Genocea Biosciences, Inc.
Q3 2015 Earnings Call Transcript

Published: 8 Nov 2015

[Operator:]

Good morning and welcome to the Genocea Third Quarter 2015 Financial Results Conference Call. At this time, all participants are in a listen-only mode. Following the formal remarks, we'll open 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 Sarah McCabe of Stern Investor Relations. Please proceed.

[Sarah McCabe:]

Thank you, operator. Good morning. This is Sarah McCabe with Stern Investor Relations and welcome to Genocea's third quarter 2015 financial and operating results conference call. This morning we issued a press release which outlines the topics we plan to discuss today. We have also prepared a Slide presentation to accompany today's webcast and that presentation along with the press release is available at www.genocea.com under the Investor Relations tab. Today on our call, Chip Clark, President and CEO, will review the company's recent clinical highlights; and along with Jessica Baker Flechtner, Genocea's Head of Research, will provide an update on the expansion of the ATLAS technology platform into immuno-oncology. Then Jonathan Poole, CFO, will review the financial results. Seth Hetherington, CMO is also with us today for the Q&A. Before we begin, I would like to direct you to Slide 2 and 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 forecast 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 2014 Annual Report on Form 10-K and other periodic reports filed with the Securities and Exchange Commission. With that, let me pass the call over to Chip.

[Chip Clark:]

Thanks, Sarah and good morning everyone. Please join me on Slide 3 from our webcast. I will begin today's call be reviewing the recent positive results from our ongoing Phase 2 dose optimization trial for GEN-003, our treatment for genital herpes. I will than review the Phase 2a results for GEN-004 and the current program status. Jess and I will than introduce the immuno-oncology initiatives we have unveiled over the past 24 hours and explain our strategy. After that Jonathan will review our financials and then we will take your questions. Let me now turn to Slide 5. We believe the positive results in early October strengthened GEN-003's value proposition for the treatment of genital herpes. These six-month Phase 3 efficacy data show an improved impacted on viral activity versus the already excellent results from our Phase 1/2a trial. GEN-003 has also demonstrated durable clinical efficacy across multiple potential Phase 3 endpoint and we have a clear development path to potential approval with an FDA end of Phase 2 meeting expected in Q4 of next year. Moving to Slide 6. The GEN-003 program provides three significant catalysts in the next year. First, the efficacy readout 12 months after dosing from the ongoing trial comes in the first quarter of 2016. We will see if GEN-003s improved efficacy through six months is sustained through 12-months, which will be upside from our target product profile. These data will also give a read on the likely timing of a booster dose. Second, in the second quarter we will report efficacy from our Phase 3 bridging study through which we will augment our end of Phase 2 meeting package with clinical data generated from GEN-003 manufactured at commercial scale. Finally, we expect to conduct the FDA end of Phase 2 meeting in the fourth quarter of 2016. Moving to Slide 7. We believe that GEN-003's profile supports the potential for it to be the cornerstone treatment for genital herpes, improving upon both the dominant treatment paradigm of episodic antiviral therapy as well as chronic suppressive antiviral therapy. First in contrast to episodic antiviral therapy which is the choice of roughly two-thirds of treated patients in the U.S., treatment with GEN-003 could reduce the frequency of outbreaks and reduce asymptomatic viral shedding, the cause of most transmission. And for the one-third of patients treated with chronic suppressive therapy, we believe that GEN-003 offers durable efficacy through a novel mechanism of action, the ability to reserve orals for use during outbreaks, should they occur and a more convenient dosing regimen that avoids the painful daily reminder of the disease and offers the potential to drive greater treatment compliance. Based on earlier market research, we believe that GEN-003's profile supported a revenue forecast of greater than $1 billion in the U.S. alone and our new results further cement our confidence in this. Now, turning to GEN-004, let's look at Slide 9. We designed GEN-004 to prevent infections by pneumococcus, a major cause of infectious disease-related deaths worldwide. Last month we reported results from a Phase 2a clinical trial and in it GEN-004 showed consistent reductions versus placebo in the rate and density of colonization but these reductions did not achieve statistical significance. At this time we believe the path to further clinical development may require investigation of dose, adjuvant or trial population. We have suspended development of GEN-004 pending further review of the data and expert consultation. Now let's switch gears. I am excited share our immuno-oncology programs and to explain specifically what ATLAS brings to the table that is both differentiated and crucial to the field. So moving to Slide 11. I think this audience knows that immuno-oncology has transformed cancer treatment in recent years. These new therapies unleash a broad T cell response but we don’t really know what the T cells are targeting for efficacy and as a consequence these products still have significant limitations. Well, what if we could find those targets of T cell responses? What if we could mine both the tumor associated antigens and neoantigens to understand the underpinnings of response or non-response. That could lead to a better understanding of which patients should or should not get these products and just as importantly could lead to new products providing clinical benefits to even more patients. Finding T cell antigens is one of the biggest pursuits in immno-oncology and finding T cell antigens is what Genocea does for a living. So let's move to Slide 12. Using ATLAS defined T cells antigens in cancer is a natural extension of our expertise in infectious disease. And finding the right T cell antigen is as essential to cancer, if not more so than it has been for us in infectious disease. And remember, GEN-003 represents we believe the only immuno-therapy against any disease built around new T cell antigens. And so with this early GEN-003 proof of concept in hand that we established last year, our collaboration with Dana-Farber to explore the potential to apply ATLAS to cancer. We set out to use ATLAS to inform two things. First, if signatures of checkpoint inhibitor response and non-response could be determined, and second by extension, if the targets in these signatures can serve as the crucial components of the T cell antigens of novel cancer vaccines. I will now ask Jess to take you through the scientific basis of our oncology strategy.

[Jessica Baker Flechtner:]

Thank you, Chip. On Slide 13, we discuss some of the challenges associated with predicating T cell antigens and what effective antigen selection requires. The growing evidence that neither immunogenicity nor immunodominance predicts protective immunity, meaning that you can't rely purely on volume signatures for antigen selection. Without a clinical association, T cell antigens are only those peptides that T cells recognize and to which they respond. So with ATLAS, we don’t face this challenge. We do not predict antigens. We find them through a clear understanding of the full range of T cell and antigen interaction and critically the ability to link T cell responses with clinically meaningful outcomes. On Slide 14, we describe the unique position which Genocea through ATLAS fills in the cancer immunotherapy landscape. There are really two side to the equation, what's going on in the tumor cell on the left and what's going on in the T cell to the right. On the left of this Slide, we have described the approaches which use predictive tools focused on tumor cells. These vary from antigen prediction through tumor cell DNA or RNA sequencing to the identification of tumor associated peptides. On the right side, we have described approaches which seek to identify the sequences of T cell receptors that have become more frequent due to the presence of a tumor through T cell DNA analysis. Critically, we believe that only ATLAS is an actual read out of the human responses to a cancer. ATLAS is the way to find smarter targets. Moving to Slide 15. I will describe in more depth how ATLAS enables smarter profiling of T cell responses and by extension than, smarter antigen selection. In contrast to other high throughput predictive tool, we believe ATLAS has a number of critical benefits. ATLAS can find antigen to which patients are actually responding. It can distinguished between clinically relevant and immunodominant responses. It works for both CD4 and CD8 positive T cells. An importantly, it is not HLA limited in contrast to predictive tools which tend to focus on a single HLA molecule and Caucasian population. Considering the potential power of ATLAS in oncology, we have made investments behind three key areas of focus. First, finding novel antigens for cancer vaccines development. Second, using ATLAS to characterize signatures of T cell responses to immunotherapy. And third, developing immunotherapies for cancers with viral origin. We are finding smarter targets. On Slide 16, the results from the Dana-Farber collaboration which we announced yesterday, show that ATLAS can find signatures of checkpoint inhibitor response. In this collaboration, we measured recall T cell responses to 23 tumor associated antigens via ATLAS in ten subjects who had been treated with checkpoint inhibitors. ATLAS successfully identified the cancer antigens to which either or both CD4 and CD8 positive T cells became activated. And although this research was not powered to draw a firm conclusion, the analysis of T cell responses in patients receiving checkpoint inhibitor therapy revealed the pattern indicating a greater breath of T cell activation for responders than non-responders. The study also revealed preliminary evidence that different characteristics of T cell responses emerge when comparing patients who respond and those who do not. Furthermore, some T cell responses do not correspond with improved patient outcomes and maybe classified as decoys, further validating the ability of ATLAS to distinguish clinically relevant targets of T cell response. We are pleased that these results were accepted for a late-breaker poster presentation SITC this Saturday, November 7. Moving on to Slide 17. With this clear proof of concept in hand from our Dana-Farber collaboration. We have been working to expand our T cell cancer antigen discover efforts and are truly delighted to have announced today a new collaboration with Tim Chan and Jedd Wolchok at Memorial Sloan Kettering Cancer Center focused on neoantigen discovery in melanoma and non-small cell lung cancer patients. They are some of the world's leading researchers into new cancer vaccine concepts. So we are pleased to be working with them. Our goals here are once again to find cancer vaccine candidates and to identify signatures of T cell response. Moving to Slide 18. I will describe the second area of focus for our oncology strategy cancer vaccine. We believe that Genocea is uniquely positioned to develop cancer vaccine because picking the right T cell antigens is likely central to efficacy and ATLAS maybe the only platform able to identify clinically relevant T cell antigen and has been proven to work. We have significant vaccine discovery and development expertise and the flexibility to work with any adjuvant or delivery system to create cancer vaccine. We expect to pursue personalized cancer vaccines initially and would look potentially to incorporate common antigens over time. Furthermore, we expect a faster path to clinic than for our infectious disease program. The third area of focus is described on Slide 19, the development of immunotherapies for cancers with viral origin. Here we have started discovery work on an Epstein-Barr virus immunotherapy. An effective immunotherapy against EBV may have therapeutic potential against a number of cancers, all linked to EBV infection with unmet need such as post-transplant lymphoproliferative disease, non-Hodgkin’s lymphoma, nasopharyngeal carcinoma and gastric carcinoma. EBV is highly suited to ATLAS because there are significant evidence that T cell responses are crucial to protection. It is a large virus so that without ATLAS making antigen predictions would be extremely challenging. And EBV is a herpesvirus, which we have shown that we can treat in GEN-003.

[Chip Clark:]

Thanks, Jess. Moving to Slide 20. Today marks a major milepost in Genocea's development as we continue our pursuit of life changing medicines in new therapeutic areas. Today we have unveiled an immunooncology strategy that plays to our T cell antigen discovery and vaccine development strengths and may open new paths to near term value creation for Genocea in three key ways. First, ATLAS positions us at the center of the emerging effort to find new cancer vaccine T cell antigens. That’s puts us on a path to create personalize vaccines that we believe offers a considerably compressed path to the clinic and proof of concept. We expect to provide more color on this in future updates. Second, these T cell antigens also comprise signatures of response and non-response to immuno-oncology therapies. We believe such signatures would be a value to the developers of such product as they seek to insure their drugs get used at the right times and in the right patients. And third, with EBV, not only are we targeting a disease with high unmet need but we have the potential to create a differentiated product in Genocea's herpes virus area of expertise. With that I will pass this over to Jonathan.

[Jonathan Poole:]

Thanks, Chip. Moving to Slide 22 to discuss the financials for the quarter. In today's press release we reported that cash, cash equivalents and investments at September 30, were $112.5 million compared to $74.6 million as of June 30. We expect that these funds will be sufficient into the second half of 2017 when we expect to be entering Phase 3 trials for GEN-003. In addition, we have further potential financial flexibility from undrawn capacity in our existing debt facility and opportunities to derive funding from business development transactions relating to our ATLAS T cell target discovery platform, our preclinical and our clinical assets. Importantly also the funding of the oncology activities which Jessica has described today is included in our expectations. R&D expenses for the quarter remain flat at $6.1 million compared to the same period in 2014, reflecting higher personnel cost and increased lab related costs offset by reductions in manufacturing and licensing fees. On a program basis, we continue to make investments in Genocea's preclinical pipeline which offset lower expenses attributable to GEN-003 and GEN-004 in the quarter. G&A expenses were $3.6 million for the quarter compared to $2.8 million in 2014, reflecting higher personnel costs and depreciation expense, supporting Genocea's expanding R&D operations and the cost of operating a public company. Finally, net loss for the quarter was $9.8 million compared to a net loss of $9.2 million for the same period in 2014. With that let me hand over to Chip to wrap up.

[Chip Clark:]

Thanks, Jonathan. I hope you all agree that we continue to have exciting times ahead of us at Genocea. In GEN-003, we have a truly foundational lead clinical asset that’s a scientific breakthrough, offers a first in class profile, has significant clinical efficacy and addresses a potentially enormous market. And with ATLAS we are opening new paths to potential near term value creation both on our own and in partnership with some of the leading institutes of cancer treatment. We believe ATLAS is the best T cell antigen discovery platform and we believe we can make important advances in oncology. With that, we will open up the call for your questions. Operator?

[Operator:]

[Operator Instructions] Our first question comes from the line of Phil Nadeau of Cowen and Company. Your line is open.

[Phil Nadeau:]

First, on the oncology program. You have noted that maybe your first goal would be to personalize cancer vaccines. In the past those vaccines have been tough to commercialize because of the margins. Curious whether you see easy things to improve upon in that business model versus what's been done in the past as a way to make those more high margin and high value commercial products.

[Chip Clark:]

Hi, Phil. It's Chip. Thanks for your question. It's a little bit preliminary for us to talk about the business model but I think the point we would make is that this is entirely about finding the right targets and in ATLAS we think we have a better way to find targets rapidly. And therefore we think that the vaccines that would result from here would compare favorable from vaccines that result from other efforts. And as a consequence of that, we think that we will be in a strong position to differentiate clinically our offerings. I think going forward we will be able to provide further color on the business operations side of this.

[Phil Nadeau:]

Got it. Okay. That makes sense. And the second, on the EBV program. Can you give us some idea of the timelines there? When do you think you could have a clinical candidate and perhaps file an IND?

[Chip Clark:]

Yes, Phil, I will take this as well. I think as we typically take sort of three to four years from whiteboard to get into the clinic. And so while we haven't provided specific guidance yet on when we would get into the clinic with EBV, I think that’s a broad timeframe to be considering here. And similarly we will provides updates in the near future.

[Phil Nadeau:]

Great. And then one last question on the booster dose for GEN-003. I appreciate that that’s going to be informed by the 12-month data. But what's your current thinking? Is there, are you leaning towards a six-month or 12-month booster or no booster at all? What's kind of the plan A given the information that you have now?

[Chip Clark:]

I will ask Seth to take that.

[Seth Hetherington:]

Yes. So, Phil, I think given the six month date that we just presented at IDWeek, that reduction in viral sheddings staying so stable at six months compared to immediately post-dose, we have more confidence now that in fact we could have still a substantial reduction in viral shedding and improvement in clinical outbreaks after 12 months. So it still remains empiric science, if you will, and we will be able to give you more specific guidance in the first quarter of next year when we report out on the 12-month data.

[Operator:]

Our next question comes from the line of Ed Tenthoff of Piper Jaffray. Your line is open.

[Ed Tenthoff:]

Exciting updates both with the oncology collaboration and Epstein-Barr. I guess, it's more with the oncology collaboration, and I apologize if I missed this in the prepared remarks, but can you give us a sense of what the scale of this could actually be. I mean how many indications could we ultimately be pursuing and I guess following up, maybe asking Sloan question but differently and applying it to oncology. How many and how rapidly could we see oncology vaccines or cancer vaccines advance into the clinic?

[Chip Clark:]

Ed, thanks for the question and Jess and I will tag team a little bit on the answer here. Let me provide some general commentary and then ask Jess to speak to the specifics for examples the Memorial Sloan collaboration. We think the evidence is such that the concept of personalized vaccines is a amenable to many cancers. And so the Dana-Farber and Memorial Sloan Kettering collaborations across a couple of indications we think are both exciting but potentially may only scratch the surface of the breadth that we could be contemplating. Now as for the timelines to go from start to the clinic, this is an involving field. I think that typically the driver of the time from discovery to clinic is the work that the FDA requires to demonstrate the safety of your program and the safety of your manufacturing program and we will be having discussions with the agency on this but there is at least some circumstantial evidence to suggest that this would be substantially shorter than the few years that we typically undertake to go from start to the clinic in infectious disease. But I will ask Jess to give you specific color on the Memorial Sloan Kettering collaborations which we did not describe in the prepared remark.

[Jessica Baker Flechtner:]

Ed, thanks for the question. The collaboration that we have established with Memorial Sloan Kettering is centered around their ability to sequence the mutations in every subject tumors. And so what we will be doing is building ATLAS library of each subject's unique mutation and studying their T cell responses pre and post-therapy to identify the hallmarks of protective immunity. And so the limitations that we will have there is simply the rate with which we can recruit subjects into this study. But we look forward to accelerating the work and really making progress in this neoantigen field.

[Chip Clark:]

Yes. And I think what we would say Ed, is that this is in a way, you could think of it as a dry run. The time from receipt of samples to output with the, sort of the antigens that pop, if I maybe non-scientific here, is exactly the timeframe we would expect to see when we are creating the personalized vaccines or the next step. And so we think it's both a great proof of concept for the platform, scientifically, as well as an operational proof of concept for the platform.

[Ed Tenthoff:]

Thanks. Well, it seems like perfect application for ATLAS, so that’s very [indiscernible]. If I may just ask one follow up. Kind from a high level, how do you see the roll of specific cancer vaccines fitting into an immuno-oncology driven world? I mean from my view, they are highly complementary but maybe you could give a little bit more color in terms of what the role of vaccines are going to be playing in combination with immunotherapy.

[Chip Clark:]

Yes. Well, I think --- thanks, Ed for the question. And the way we see it is that checkpoint inhibitors and other similar products are going to be and deserve to be the foundational treatment for cancers. We think that cancer vaccines are a natural complement. So for the patients who have these tremendous responses on checkpoint inhibitors, that’s fantastic. Probably cancer vaccines are less important to those patients but for the still majority of patients where the checkpoint inhibitors are not providing sufficient efficacy and/or for whom the clinical benefits comes with toxicity, we see cancer vaccines as boosting the immune response or directing the immune response to respond to the right targets in order to improve the clinical outcomes. So we agree with you that there is a natural complementarity here and we are excited about the application of ATLAS here both because we think we can in a high throughput way identify personal differences. Personal targets that we want to direct the immune system to, but we think we are also optimally placed to find if they exist, common antigens. So that the effective vaccines going forward will end up being a blend of personalized and common antigens.

[Operator:]

Our next question comes from the line of Stephen Willey of Stifel. Your line is open.

[Prakhar Verma:]

This is Prakhar on for Steve today. Thank you for taking my question. So on GEN-003, I have couple of questions. One on, so you talked about -- previously you talked about using some of the [indiscernible] measurements or recording devices to improve the compliance. Are you going to be employing those and the bridging study?

[Chip Clark:]

Thanks, Prakhar. I will have Seth answer that question.

[Seth Hetherington:]

Yes. We are. We are piloting an electronic data capture method for patients through the use of a tablet computer or Smartphone.

[Prakhar Verma:]

Okay. And then on GEN-003, what's the timeline or current thinking on the combination of studies with [indiscernible]?

[Seth Hetherington:]

We [internally] [ph] have a combination study planned for the middle of next year.

[Chip Clark:]

And near future update, Prakhar, we will be able to provide clarity on when we would expect efficacy from that.

[Prakhar Verma:]

Okay. And on the Memorial collaboration? So these patients have received [CTLF4 or PB1s] [ph] or what kind of therapy these patients have seen in the clinical [indiscernible]...

[Chip Clark:]

Yes. Prakhar, we have not yet disclosed the specific product or products they maybe on but you are talking about the right classes.

[Operator:]

Our next question comes from the line of Alan Carr of Needham & Company. Your line is open.

[Alan Carr:]

A couple of them. I guess to touch on some of the previous ones. Can you, I guess, clarify a bit more around -- you have a few phase 2s planned here, bridging regimen and a combo. Give us a sense of timing for starter dose and when you get data from each one of those and which one of those or which of these are important for end of Phase 2 meeting. And then the other one is, you have mentioned three different infectious disease programs, the earlier stage ones. EBV, malaria and Chlamydia. I am wondering if you can give us a sense of priorities amongst these three and actually how they relate in priority relative to the oncology program that you are making progress with. Thanks.

[Chip Clark:]

So I will first ask Seth to briefly review the timelines on the GEN-003 questions you asked Alan and then after that if we have answered those questions we will turn to the pipeline question that you asked.

[Seth Hetherington:]

Right. So the timing questions, first for the bridging study. As we have said previously, sometime around, the end of this year, preparations are already being made. So we expect to start that again around the end of the year. Data would come out probably around the second quarter of 2016, which is immediately after the third dose. Data from that. The other study, you mentioned the dose regimen and any [role] [ph] combination, our plan is to start those in the middle of 2016. We would expect six month data coming out of those two studies around the first half of 2017. Now to the point about the end of Phase 2 meeting with the FDA, we still anticipate hitting that target of fourth quarter 2016. The data that we will need for that include the two studies which we are already, one is completed and the second study of course, we just presented the six month data. We have plenty of information from those two studies. We will have additional data from the bridging study demonstrating the suitability of our scaling up of the manufacturing techniques. That’s the only -- those are only data that we actually need for that end of Phase 2 meeting to accomplish what we need to. Anything that might be available from the dose regimen study or the antiviral combination study, it's unlikely but we could have some supplemental safety data that would be included in a briefing package. But it's not really [indiscernible].

[Chip Clark:]

Alan, does that answer your GEN-003 questions before we turn...

[Alan Carr:]

It does.

[Chip Clark:]

Okay. Great. So let me make sort of a general comment on the pipeline before asking Jess to just list the specific preclinical programs that we have and what we have said already about when we expect to be in the clinic. And so, I think the most important thing to do is to remind you of the financial guidance that Jonathan gave you. Everything that we are doing, the new stuff that we are talking about today, as well as the ongoing preclinical work, is all factored into our use of proceeds. And I think that speaks to the relative capital efficiency with which ATLAS can enable us to discover and advance new novel products. But I will ask Jess to just walk through the specific pre-clinical and discovery stage programs and where we expect them to be landing.

[Jessica Baker Flechtner:]

Hi, Alan. We have four preclinical programs. You mentioned three of them EBV, malaria, Chlamydia and our next generation herpes vaccine. And the reason that we can maintain all of these programs is because they are all at different stages of development. So in order to be able to accommodate the EBV and the oncology projects that we have discussed, the other programs are more or less out of the screening portion of their development and are emerging into the animal modeling and development of the vaccine portion. And so we are wrapping up our screens for the malaria program. We are beginning animal modeling in Chlamydia. We have been developing our next generation HSB vaccine. And so we are in really good shape to be able to continue to make progress on these. And as we have mentioned in the past, I think that the next major milestone from these pipeline products would be at the end of 2017 with an IND for the next generation HSB product.

[Alan Carr:]

Okay. And then, actually Chip, you mentioned before that for EBV, three to four years from whiteboard to clinic, I take it that you are implying that EBV is at whiteboard right now?

[Chip Clark:]

At the whiteboard but not years passed. We have been working on it for several months.

[Operator:]

Our next question comes from the line of Christopher James of FBR & Co. Your line is open.

[Christopher James:]

Congrats on the progress and thanks for taking my question. My first question relates to GEN-003. Maybe Seth, can you talk a little bit about the booster dose. What would that potentially entail in terms of both antigen and adjuvant, also dose and would this require a separate study?

[Seth Hetherington:]

Sure. We anticipate that the composition of the booster dose would be identical to what's used in the primary [steers] [ph]. There is no reason to expect to change that. It's really the timing of the booster dose, as we mentioned earlier, that’s the variable. It's need to be defined. We know that we have very durable efficacy up to six months. We have got 12 month data coming out in the first quarter of next year and based on that data we will make a decision as to whether or not a booster dose needs to be given at 12-months. Theoretically, it could be even longer than that. But, let's for the sake of argument say, it's a year's interval between doses. It would not require a separate study. We would incorporate booster doses either as amendments to ongoing protocols or to include it in future protocols depending upon what's active at the time when we make the decision.

[Christopher James:]

Great. No, that’s helpful. And then on your new oncology program. Do you anticipate combination studies with existing checkpoint inhibitors or how should we think about that?

[Chip Clark:]

Yes. I think that’s the right way to be thinking about it.

[Christopher James:]

Okay. And then maybe, can you expand on the use of adjuvants in oncology? Are you going to be using, I guess, what sort of adjuvants, you expect to use? It seems like you are able to identify the antigen quite nicely but how should we think about the adjuvant side a bit?

[Chip Clark:]

Yes, Chris, that’s an important point. Vaccine, we think that initially what distinguishes us is our ability to find the right targets and, again, we have contrasted that with these predictive methods that others are using. We think today we have the flexibility to pair with whatever we think the right adjuvant or delivery system will be and that may vary depending on disease. And that’s why, but similar to the strategy we have employed in our infectious disease program. The GEN-003 adjuvant is different from, or is or maybe different from the adjuvants we employ in other diseases.

[Operator:]

We have a follow-up question from the line of Stephen Willey of Stifel. Your line is open.

[Stephen Willey:]

This is Stephen up on the call late, so my apologies if I ask a question that was already covered. But with respect to the immuno-oncology collaboration, is the intent there to actually guide treatment decisions with respect to the work that you are doing with ATLAS, or is it just kind of a more of a retrospective collagen of information post checkpoint inhibitor therapy?

[Chip Clark:]

Steve, I am delighted to say that the question has not been asked, but I think it's an important point. This is prospective. The tantalizing evidence emerging from our Dana-Farber collaboration is that there do appear to be signatures and that information is really valuable and could be valuable going forward for finding the right patients to get the right drugs at the right time. And in the Memorial Sloan Kettering collaboration, we are looking at neoantigens rather than the tumor associated antigens, so it's sort of a different way of looking at a similar question. But we expect that both these signatures of response as well as cancer vaccine candidates could emerge from this collaboration.

[Stephen Willey:]

Okay. And does the current throughput time allow ATLAS to leverage as a tool for determining treatment visions and I guess, if not, are there improvements you can make to the throughput time of the antigen identification process.

[Chip Clark:]

Yes. I mean the short answer is, yes. ATLAS has always been a high throughout engine and a Jess said earlier, it's a function of just getting the material.

[Jessica Baker Flechtner:]

But we do have work ongoing as a project in order to see how much faster we can do it and how much more less resources we will require to automate parts of the process to make it even faster.

[Operator:]

And I am showing no further questions in the queue. I would like to turn the program back to Chip for closing remarks.

[Chip Clark:]

Yes. Thank you, operator. Thank you all for your questions and your interest. As I said before, this is just a really exciting time for Genocea. We are really excited about GEN-003 and we are very pleased not only to be continuing to invest in the existing pipeline but to now share with you the ongoing work we have had to show that the ATLAS platform can be valuable in an areas of extreme clinical and by extension, pharma biotech and investor interest, namely immuno-oncology. We like where we sit from a competitive differentiation standpoint and look forward to delivering on the milestones that we have outlined. So with that, I thank you all for your time.

[Operator:]

Ladies and gentlemen, thank you for participating in today's conference. This does conclude the call. You may now disconnect. Everyone have a wonderful day.