Genocea Biosciences, Inc.
Q4 2019 Earnings Call Transcript

Published: 13 Feb 2020

[Operator:]

Good morning, ladies and gentlemen. And welcome to the Genocea Fourth Quarter 2019 Conference Call. At this time, all participants are in a listen-only mode. Later, we will conduct a question-and-answer session and instructions will follow at that time. [Operator Instructions] As a reminder, this conference is being recorded.I would now like to turn the conference over to your host, Mr. Dan Ferry. Go ahead, sir.

[Dan Ferry:]

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 brief 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, Genocea's, Chief Medical Officer; and Jessica Flechtner, Genocea's, 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.

[Chip Clark:]

Thanks, Dan. And thank you all for joining us today. Genocea made important scientific and clinical progress in the fourth quarter of 2019. I want first to review our path-breaking work on neoantigen profiling and selection.Specifically I want to talk about our unique work on inhibitory neoantigens which we're now calling inhibigen. We think through the inhibigen work we are once again reshaping antigen selection conventional wisdom.We first showed conclusively through our GEN-009 immunogenicity data that only a bioassay such as ours can systematically and faithfully identify the right neoantigens. In other words, we showed that the right neoantigens are those which have been expressed by the tumor, presented to the patient's immune system and can trigger anti-tumor T cell responses.But what if GEN-009’s compelling immune responses stem not just from ATLAS’s ability to find the right antigens? What if there's such a thing as a truly wrong antigen. Surely, we would want to find these and ensure we are not relying on them for our vaccines and cell therapies.This is exactly what we showed at SITC in November. We showed that certain antigens can drive immune responses that run counter to the cancer immunotherapy goals by dampening anti-tumor T cell responses.To recap, we showed that vaccination with inhibigens actually promotes tumor growth in the stringent B16F10 mouse melanoma model. Even more compellingly inhibigens reversed anti-tumor responses in an otherwise protected vaccine in that same model.Think about the implications, to us this demonstrates that maximizing the immune responses to a cancer immunotherapy requires both including the right antigens and also excluding inhibigens.There are two reasons in other words for the unparalleled immune responses we've demonstrated in GEN-009, and two reasons to expect good things from our cell therapy GEN-011.We continue to investigate inhibigens and expect to share more on their actions and implications this year. We also continue to advance our GEN-009 neoantigen vaccine. At SITC we reported that we completed patient dosing in the monotherapy Part A of our Phase 1/2a trial with no disease progression observed in vaccinated study participants. GEN-009 was well tolerated by this patient cohort.The Part A immunogenicity results confirmed the importance of ATLAS for antigen selection GEN-009 generated immune responses to essentially all of its cargo, 99% of the vaccine neoantigens and we should note that because of ATLAS the immune responses were not just high, but also relevant.Those of us who received this year's flu vaccine but still succumbed to the flu can attest to the seeming pointlessness of strong immune responses to the wrong antigens. ATLAS ensures that the GEN-009 immune responses should be to tumor relevant antigens.That is why we continue to believe that these strong immune responses position GEN-009 to potentially be the first neoantigenvaccine to demonstrate meaningful tumor shrinkage on top of immune checkpoint inhibitor therapy.This would come from Part B of the GEN-009 study which is designed to evaluate the vaccine in combination with standard of care immune checkpoint inhibitors in patients with advanced disease, including head and neck and non-small cell lung cancers. We have begun dosing and we anticipate reporting preliminary clinical results in Q2, Q3.I next want to speak to our exciting new T cell therapy program, GEN-011. We think the case for GEN-011rests on several converging trends. First is the solidifying confidence that adaptive cell therapy using neoantigen specific, but bulk unselected tumor-infiltrating lymphocytes or TILs can provide new hope to refractory patients with solid tumors.Second, as pioneers at the National Cancer Institute or NCI have reported sorting TILs for neoantigen specific T cells can improve patient outcomes. Third, as the team at the NCI have very recently confirmed the T cell cohort in the periphery can mirror those in the tumor.These points together argue for a product that uses T cells from the periphery that are sorted for the right neoantigens and that of course exclude inhibigens. This is GEN-011 and we're really excited to get it into the clinic.We have made significant progress in developing a productive and efficient manufacturing process for GEN-011. We intend to file an investigational new drug application next quarter and anticipate reporting preliminary clinical results in the first half of 2021.One more piece of news. Yesterday we appointed Dr. Gisela Schwab, President, Product Development and Medical Affairs and Chief Medical Officer of Exelixis to our Board of Directors effective February 14th, 2020. I think she's going to make a terrific addition.For 2019, it was a pivotal year as we continue to demonstrate positive preclinical and clinical data in support of both our proprietary platform and our pipeline. We look forward to continuing this momentum in 2020 through a range of data and regulatory milestones.I'm now going to pass the call over to Diantha, to summarize our financials from this quarter before opening the call to questions. Diantha?

[Diantha Duvall:]

Thanks, Chip. And good morning, everyone. We ended the quarter with $40.1 million of cash and cash equivalents. Our operating results for the quarter ended December 31, 2019 are as follows, R&D expenses were $6.8 million compared to $6.3 million for the same period in 2018.G&A expenses were $3 million compared to $2.6 million for the same period in 2018. And our net loss was $9.4 million compared to net income of $0.4 million for the same period in 2018.We also reaffirm that our existing cash resources will be sufficient to support our operations into the first quarter of 2021.With that, let's now open up the call for questions. Operator?

[Operator:]

[Operator Instructions] Your first question comes from Joe Pantginis from H.C. Wainwright.

[Joe Pantginis:]

Thanks for taking the question. Guys, I was just curious, in 2019 the new antigen space surely saw a lot of volatility both to the upside and the downside with various events. So I was just curious more on the macro side when maybe for Jess and Tom, as you presented your initial inhibigen data at CITI [ph] 2018 and then more in-depth data in ‘19. Can you describe your sort of broader discussions with other scientists and physicians in the field and KOLs and immunotherapy, how they've been reacting to these - to the inhibigen thesis?

[Chip Clark:]

Thanks, Joe for the question. This is Chip I'll ask Tom to kick the comments off.

[Tom Davis:]

Well it's been a - I think a fairly dramatic progression over the last 12 to 18 months when we initially were discussing the inhibigens. Clearly there was some skepticism since it is truly a novel finding, a potentially critical element of the immune system that had not yet been identified.However, over the last year as you pointed out Joe, we were able to present more data including consistent evidence that in the clinic inhibigens appear to play some role in the recurrence disease. But more importantly in a very challenging mouse model, we've been able to show that inhibigens have a very active role both in preventing immune responses, as well as preventing vaccines from working effectively and as a consequence also encouraging tumor growth.This has been a very consistent story where we're actively pursuing what the mechanism might be in order to better understand what we can do to control it. But obviously our current situation where we are the only ones to identify inhibigens and can exclude them from our therapeutics and as such are probably taking a very important step in assuring the success of our immune therapy.

[Joe Pantginis:]

So more like any feedback about how your colleagues in the space have been adjusting and reacting to the data?

[Chip Clark:]

So Joe, this is Chip and I’ll make a couple of comments. I mean, I think the other important sort of piece of feedback from the scientific and clinical community came from becoming a top 10 abstract at ASCO. I think that immuno-oncology at ASCO I think that's a clear reflection that we were you know sort of moving the needle clinically and scientifically.I think that as Tom said just because no one else can identify inhibigens, our peers don't really have much of an answer for how they might address those for their immunotherapies. And we obviously intend to continue to push the advantage as much as we can.

[Joe Pantginis:]

Got it. I appreciate the added color guys.

[Chip Clark:]

Thank, Joe.

[Operator:]

Your next question comes from Daina Graybosch from SVB Leerink.

[Daina Graybosch:]

Chip, maybe starting more top and then getting more detailed. You mentioned that we would see the next clinical results in Q2 or Q3. Is that a little bit of a delay? And can you give us any guidance on which conference that may be at and how many patients - and if there is a little bit of delay, what's driving it?

[Chip Clark:]

Thanks, Daina. That is not a delay. I think it's just a reflection of wanting to make sure we have a robust data set when we do present results. And Tom can speak to sort of the when and the where.

[Tom Davis:]

So we activated the study the second half last year and accrual has been going very well from our perspective. It is a complicated study and right now we want to be sure we have adequate amounts of data for people to interpret the results.So we're not pointing to any specific meaning at this time, but as you can tell from the range, we provided that we believe we'll have adequate patients in the middle of this year, most likely late Q2, Q3.

[Daina Graybosch:]

That's great. Thank you. And ahead of that, should we expect more preclinical data in any publications or conferences?

[Chip Clark:]

Absolutely as you know strive to present our data at major medical centers conferences rather. And so I am hopeful that at such conferences we will be present, but until abstracts have been accepted and things like that, we're not going to be providing any specific guidance.

[Daina Graybosch:]

Okay. That’s fine. And then I - a slight question on the cell therapy and inhibigen, if you - do you think the inhibigens are as relevant for cell therapy, let's say competitors are doing something similar taking peripheral blood T cells or TILs and then using their various platforms to select and stimulate the neoantigen specific? Would those - if they are using inhibigens, and that with those T cells just wouldn't proliferate, and so when they go and put T cell product back into the patients it wouldn't make as much of a difference as an vivo [ph] vaccine? I'd love to better understand that.

[Chip Clark:]

Thanks, Daina. I'll have Jess tackle that question.

[Jessica Flechtner:]

Thanks, Daina. I think your question is very relevant. These are as important, if not more important in cell therapy approaches both from TIL and from peripheral blood. What we know today about these T cells is that they – they do proliferate in response to the non-specific stimulation that many of these approaches are using to grow the TIL product or the peripheral T cell product and that they can exert their influence over their neighbors, the other T cells in the pool of these products.I'd also remind you that the majority of these products are not pure neoantigens specific TIL products, as ours is intended to be. They are mix of tumor relevant antigen, inhibigen specific T cells and totally irrelevant [ph] you know, viral specific T cells that get transferred as well.And so by selecting the right targets with ATLAS and avoiding the inhibigens for growing the new antigen specific T cells from the periphery and then putting back a more pure and enriched new antigen specific T cell pool, we believe that we have the opportunity to really benefit these patients in a way that they haven't been benefited before.

[Daina Graybosch:]

Great. Thank you.

[Chip Clark:]

Thanks, Diana.

[Operator:]

Your next question comes from Ben Burnett from Stifel.

[Ben Burnett:]

Great. Thanks so much. Just two quick questions. You announced that a patient has now been dosed in Part B of the GEN-009 study. I guess can you comment on how long it took to manufacture that patient’s vaccine?

[Chip Clark:]

Yeah, Ben. So the needle to needle time for the Part B of our clinical study is I think broadly reflective, possibly a little bit better than what we showed in Part A. Remember there that we reported that our overall needle to needle time was a little bit under 16 weeks, which I think compared favorably to the needle to needle times that others in the space have shown at a similar stage of development.And so that gives us confidence that assuming we scale that we can make GEN-009 not just available for the products who are eligible for a clinical trial as currently designed, but in future potential - potentially more expanded settings to be able to make the product faster for more patients.

[Ben Burnett:]

Okay. Great. Thank you for that. And then maybe just one more question on GEN-011. I guess what patient population where you test this once you began clinical trials this year? And then I guess separately, is there a limit to a number of different neoantigen T cells you can include in this product?

[Chip Clark:]

So I'm going to divide that question up, I'll Jess speak to the number of neoantigens in the product and then I'll have Tom speak to the target patient population in the initial clinical study. So Jess?

[Jessica Flechtner:]

Right. So currently we will put the number of neoantigens that we find in neo - we will put the number of neoantigens that we identify with ATLAS in the process for amplifying the T cells for our product. The upper limit that we have set today is 30 and that is mostly just for defining a process under which we're going to develop these products. But theoretically there is no upper limit and we intend to continue to put in everything that we find.

[Chip Clark:]

Tom?

[Tom Davis:]

So of course, as an ideal target for these treatments for GEN-011 in patients, one would want tumor types that have a high level of new antigens to take advantage of what Jess is just describing, but also tumors that [indiscernible] immune responses. So our focus to date like other companies has been tumors along the lines of head and neck, lung, urothelial and renal, which do have response rates where there's plenty of room for improvement.However it has an interesting process as we refine the protocol in preparation for filing with the IND and there are a lot of other great ideas out there. So we haven't a final list of tumors that we're going after, but I do think we'll have some challenging ones in there in order to test really what potential for this treatment is.

[Ben Burnett:]

Okay, great. Thanks for that color.

[Chip Clark:]

Thanks, Ben.

[Operator:]

[Operator Instructions] Your next question comes from Gil Blum from Needham and Company.

[Gil Blum:]

Hi, everyone. How are you doing today? Thanks for taking my question. So going back to the inhibigen to immunogen ratio, is there - considering this is a naturally occurring phenomenon. Is there a chance that if you have a poor inhibigen ratio to begin with you would be unresponsive to CPI or pretty much any other immunogenic therapy?

[Chip Clark:]

Thanks, Gill. I’ll have Jess to take that question.

[Jessica Flechtner:]

That is exactly what we are finding. If I interpret your question correctly, when we have done retrospective studies of humans who have been treated with checkpoint and we have profiles, the number of inhibigens that we find and the number of new antigens that we find in each of those subjects prior to their treatment.We have shown that it is the relative proportion of inhibigen to neoantigens that appear to predict whether they will subsequently respond to checkpoint blockade. We think this is a very interesting observation and we are currently collecting additional data in our clinical trial, as well as in some prospective research study to more definitively answer this question.

[Gil Blum:]

Would you consider excluding such patients in your own clinical studies?

[Chip Clark:]

I have Tom to tackle that part.

[Tom Davis:]

Of course, it's very early in development and I think too early to start selecting patients. First you have to confirm the finding that Jess described. But I do think long term there's a strong possibility that the ATLAS type, the picture of the immune system that we get from ATLAS can tell us a lot about each individual patient. And we may be able to identify not just those who might not respond to a certain type of therapy, but perhaps allow us to select the therapy that will work in that patient. So we're excited about potential here - and this will be used in clinical decisions down the line. But right now we're creating the data to justify that.

[Gil Blum:]

All right. Thank you for taking my questions and for the added color and I hope the flu season will be over soon.

[Chip Clark:]

We are with you on that, Gill. Thank you.

[Operator:]

At this time I would like to turn it back to the speakers for any further comment. Please go ahead Mr. Clark.

[Chip Clark:]

Thank you, operator. And thanks again everyone for joining us today. We'll speak to you again soon.

[Operator:]

Ladies and gentlemen, this concludes today's conference. Thank you for participating and have a wonderful day. You may now disconnect.