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Edited Transcript of GNCA earnings conference call or presentation 24-Oct-19 12:30pm GMT

Q3 2019 Genocea Biosciences Inc Earnings Call

Cambridge Oct 29, 2019 (Thomson StreetEvents) -- Edited Transcript of Genocea Biosciences Inc earnings conference call or presentation Thursday, October 24, 2019 at 12:30:00pm GMT

TEXT version of Transcript

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Corporate Participants

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* Diantha Duvall

Genocea Biosciences, Inc. - CFO

* Jessica Baker Flechtner

Genocea Biosciences, Inc. - Chief Scientific Officer

* Thomas A. Davis

Genocea Biosciences, Inc. - Chief Medical Officer

* William D. Clark

Genocea Biosciences, Inc. - President, CEO & Director

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Conference Call Participants

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* Benjamin Jay Burnett

Stifel, Nicolaus & Company, Incorporated, Research Division - Associate

* Chad Jason Messer

Needham & Company, LLC, Research Division - Senior Analyst

* Colleen Margaret Hanley

Robert W. Baird & Co. Incorporated, Research Division - Research Analyst

* Daina Michelle Graybosch

SVB Leerink LLC, Research Division - MD & Senior Research Analyst

* Gil Joseph Blum

Needham & Company, LLC, Research Division - Analyst

* Daniel Ferry

LifeSci Advisors, LLC - MD & Relationship Manager

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Presentation

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Operator [1]

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Ladies and gentlemen, thank you for standing by, and welcome to the Genocea Biosciences Third Quarter 2019 Financial Results Conference Call. (Operator Instructions)

I would now like to turn the conference over to your speaker today, Mr. Dan Ferry, Managing Director at LifeSci Advisors. Thank you. Please go ahead, sir.

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Daniel Ferry, LifeSci Advisors, LLC - MD & Relationship Manager [2]

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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 genocea.com under the Investors tab.

During the call today, Chip Clark, President and CEO, will provide a corporate update; and the company's Chief Financial Officer, Diantha Duvall, will review the financial results. After the prepared remarks, we will open up the call for Q&A and Chip; Diantha; Tom Davis, Chief Medical Officer; and Jessica Flechtner, Chief Scientific Officer, will 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's 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. 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's 2018 annual report on Form 10-K and other periodic reports filed with the Securities and Exchange Commission.

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

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William D. Clark, Genocea Biosciences, Inc. - President, CEO & Director [3]

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Thanks, Dan, and thank you all for joining us today. We continue to make important progress in the third quarter across each of our areas of operational focus, namely: our neoantigen vaccine, GEN-009; our neoantigen T cell therapy, GEN-011; and our ATLAS antigen discovery platform.

Let me first summarize our GEN-009 progress. As most of you know, we presented immunogenicity data from Part A of our Phase I/IIa study at the European Society for Medical Oncology Conference 2019, or ESMO. Our preliminary analysis of patients with both ex vivo and IVS data showed GEN-009 generated immune responses to 98% of all immunized neoantigens, which is both unprecedented for neoantigen vaccinations and a clear reminder of the power of our ATLAS platform for antigen selection. We expect to present substantially all of the remainder of Part A short-term immunogenicity results at the Society of Immunotherapy for Cancer (sic) [Society for Immunotherapy of Cancer], or SITC, Conference in early November.

With that in mind, I want to reflect on the immunogenicity goals of a neoantigen vaccine and our progress against these goals. We first want immune responses to substantially all vaccinated neoantigens. Second, we want responses from both CD8 as well as CD4 T cell subsets, which are together essential for sustained efficacy. Finally, we want to be able to detect such immune responses in a conventional ex vivo assay to confirm T cell effector function as well as in an IVS assay to demonstrate memory response.

A vaccine that elicits such broad CD8 and CD4 immune responses to substantially all vaccinated neoantigens should greatly increase the number and concentration of T cells primed to kill tumors and prevent them from recurring. And on each of these measures, we continue to believe GEN-009 has generated unprecedented results. These data offer compelling clinical proof that ATLAS selects the right antigens for cancer immunotherapy. They also showcase the importance of identifying for exclusions the antigens of inhibitory responses that only ATLAS can identify and that thus far appear to be present in nearly every cancer patient.

For all these reasons, we remain excited about GEN-009. We are accruing patients for Part B of our Phase I/IIa clinical trial, which we designed to evaluate GEN-009 in combination with standard-of-care checkpoint inhibitor therapy in patients with advanced disease, including melanoma and non-small cell lung cancer. We anticipate that we'll provide preliminary clinical efficacy data from an initial cohort of Part B patients in mid-2020.

Now let me turn to GEN-011, our neoantigen-specific adoptive T cell therapy. We believe this may represent a best-in-class T cell therapy for treating solid tumors with potential advantages over tumor-infiltrating lymphocyte, or TIL therapy, and TCR therapy. We've made substantial progress this quarter and intend to file an IND for it in the first half of next year.

Finally, let me provide an ATLAS update. Even as we advanced the GEN-009 and GEN-011 programs with ATLAS, we continued to conduct critical research in a variety of other ATLAS applications. We are particularly excited to continue to explore inhibitory neoantigens and their implications. We intend to present exciting new data from this research at next month's SITC Conference.

With that, 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. Diantha?

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Diantha Duvall, Genocea Biosciences, Inc. - CFO [4]

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Thank you, Chip, and good morning, everyone. Our operating results for the quarter ended September 30, 2019, are as follows. R&D expenses were $6.8 million compared to $6.4 million for the same period in 2018. G&A expenses were $2.8 million compared to $4.1 million for the same period in 2018. Our net loss was $7.5 million compared to a net loss of $7.8 million for the quarter ended September 30, 2018.

Yesterday, we entered into a stock purchase agreement with Lincoln Park Capital for up to $30 million, including an initial investment of $2.5 million. Lincoln Park is an existing investor of ours having participated in both of the 2019 financings. This agreement will allow us access to capital similar to our existing ATM. We expect to use it strategically to fund continued advancement of both GEN-009 and GEN-011. We expect our existing cash and cash equivalents are sufficient to support our operations into the first quarter of 2021.

With that, let's now open up the call for questions. Operator?

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Questions and Answers

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Operator [1]

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(Operator Instructions) Our first question comes from the line of Ben Burnett with Stifel.

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Benjamin Jay Burnett, Stifel, Nicolaus & Company, Incorporated, Research Division - Associate [2]

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I had a question about something you disclosed at the ESMO update recently. So it was found that 1 patient had insufficient antigens to vaccinate against. I guess is there anything you can discern about this patient and maybe also discern from patient I who didn't have stimulatory antigens? Is anything you can learn from these cases that can be leveraged towards guiding enrollment into Part B?

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William D. Clark, Genocea Biosciences, Inc. - President, CEO & Director [3]

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Thanks, Ben. It's an important question, and it's insight that really only ATLAS can provide because only we are doing this kind of biological assessment of all candidate neoantigens. I'm going to ask Tom to discuss the potential, I guess, you're saying biomarker implications of ATLAS in our clinical study.

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Thomas A. Davis, Genocea Biosciences, Inc. - Chief Medical Officer [4]

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Thanks, Chip. It's a great question, Ben. I wish I had a complete answer for you. But what ATLAS is telling us is that each patient does have a different ability to react to their own antigens, their own mutations, which kind of make sense because these tumors are able to develop and in some way they are escaping from the immune system. But ATLAS points out both, that some patients are unable to make significant immune reactions, but also that others may have these suppressive inhibitory antigens that Chip alluded to. So that those are important facets as we move forward in the clinical trial.

We do need to determine whether or not these patients truly will be unable to respond. We have to have some stimulatory antigens in order to make a vaccine. But we're evaluating the true meaning of what you've alluded to here, the patients who don't appear to have an immune repertoire that will work against the tumors. So it's the initial part of the study. We are looking at all patients and attempting to make vaccines where we can.

But I think the important facet of ATLAS is that it does sort of give us 2 pieces of information. First, it tells us what targets will work in that patient. And as you've heard, we succeeded 98% of the time when we've had stimulatory antigens that we can go after. The second, it will tell us those patients who are unable to benefit from this particular approach. And we do also have data, more of which will be presented at SITC, that shows the ATLAS readout can predict who's going to respond and who's not. So it serves both to help us design the vaccines but also to predict who will respond and to thereby enrich our ability to benefit patients down the line.

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Benjamin Jay Burnett, Stifel, Nicolaus & Company, Incorporated, Research Division - Associate [5]

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Okay. Great. I wanted to ask just one more follow-up. Just with regards to the Part B disclosure next year, I understand that it's early now, but based on enrollment, I guess what are your expectations for sort of the number of patients and kind of the duration of response that you expect to have by midyear? I think the press release maybe noted this as a preliminary look. So I guess what are your internal expectations for this update?

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William D. Clark, Genocea Biosciences, Inc. - President, CEO & Director [6]

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Tom, why don't you address that as well?

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Thomas A. Davis, Genocea Biosciences, Inc. - Chief Medical Officer [7]

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I'm sorry. Could I ask you to repeat that question just quickly?

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Benjamin Jay Burnett, Stifel, Nicolaus & Company, Incorporated, Research Division - Associate [8]

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Yes. So I was just asking about the Part B disclosure in midyear next year. I think the press release noted this as a sort of preliminary look. Is there anything you can say about the number of patients, duration of response and sort of what your internal expectations are for this update?

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Thomas A. Davis, Genocea Biosciences, Inc. - Chief Medical Officer [9]

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We are actively accruing patients at this point, and I think there's some tremendous enthusiasm besides our screening for patients avidly and we believe accruals going particularly well. It is, of course, impossible to predict exactly how many patients and how much data we'll have midyear. But we do think we'll have adequate numbers to assess whether or not we're significantly adding to the standard of care in those patients. So we're not providing specific guidance as to how many patients since we don't know how many come in over the next 6 months or so. But it certainly will be enough for us to get a sense of what the vaccine is able to contribute.

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Operator [10]

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And our next question is from Mike Ulz with Baird.

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Colleen Margaret Hanley, Robert W. Baird & Co. Incorporated, Research Division - Research Analyst [11]

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This is Colleen on for Mike. Just looking forward to the SITC update in early November, I know you said probably substantially all of the data so assuming all 8 patients. And then will they all have completed all 5 doses at that point?

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William D. Clark, Genocea Biosciences, Inc. - President, CEO & Director [12]

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Thanks, Colleen. I'll have Jess speak to the immune response data that we are expecting to be able to present at SITC.

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Jessica Baker Flechtner, Genocea Biosciences, Inc. - Chief Scientific Officer [13]

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Right. I think it's accurate that we will have immune response data from all 8 patients. The data that we anticipate presenting will be focused on the baseline and times 50 post the primary series time point. So it will not be all of the patients post all the doses immune responses. They are not all through yet.

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Colleen Margaret Hanley, Robert W. Baird & Co. Incorporated, Research Division - Research Analyst [14]

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Okay. And then just a follow-up. So the -- can you comment on looking at Part B, the dosing? I know you've said the PD-1 will be dosed according to the label, but can you talk about a little bit of the sequencing of the PD-1 with GEN-009? Whether they'll be on PD-1 first and then going on GEN-009, and whether it will be the same amount of time or different for the different patients?

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William D. Clark, Genocea Biosciences, Inc. - President, CEO & Director [15]

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Got it. Thanks. Tom, could you address that, please?

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Thomas A. Davis, Genocea Biosciences, Inc. - Chief Medical Officer [16]

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Sure. So our goal here is to combine GEN-009 with the standard-of-care regimen. So in some cases, that may represent just a PD-1-targeted agent. But in others, it is a combination regimen that's based on PD-1 targeting. So the trial is designed that while we are manufacturing the vaccine, the patients can complete their combination therapy. So if they're receiving a PD-1 and a CTLA-4-targeted agent, characteristically, those are given over a period of about 3 to 4 months. And then the patients continue on the PD-1. And in general, it's similar for chemo combinations as well.

The timing actually works out well for us because we can then initiate GEN-009 when we've completed manufacturing, but that tends to fit in nicely for when the combinations are discontinued and the patients adjust on their PD-1 therapy. We have publicly announced that it takes us approximately 14 to 16 weeks in order to manufacture. So that's generally the time line between when the patients would have started their combination therapy and when the vaccine initiates.

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Operator [17]

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And our next question is from Chad Messer with Needham & Company.

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Chad Jason Messer, Needham & Company, LLC, Research Division - Senior Analyst [18]

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Another one on the ESMO poster. It includes an analysis we didn't see at ASCO on indels and frameshifts and kind of makes the point that those aren't enriched. Could you maybe explain the significance of that finding? It's something you included in the poster and also in the conclusions, but I can't quite wrap my head around the meaning of that.

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William D. Clark, Genocea Biosciences, Inc. - President, CEO & Director [19]

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Thanks, Chad. I'm going to have Jess take that question.

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Jessica Baker Flechtner, Genocea Biosciences, Inc. - Chief Scientific Officer [20]

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Chad, thanks for the question. So there's a theory in the field. This is just a nuanced scientific point. There's a theory in the field that these entirely new sequences that emerge because, for example, there is a stop-loss and there's a read-through into an intron would be a better antigen because the immune system hasn't been tolerized to it or previously educated to avoid it. And a lot of people who are trying to predict what might be a good antigen to include in a vaccine would naturally trend toward these if they have to down-select from their epitope prediction algorithm. And so what we have found is that it is not the case that neoantigens are enriched for these truly novel sequences. When we find them, they're not more antigenic than, for example, a single amino acid change.

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Chad Jason Messer, Needham & Company, LLC, Research Division - Senior Analyst [21]

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Okay. Great. We learn something every day. Looking forward to SITC, I know Tom alluded we're going to get some data on how ATLAS can predict who's going to respond to vaccines. And you've already told us sort of what to expect in terms of the immunogenicity data. Any other kinds of novel findings or analyses that we should look for? I'm just trying to prime my brain for a few weeks from now.

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William D. Clark, Genocea Biosciences, Inc. - President, CEO & Director [22]

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Yes, Chad. So I think the other point that we'll be emphasizing, and this will be in a separate presentation, is inhibitory antigens and their importance in clinical treatment. So keep your ears to the ground for those revelations.

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Operator [23]

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And our next question is from Gil Blum with Needham & Company.

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Gil Joseph Blum, Needham & Company, LLC, Research Division - Analyst [24]

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This is kind of going a little backwards for the data presented from the Neon program back at AACR. They did show some responses for CD8 and the ex vivo assay. I'm just wondering if you kind of expect even higher responses in the Part B kind of looking forward.

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William D. Clark, Genocea Biosciences, Inc. - President, CEO & Director [25]

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So Chad, so I think we probably nitpick a little bit about whether the Neon assay is a true ex vivo assay. But let's leave that point aside. You're asking essentially if on checkpoint inhibitor we would expect there to be some immune system priming that would make -- there would be some synergy in immune response between vaccine and therapy. Is that correct?

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Gil Joseph Blum, Needham & Company, LLC, Research Division - Analyst [26]

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Exactly.

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William D. Clark, Genocea Biosciences, Inc. - President, CEO & Director [27]

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I will ask Tom to handle that question.

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Thomas A. Davis, Genocea Biosciences, Inc. - Chief Medical Officer [28]

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Sure. Give me the tough ones. No, it's an excellent question. Checkpoint inhibitors have been available for quite some time now, and it's clear that they do significantly alter the patient's immune system and do alter immune responses. But it's not clear exactly how it does that and hard to predict exactly what immune responses you'd see. We would, however, expect to see a greater array of immune responses and hopefully some evidence of epitope spread in that context because, of course, these patients will have tumor on board, and the patients with checkpoint inhibitors will hopefully be seeing tumor death. I don't think that there's a clear picture as to what's going to happen here. But I think in the Neon experience, they clearly saw that the addition of checkpoint inhibition did improve their immune response profile.

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Operator [29]

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(Operator Instructions) Our next question comes from the line of Daina Graybosch with SVB Leerink.

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Daina Michelle Graybosch, SVB Leerink LLC, Research Division - MD & Senior Research Analyst [30]

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I have 3. The first one is, Chip, to your assertion that you get 98% of the neoantigens, and correct me if I got the number wrong, are stimulating an immune response. I wonder if you guys have been able to validate or plan to validate in vitro tumor killing of these T cells that are stimulated.

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William D. Clark, Genocea Biosciences, Inc. - President, CEO & Director [31]

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Thanks for the question, Daina. I'm turning to Jess to answer that question.

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Jessica Baker Flechtner, Genocea Biosciences, Inc. - Chief Scientific Officer [32]

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Thanks, Daina. Unfortunately, in the clinical trial, we don't have viable tumor from these patients where we can grow the cells to do those killing assays. We have been generating those data in our animal models. So we are confident that what we're finding with ATLAS is valuable to killing tumors. But unfortunately, because we don't have access to the viable tumors, we can't do that assay.

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Daina Michelle Graybosch, SVB Leerink LLC, Research Division - MD & Senior Research Analyst [33]

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Will you in the clinical trial undergoing right now have some tumor samples to do those kind of assays?

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Jessica Baker Flechtner, Genocea Biosciences, Inc. - Chief Scientific Officer [34]

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The way that we have planned this trial, we will have biopsies of tumors, but they will be for -- they will be FFPE sections, so not viable tumors. We will look for other indicators that there is immune response happening such as perhaps infiltration into the tumors, sequencing of TCRs or other type assays that you can do by staining or RNA techniques.

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Daina Michelle Graybosch, SVB Leerink LLC, Research Division - MD & Senior Research Analyst [35]

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Got it. My next question is perhaps a theoretical one clinically about the patients that we should expect to respond best and sort of following up the question from -- that you got earlier. In that if a patient doesn't have enough neoantigen, then you can't create a vaccine unfortunately for that patient. What about a patient with a lot of neoantigens? Would we ever expect that those patients already have sufficient neoantigen T cells and so the incremental benefit for a vaccine wouldn't be good enough? Is there some sort of middle ground? And are you thinking about doing any assays to try to assess whether there are patients that just wouldn't benefit from a vaccine given their de novo responses?

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William D. Clark, Genocea Biosciences, Inc. - President, CEO & Director [36]

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Daina, I'll ask Tom to take that one.

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Thomas A. Davis, Genocea Biosciences, Inc. - Chief Medical Officer [37]

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Well, another tough one. Again, ATLAS gives us a tremendous insight into these patients. And there doesn't appear to be a clear correlation between the mutational burden in patient and the ones that the patient themselves can react again. We've seen some patients with many mutations with up to 200 possible targets. So when we look at the ATLAS outcomes, it tends to be a much lower level, which sort of raises the question, is there a certain number of immune responses that your immune system is limited to when it comes to these tumors?

Obviously, more are better. We certainly think that there's a lack of immune response in order for the tumors to grow. So being able to augment immune responses are very important, and GEN-009 should be able to do that. Although I will pause and remind everyone of GEN-011, which is actually a cell therapy. We're the only ones, I think, who are really moving forward to target as many new antigens as possible in a comprehensive, individualized cell therapy. And we're quite excited to be able to take that to patients where we will be introducing an externally generated immune response against many targets. And that is probably critically important when you look at the heterogeneity of tumors.

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Daina Michelle Graybosch, SVB Leerink LLC, Research Division - MD & Senior Research Analyst [38]

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Great. And maybe an easy one to end. We hear you and others often complain about certain types of ex vivo assays. And I wonder if you could help us understand what should we be looking for with your competitors or academic publications to get confidence that an ex vivo assay results reported are relatively apples-to-apples to yours and to others who you think are doing them well?

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William D. Clark, Genocea Biosciences, Inc. - President, CEO & Director [39]

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So Daina, essentially, what are the principles of what we would consider to be a sound ex vivo assay. So I'll have...

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Daina Michelle Graybosch, SVB Leerink LLC, Research Division - MD & Senior Research Analyst [40]

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Yes. That's much better put than me, yes.

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William D. Clark, Genocea Biosciences, Inc. - President, CEO & Director [41]

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Not -- I'm seeking clarification, not trying to be critical, but I'll have Jess answer the question.

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Jessica Baker Flechtner, Genocea Biosciences, Inc. - Chief Scientific Officer [42]

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Thanks, Daina. I think the definitions around both assays are actually really critical. The intention of an ex vivo assay is to actually measure what is present in the blood when you took it from the patients. And so you try to manipulate it as little as possible. So the timing varies depending on the analytes that you're looking at. But in -- by classical definition, an ex vivo assay is one -- an overnight to 48-hour assay, depending on the analyte that you're looking at. The IVS assay, on the other hand, is an intention to culture cells that are present in the blood and perhaps turn memory cells back into effector cells that you can measure. And in those cases, the timing in classical definitions of the assay have been about 7 to 10 days of culture before you read out the immune response. And in some cases, there have just been wildly variable timing ascribed to either of those assays in publications. And we would like some consistency in the field.

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Operator [43]

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And I'm not showing any further questions. So I'll now turn the call back over to Chip Clark for closing remarks.

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William D. Clark, Genocea Biosciences, Inc. - President, CEO & Director [44]

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I will simply thank you, operator, and thank everyone for joining us today. We look forward to future updates.

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Operator [45]

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