about the general 11 clinical program.

I guess have you started manufacturing clinical material for Gen 11, and are you able to say anything about the manufacturing experienced thus far.

Hi, Ben Thanks for the question.

We are in the middle of our needle to needle process as you might call. It four Gen 11, it's a little bit too early to comment specifically on the patient experience, but based on the 15 plus developments in engineering runs we conducted with the Gen 11 process we are.

Have a high degree of confidence in the processes overall robustness and as I said, we intend to provide an update on.

Dates rather throughout the year, so we will certainly.

Manufacturing success is one of those things, we expect to be able to report on.

Okay excellent.

And then just one other question about the Sars Covid two program.

And just genocea his role in the collaboration with Dr. <unk> Dr Finberg.

I guess, what kind of data could we see from this collaboration and when.

Might we get this.

And also just from a cash perspective, what sort of impact is this there's a sars COVID-19 two antigen discovery program have on cash burn.

So.

So thanks, Ben for the question I'll have Jeff speak to that.

Scientific nature of your question and then I'll ask afterwards, diantha to speak to the cash impact.

Okay.

Thanks, Dan So as you know and as chip laid out T cells help antibodies do their jobs and they persist when the antibodies are gone and so our role with this.

Collaboration with Umass is to use Atlas to help us identify the right targets of T cell responses to include in a vaccine a next generation vaccine against this virus. So we published many years ago that.

Antibody targets changed right, that's what's happening right now with spike that because of antibodies. They all bind to essentially the same region. The protein the virus mutates away to try to evade the antibody response.

T cell.

The targets of T cells don't do that they don't change.

We are not under selective pressure and the virus because everybody presents a different piece of the same protein to their immune system to make our response to so what we are trying to find those conserved antigens that are targets of T cells that are associated with protective immunity and not enhanced disease, which is where the <unk> inhibitor <unk>.

May come into play.

And.

That are going to help.

Target any variant of the virus and not just <unk>.

Particular strain.

So we're really excited to see the continued data from this collaboration we have certainly begun already looking and we find very interesting results with our Atlas screen.

Diantha.

Thanks, Jeff So then as far as sort of a cash.

Impact our investment the investment is relatively modest I mean on.

Obviously, our focus is on our two clinical programs in the preclinical.

So this is this is a relatively modest investment at this stage.

Okay. That's fantastic great. Thank you so much from the call it.

Thanks Ben.

Your next question comes from the line of buying Ugly.

Cash from SBB Leerink your line is open.

Hi, Thank you all for the question I Wonder if we could get into Jan 11, and.

On the 60 data that you guys presented last year I think.

You I think you said again that you had a response.

And Genesis he responds to 89% on the targeted neo antigens and I also noted that you have an increase in poly commonality of TCR I Wonder if you could help us understand.

Quickly patient by patient.

Sort of how many <unk> are dominating the product beginning one dominate.

Five non dominance and average of two dominant I just wonder a patient by patient how consistent it is and how.

How spread the dominant says for the journey 11 that you actually stimulated ex vivo and then also how much there is instead of antigen spread polyclonal holiday afterwards.

Thanks, Dana a bunch of related questions.

I think we kept track of them, but of course have Jeff speak to them.

Hi, Dana Thanks for the question.

So I think that there was a few pieces in there one yes, we said that in our manufacturing process.

We maintain responses to about 90% of the targets that we want the T cells to be responding against and so if we are growing that patients T cells against 30 Neo antigen. What it means is that at the end of our manufacturing process. We have responses still to 27 of those neo antigen.

Now we also presented that the product is purely functional.

That analysis was not.

Related to the TCR that was related to the characteristics of the T cells that were responding and it meant that they were secreting multiple cytokines that we would believe to be very good once we transfer those sales into the body to help them in graft to help them kill the tumor so that's where the polyclonal <unk> came from.

Your last question was what was on <unk>.

TCR and how to narrow the coloniality or how many TCR emerge and if there is a dominant one we.

We have looked at some of our development run TCR profile overall and what I can tell you is that there is not an outgrowth of a dominant TCR. So that 97 per cent of the product is all one T cell type in fact, what we just see is that there isn't any enrichment of TCR specific.

For the antigens that we want to target with our product and this is exactly what we imagine that we would.

Want to have as we go through our process. So in the peripheral blood youre going to have millions of different <unk> and as we hone in on the antigen specific ones you should see a reduction in the overall number of TCR is that you find and the outgrowth of specific tcr's to your product, which is what we want.

Your last question was on antigen spread and we won't see that until we transfer the product into the patience and.

Look at immune responses or in graft meant after the transfer and Thats what will happen in our clinical trial as we start treating our patients.

Perfect and thank you for taking my meandering question on making it more specifics let me just make sure I understand so.

<unk>, you're getting 90% of the T cells that you want and you're not seeing dominance in that product are you seeing pretty even spread across let's say in your example, the 27.

Just to put a finer point on it you're correct, we see that 96% of the T cells in our product.

Specific for Neo antigen.

And then if we look at the breadth of their responses. What we're seeing is that we wanted them to respond to 30 things.

And at the end of the process. They are still responding to 27% to 30 things that we targeted so I just.

I know, it's really nuanced argument, but the point is that nearly every single T cell in the product is specific for the cancer, which is different than what has been reported for til therapies. For example, where there are a lot of bystander cells that get grown up alongside the tumor specific cells instead of the T cell <unk>.

<unk> is not purely targeting cancer antigens.

That's very helpful. Thank you.

Thank you Dana.

Your next question comes from the line of Michael <unk> from Baird. Your line is open.

Hi, This is Colin cousy on for Mike Thanks for taking our questions and congrats on all the progress.

On the on the General 11 study can you talk about.

Kind of.

How many more additional price youre looking to add throughout the year on any sort of initial feedback on if theres any interest and one dosing regimen over the others.

Thanks for the question Colin.

Tom would you handle that please.

Sure certainly good question.

As you know the protocol has two cohorts.

An initial one that serves as a dose escalation step for safety.

What's important to free.

That perspective is.

Is that we'll be able to tell what the product itself does when we infused into patients.

Not going to be the patients will not be giving limited kitchen.

But they will be given low dose IL two so this would be a very patient friendly regimen, but we then can rapidly dose escalate to the til type regimen that uses food limber depletion as well as high dose IL. Two I know your question is focused on how many patients will be putting in each arm book.

But in reality, we will see what happens as the protocol progresses, but we'll be focused on the high dose regimen. Since that's the one that's most likely to be effective.

That said, we certainly think that the low dose could be effective and could be very appropriate for patients who can't tolerate til type of therapies. So we will basically be assigning patients to either on dependent on what's appropriate for that patient.

Great. Thank you that's very helpful.

And then on congrats on a multiple collaborations announced here on the on.

On the T cell targeted proprietary shared neo antigens program I guess, you got a little bit more about where you are in the process and if there's any clarity on when we might see an update from that program.

Yes.

Maybe just could you answer that first by speaking to what we have found in terms of share of new antigens, Thus far and then reported on the progress.

Yes.

It's a really good question, what we have found so far is quite interesting so while we find common mutation.

People that we have screened over the past several years that we have been doing our atlas screening of mutant <unk>.

Just because they're common mutation does not mean that they are a common antigen that people can actually make a T cell response to them and in fact some of the common mutations that we have found across subjects are not.

Not never antigen.

In some cases some of the common mutations are dominant inhibiting that anytime we find that T cell response to them. They are inhibitory responses, which we would want to necessarily avoid and then there are some that are actually very good T cell targets. There every time that we have screened them. They are indeed no.

Antigens for the patients who.

We have had screened.

So the first one is the one that we are working on with the University of Minnesota and this.

Common neo antigen is quite interesting because we found it in about 10 per cent of the subjects that we screen across multiple different solid tumor types, which means that we're not limited in our ability to target different cancers with the same product.

And so we are currently.

Cloning this tcr's and showing that we can create a TCR T against this common mutation and then we have others in the queue that we will pursue next.

Okay. Thanks, so much.

Yeah.

Thanks Colin.

Again, if you have a question at this time, please press star one.

On your Touchtone telephone.

Question comes from the line up.

He'll bloom from Needham and company your line is open.

Good morning, everyone and thank you for taking our questions.

So maybe kind of a simple one could you set our expectations for the data update coming out of <unk> in the second quarter.

Are we going to look on.

Longer time here and is there a potential for some of these disease control patients to improve.

Yeah.

Thanks Gil for the question.

Tom could you speak to that.

Sure.

At this point following these patients for outcome as you suggested so the data that we're generating at this point in time is long term follow up.

So we will be able to talk about the patients that we have presented but what has happened to them over time.

And in all of these patients of course with a broad Lee targeted drug like Gen. Nine we would hope that we can not only shrink tumors, but also that we can stop them from growing.

So at this point the follow up is going to focus primarily on the durability of these responses.

And particularly in the refractory patients where they are expected to grow quite quickly if we see stability there, particularly if it's durable that would be a clear sign that we have helped these patients are you really don't see refractory patients.

Developed stable disease that lasts for six months to 12 months and those are the kind of follow ups that we will have.

Of course, we'll also be looking at other correlative science.

Significant amount of data to still come out showing really the connection between the vaccination and what has happened to the patients.

Okay excellent.

Maybe a bit of a follow on to Dana's question just to make sure that I also.

I understand what you guys talked about so.

Once you give the therapy, even if there is.

Different.

T cells responding to different.

I'm sorry.

On antigens.

Overtime, we expect less flow mallaby as the immune system is focusing on the right targets is that the right way to think about it.

Joe I'll have Jess take that question. Please.

I think that's a very difficult question to answer, especially without data.

So.

What we will do is we will track the dominant clone of types present in our product and our cell therapy product.

After we transfer them into the patient to <unk>.

Identify if some of those claims persist and grow if some disappear altogether.

And we will of course look for them infiltrating the tumor that is the best that I can answer your question at this point in time.

Okay that makes sense on data will will help clarify thanks Dan.

Got it maybe share.

Last theoretical one here.

You guys. Thank you, hey, Ralph or inhibit Jensen and infectious disease could you find on the hesitant for Covid.

Possibility.

[laughter] yeah.

Absolutely.

Absolutely. So I can give you the anecdote from our Epstein Barr virus program that we have reported publicly on in.

Maybe it was in 2017, we inhibit <unk> are very much in play in infectious disease.

And what's very interesting is that they're they.

They may they have the opportunity to serve either as something bad and dangerous as we've seen in cancer or potentially protective as we saw in SDN Barr virus and so in the case of Epstein Barr virus, we showed that.

People, who had inhibitor <unk> specific T cell responses did not develop them.

Mononucleosis after EBV infection, which is.

Went though proliferative disorder, they basically the immune system growth out of control.

And those that did not develop these inhibitors specific responses did develop on them.

And so it's exactly this question or this type of question that we can answer in the context of Covid with Atlas and it's possible that inhibits <unk> me it could be good that they put they protect the patients from getting that really severe syndrome that occurred in response to infection or Conversely, it could be driving the wrong kind of it.

In response that is driving this pathology and we will be answering that question with our screen.

Really interesting stuff, thanks for taking our questions.

Congrats on the progress.

Thanks Gil.

Yeah.

And I am showing no further questions at this time I would like to turn it back to the speakers for further comments.

Thank you operator.

And thanks again, everyone for joining us today.

Yeah.

Okay.

Ladies and gentlemen, this concludes today's conference call. Thank you all for joining you may now disconnect.

[music].

Sure.

[music].

Good morning, and welcome to channel shaft fourth quarter 2020 conference call. At this time all participants are in a listen only mode. Following the formal remarks, we will begin to call up from your questions. Please be advised that the call is being recorded at the company's request at this time I'd like to turn the call on.

Over to Dan Ferry of life by Advisors. Please proceed.

Thank you operator, and good morning, everyone.

Earlier today, we issued a press release that outlines the topics we plan to discuss today.

This release is available at you know should I com under the investors tab.

During the call today Chip Clark President and CEO.

Who will provide a brief corporate update and the company's Chief Financial Officer, Dan Duvall.

We will review the financial results.

After the prepared remarks, we will open up the call for Q&A.

And chip Diantha Tom.

Tom Davis, <unk>, Chief Medical Officer, and Jessica Fuck Theyre Genocea as Chief Scientific Officer.

We'll then be available to answer your questions.

Before we begin I would like to remind everyone that statements made during this conference call.

Relating to <unk> expected future performance future.

Future business prospects or future events or plans may include forward looking statements as defined under the private Securities Litigation Reform Act of 1995.

Genocea expressly disclaims any duty to provide updates to its forward looking statements, whether as a result of new information future events or otherwise.

Participants are directed to the risk factors set forth in Genocea is 2019 annual report on form 10-K and.

And other periodic reports filed with the Securities Exchange Securities and Exchange Commission.

It's now my pleasure to pass the call over to chip.

Thanks, Dan and thank you all for joining us today.

We're pleased to provide updates on several important efforts on.

I'll start with our two clinical programs Gen nine and Gen 11.

As a reminder, Gen 11 is genocea is neo antigen targeted peripheral T cell therapy or N P T therapy.

Which we're testing initially in checkpoint inhibitor refractory patients.

And the other with Gen 11 administered as multiple low doses.

We have initiated two clinical sites and have begun accruing patients.

We will provide updates throughout the year and expect to report initial efficacy data from a patient subset.

The fourth quarter on this year or the first quarter from 'twenty to 'twenty two.

Next let me update you on <unk> nine our adjuvant and peptide neo antigen vaccine.

In November we presented expanded clinical and Immunogenicity findings for the ongoing phase <unk> trial.

The 2020 society for immunotherapy of cancer or <unk> annual meeting.

We were pleased to find evidence.

Excuse me the Gen nine clinical activity on top of checkpoint inhibitor responses.

Among the nine CPI sensitive patients dosed with Jack on.

Three patients experienced a novel reduction in tumor volume and achieved independent resist responses posted gen nine dosing, including two Prs and one C. R.

Five additional CPI sensitive patients have shown disease control post vaccination for up to 11 months.

Within the CPI resistant population five of seven patients appear to have stabilized the disease lasting up to seven months.

And these results could become even more compelling with additional follow up.

Gen nine elicited strong.

Anti tumor see before and CDA T cell responses.

We look forward to providing additional clinical and immunogenicity data from these patients in Q2.

Now, let me move on to some other news.

A few weeks ago, we announced a milestone publication in cancer discovery, which shares preclinical and clinical research confirming that Atlas is the only antigen selection platform able to identify the tumor surface presented antigens that induce T cell responses, whether they are neo antigens.

Anti tumor T cell responses or <unk>.

Uniquely to Atlas inhibitory antigens, which we call inhibitors of pro tumor C. D E and CD four T cell responses.

We also demonstrated and the B 16 F 10 mouse melanoma model.

Including an Atlas identified <unk> inhibitor in an otherwise protective cancer vaccine can completely abrogate such protection.

And showed that inhibits renin mediated suppression of antitumor T cell responses cannot be overcome by checkpoint inhibitor therapy.

Finally, bringing it back to part a of the Gen. <unk> clinical trial, we showed that by selecting the right antigens with Atlas.

We were able to elicit T cell responses to 19, 9% of the vaccine antigens.

Collectively.

These findings further validate our unique Atlas platform and highlight the potential importance not just of targeting the right Neo antigens, but also of identifying and excluding inhibitors.

And as a cancer immunotherapy targets to maximize patient clinical efficacy benefits.

As part of our efforts to investigate inhibits <unk> further.

We're excited to report our research collaboration with Dr. <unk> Laboratory at the University of Minnesota.

Leading group in cancer immunotherapy and T cell engineering methods.

Together, we will also develop T cell receptor targeting proprietary shared neo antigens identified via Atlas.

Now like everyone, we've been deeply affected by the global pandemic.

And we believe we may be able to help enable our next generation COVID-19 vaccine with the potential to protect universally against Sars Covid two.

And so we're pleased to unveil our ongoing effort to identify novel T cell antigens on the virus.

As part of this effort, we have initiated a collaboration with Dr. Robert Finberg.

Share of the Department of Medicine at the University of Massachusetts to identify conserved antigens of protective T cell responses to Sars Covid two.

Pairing atlas's antigen selection capabilities with Dr. Finberg expertise may lead to a better understanding around the role of T cells, and inhibits <unk> and the severity and duration of Sars Covid two symptoms.

In addition to this operational progress we recently strengthened our executive leadership team appointing Dr. Raymond Stapleton.

<unk> executive Vice President of pharmaceutical Sciences and manufacturing.

Ray brings 20 plus years of industry experience, leading technical quality control and manufacturing operations at commercial and clinical stage biopharmaceutical companies.

I have no doubt that his leadership and expertise will prove essential to our plans to scale and commercialize our cancer Immunotherapies.

We are pleased that our progress on multiple fronts, not only this quarter, but throughout a very challenging 2020.

We believe this momentum has set us up well for success in 2021.

I'm now going to pass the call over to Diantha to summarize our financials from this quarter before opening the call up to questions.

Thank you chip and good morning, everyone.

We ended the quarter with $79 8 million of cash and cash equivalents compared with $40 1 million at December 31, 2019.

Our operating results for the quarter ended December 31, 2020, our installers.

<unk> expenses were $7 8 million compared to $6 8 million for the same period in 2019.

G&A expenses were $3 9 million compared to $3 million.

Same period in 2019.

And our net loss was $15 million compared to $9 4 million same period in 2019.

<unk> operating plan extended cash runway to the end of 'twenty two.

With that let's now open the call up for questions operator.

Okay.

Yes.

At this time.

Alright, and then the number one.

If your question has been answered or you wish to go.

I'm curious on from the queue. Please.

Power.

Well for a momentum.

Your first question comes from the line.

Okay.

Yeah.

Okay.

Great. Thank you very much and congratulations on the update this morning.

Wanted to ask a question first about the general 11 clinical program.

I guess have you started manufacturing clinical material for June 11th and are you able to say anything about the manufacturing experienced thus far.

Hi, Ben Thanks for the question.

We are in the middle of our needle to needle process as you might call. It four Gen 11, it's a little bit too early to comment specifically on the patient experience, but based on the 15th plus developments in engineering runs we conducted with the Gen 11 process we are.

Have a high degree of confidence in the processes overall robustness and as I said, we intend to provide an update on <unk>.

Dates rather throughout the year, so we will certainly.

Manufacturing success is one of those things and do you expect to be able to report on.

Okay excellent.

And then just one other question about the Sars Covid two program.

And just genocea his role in the collaboration with Doctor Dr. Steinberg, I guess, what what kind of data could we see from this collaboration and when.

Might we get there.

And also just from a cash perspective, what sort of impact is this does this sars COVID-19 two antigen discovery program have on cash burn.

So.

So thanks, Ben for the question I'll have Jeff speak to the.

Scientific nature of your question and then I'll ask afterwards, diantha to speak to the cash impact.

Yeah.

Thanks, Tim So yeah, as you know and as chip laid out on T cells help antibody do their jobs and they persist when the antibodies are gone and so our goal with this collaborations.

<unk> I'm with your math is to use Atlas to help us identify the right targets of T cell responses to include in a vaccine a next generation vaccine against this virus.

You know, we published many years ago that.

Antibody targets changed right, that's what's happening right now with spike that because of antibodies. They all buy into essentially the same region of the protein the virus mutates away to try to evade the antibody response.

T cell.

<unk> targets of T cells don't do that they don't change.

They are not under selective pressure and the virus because everybody presents a different piece of the same protein to their immune system to make our response to say what we are trying to find are those conserved antigens that are targets of T cells that are associated with protective immunity and not enhanced disease, which is where the <unk>.

Jim May come into play.

And.

Net are going to help.

On target any variant of the virus and not just a particular strain.

So we're really excited to see the continued data from this collaboration we have certainly begun already looking and we find very interesting results with our Atlas screen.

Diantha.

Thanks, Jeff.

As far as sort of a cash.

Impact on our investment the investments relatively modest I mean, obviously, our focus is on our two clinical programs and preclinical.

So this is this is a relatively modest investment at this stage.

Okay. That's fantastic great. Thank you so much from the call it.

Thanks Ben.

Your next question comes from the line of buying Ugly like Marsh from SBB Leerink. Your line is open.

Hi, Thank you all for the question I Wonder if we could get into Jonny 11, and.

On the safety data that you guys presented last year I think you I think you said again that you had a response.

Immunogenicity response to 89% on the targeted neo antigens and I also noted that you have an increase in poly commonality of TCR I Wonder if you could help us understand statistically patient by patient sort of how many TCR is on dominating the product youre getting one.

On dominate.

Five non dominance in average of two dominant I just wonder if patient by patient how consistent it is and how how spread the dominant says for the journey of 11 that you actually stimulated ex vivo and then also how much there is instead of antigenic spread polyclonal holiday afterwards.

Thanks, Dana a bunch of related questions.

I think we kept track of them, but of course have Jeff speak to them.

Hi, Dana Thanks for the question.

So I think that there was a few pieces in there one yes, we said that in our manufacturing process, we maintain responses to about 90% of the targets that we want the T cells to be responding against and so if we are growing that patients T cells against 30 Neo antigen.

What it means is that at the end of our manufacturing process, we have responses still to 27 of those neo antigen.

Now we also presented that the product is polyfunctional that that analysis was not.

Your last question was what was on.

TCR and how to narrow the coloniality or how many TCR emerge and if there is a dominant one we.

For the antigens that you want to target with our product and this is exactly what we imagined that we would.

Want to have as we go through our process. So in the peripheral blood youre going to have millions of different <unk> and as we hone in on the antigen specific ones you should see a reduction in the overall number of TCR is that you find and the outgrowth that specific tcr's to your product, which is what we want.

Your last question was on antigen spread and we won't see that until we transfer the product into the patience and.

Look at immune responses or an grassman after the transfer and Thats what will happen in our clinical trial as we start treating a patient.

Perfect and thank you for taking my meandering question and making it more specifics let me just make sure I understand so.

Product, you're getting 90% of the T cells that you want and you're not seeing dominance in that product on your <unk>.

Pretty even spread across let's say in your example, the 27.

Just to put a finer point on it you're correct.

You see that 96 per cent of the T cells in our product.

Our specific for neo antigen.

And then <unk>.

If we look at the breadth of their responses. What we're seeing is that we wanted them to respond to 30 things.

And at the end of the process. They are still responding to 27 of the 30 things that we targeted so I just.

I know, it's a really nuanced argument, but the point is that nearly every single T cell in the product is specific for the cancer, which is different than what has been reported for til therapies. For example, where there are a lot of them by stand ourselves that get grown up alongside the tumor specific cells instead of the T cell.

It is not purely targeting cancer antigen.

That's very helpful. Thank you.

Thank you Dana.

Your next question comes from the line of Michael <unk> from Baird. Your line is open.

Hi, This is Colin Suzie on for Mike Thanks for taking our questions and congrats on the progress on the.

On the General 11 study can you talk about.

Kind of.

How many more additional sites youre looking to add throughout the year.

Any sort of initial feedback on if theres any interest and one dosing regimen over the others.

Thanks for the question Colin.

Tom would you handle that please.

Sure certainly a good question.

As you know the protocol has two cohorts.

An initial one that serves as a dose escalation step for safety.

What's important to free.

That perspective.

Is that we will be able to tell what the product itself does when we infused into patients.

Not going to be the patients will not be given the Olympics kitchen.

But they will be given low dose IL two so this would be a very patient friendly regimen, but we then can rapidly dose escalate to the til type regimen that uses food depletion as well as high dose IL. Two I know your question is focused on how many patients will be putting in each arm.

But in reality, we will see what happens as the protocol progresses, but we'll be focused on the high dose regimen. Since that's the one that's most likely to be effective.

Great. Thank you that's very helpful. And then on congrats on the multiple collaborations announced here on the on the T cell targeted proprietary shared neo antigens program I guess, you talked a little bit more about where you are in the process and if there's any clarity on when we might see an update from that program.

Yeah.

Maybe just could you answer that first by speaking to.

What we have found in terms of share of new antigen, thus far and then reported on the progress.

Yes.

It's a really good question, what we have found so far is quite interesting so while we find common mutations.

People that we have screened over the past several years that we have been doing our atlas screening of mutant zone.

Just because they're common mutation does not mean that they are a common antigens that people can actually make a T cell response to them and in fact some of the common mutations that we have found across subjects are.

Not never antigen.

Antigens for the patients who.

We have had screened and so there is the first one is the one that we are working on with them the University of Minnesota and this.

So we are currently.

Cloning this tcr's and showing that we can create a TCR T against this common mutation and then we have others in the queue that we will pursue next.

Okay. Thanks, so much.

Yeah.

Thanks Holly.

Again, if you have a question at this time, please press star one.

On you touched on California.

<unk> comes from the lineup.

He'll bloom from Needham and company your line is open.

Good morning, everyone and thank you for taking our questions.

So maybe kind of a simple on could you set our expectations for the data update coming out of <unk> in the second quarter.

Are we going to look on.

Longer time here and is there a potential for some of these disease control patients to improve.

Yeah.

Thanks Gil for the question.

Tom could you speak to that.

Sure.

Yeah.

At this point following these patients for outcome as you suggested so the data that we're generating at this point in time is long term follow up.

So we will be able to talk about the patients that we have presented but what has happened to them over time.

And in all of these patients of course with a broad <unk> targeted drug like Gen. Nine we would hope that we can not only shrink tumors, but also that we can stop them from growing.

So at this point the follow up is going to focus primarily on the durability of these responses and.

In the refractory patients where they are expected to grow quite quickly if we see stability there, particularly if it's durable that would be a clear sign that we have helped these patients you really don't see refractory patients developed.

Developed stable disease that lasts for six months to 12 months and those are the kind of follow ups that we will have.

Of course, we'll also be looking at on a correlative science.

Significant amount of data to still come out showing really the connection between the vaccination and what has happened to the patients.

Okay excellent.

Maybe a bit of a follow on to Dana's question just to make sure that I also.

I understand what you guys talked about.

So once you give the therapy, even if there is.

T cells responding to different inhibit them sorry different antigens.

Over time, we expect less flow now levy as the immune system is focusing on the right targets is that the right way to think about it.

I'll have Jess take that question. Please.

I think that's a very difficult question to answer, especially without data so.

What we will do is we will track the dominant clone of types present in our product and our cell therapy product after we transfer them into the patient.

To identify if some of those closed persist and grow if some disappear altogether and.

And we will of course look for them infiltrating the tumor that is the best that I can answer your question at this point in time.

Okay that makes sense, so data will will help clarify thanks Dan.

Sure.

Last theoretical on here.

You guys think of my tenure growth for inhibitor Jensen and infectious disease could you find on the inhibitor for Covid.

Possibility.

Okay.

Yes.

Okay.

Absolutely so.

Can give you the anecdote from our Epstein Barr virus program that we have reported publicly on.

And maybe it was in 2017, we inhibit gins are very much in play in infectious disease.

And what's very interesting is that they they.

They may they have the opportunity to serve either as something bad and dangerous as we've seen in cancer or potentially protective as we saw an Epstein Barr virus and so in the case of Epstein Barr virus, we showed that.

People, who had inhibitor <unk> specific T cell responses did not develop them.

Mononucleosis after EBV infection, which is.

Lymphoproliferative disorder, they basically the immune system growth out of control.

And those that did not develop these inhibitors specific responses did develop on them and so it's.

Exactly this question or this type of question that we can answer in the context of Covid with Atlas and it's possible that inhibit Ginnie Mae <unk>.

Could be good that they put they protect the patients from getting that relates to veer syndrome that occurs in response to infection or Conversely, it could be driving the wrong kind of immune response that is driving this pathology and we will be answering that question with our screen.

Really interesting stuff, thanks for taking our questions and.

Congrats on the progress.

Thanks Kyle.

Okay.

And I am showing no further questions at this time I would like to turn it back to the speakers for further comments.

Thank you operator.

And thanks again, everyone for joining us today.

Yes.

Yeah.

Ladies and gentlemen, this concludes today's conference call. Thank you all for joining you may now disconnect.

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