Good day, ladies and gentlemen, and welcome to Agenus First Quarter 2016 Financial Results 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 call is being recorded. I will now like to turn the conference over to Michelle Linn, with Corporate Communications. Please begin.

Thank you, operator. Welcome to the Agenus first quarter 2016 conference call. Before I continue, I would like to remind you that this conference call will contain forward-looking statements, including statements regarding the company’s potential income stream, research and development, and clinical trial activities, the publication of data and potential application of the company’s technologies, and product candidates toward the prevention and treatment of diseases. These forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially. Reference to these risks and uncertainties is made in today’s press release and they are disclosed in more detail in our most recent filings with the U.S. Securities and Exchange Commission. These statements speak only as of the date of this call and Agenus undertakes no obligation to update or revise these statements. All forward-looking statements are expressly qualified in their entirety by this cautionary statement. When evaluating Agenus’ business and securities, investors should give careful consideration to these risks and uncertainties. As a reminder, this call is being recorded for audio broadcast. With me today are Dr. Garo Armen, Chairman and Chief Executive Officer; Dr. Robert Stein, President of R&D; and Evan Ballantyne, our Chief Financial Officer. During this call, Garo will provide a corporate update, Bob will provide an R&D update, and then Evan will review our financial results. We will then open up the call for questions. I will now turn the call over to Garo.

Thank you, Michelle, and thank you all for joining us this morning. We began the year with notable milestones for our proprietary portfolio of checkpoint antibodies as well as those included in our collaborations portfolios. In the quarter, we gained FDA clearance for the IND applications for our Agenus own CTLA-4 antibody, AGEN1884; and for our partner GITR antibody, INCAGN1876. Yesterday, we announced that the first patient in our trial to test our CTLA-4 antibody, AGEN1884, received their first - very first dose of this anybody. This is a Phase 1 trial in solid tumors. Last week, we presented three posters at AACR conference, and our partnered GITR and OX40 program, and our CTLA-4 program. GITR and OX40 programs in oncology are partnered 50-50 with Incyte. Dr. Stein will provide more details on the data presented at AACR. Looking ahead to the remainder of 2016, we expect to begin additional clinical studies of our checkpoint antibodies, randomized trials of our Prophage vaccine in combination with immuno-oncology agents in newly diagnosed glioma. We are continuing to evaluate the best path forward for a potential registrational trial of Prophage in glioma, including combination approaches with checkpoint antibodies. We will update you on our decision regarding this on regulatory and business considerations within the third quarter. We are also advancing a number of other immuno-oncology programs, including both disclosed and undisclosed immuno-oncology checkpoint antibodies, neoantigen vaccines as well as others, which we will provide update on as we initiate clinical trials or upon entering collaborative transactions. We expect some of these to occur during the balance of this year. I would also like to provide a quick update on our other partnered programs. GSK, our partner for our vaccine adjuvant program, has disclosed their plans to file for regulatory approval of their highly…

Thank you, Garo. We are very pleased to announce that we initiated a Phase I trial of Agenus-1884, our antibody drug candidate which targets the clinically and commercially validated immune checkpoint receptor CTLA-4. Looking ahead to the rest of the year, we and our partner Incyte expect to initiate additional checkpoint modulator antibody clinical trials. Earlier this month, at the AACR conference, we presented preclinical data showing that our two different CTLA-4 antagonist antibodies, 1884 and 2041, are functionally distinct with different Fc γ receptor binding activity expected to mediate either antibody-dependent cellular cytotoxicity or ADCC through natural killer cells in the case of the IgG1 isotype antibody 1884 or antibody dependent cellular phagocytosis or ADCP through macrophages in the case of the IgG2 isotype antibody 2041. We have also shown that CTLA-4 antagonist antibody synergize with our heat shock protein-based vaccines in preclinical mouse. We’ve demonstrated that both our CTLA-4 antibodies, slated for clinical development, enhance T-cell dependent vaccine responses in primate models. Notably, Agenus-1884 is expected to deplete intratumoral Treg cells, thereby enhancing the antitumor activity of T effector cells. At AACR, we also presented preclinical data, showing that our GITR agonist antibody, INCAGN1876, which is partnered 50-50 with Incyte, functions as a potent activator of GITR signaling in effector T-cells, and then in the context of suboptimal TCR signaling GITR binding by 1876 enhanced T-cell responsiveness only in the presence of TCR stimulation. Notably, the data also show a high-expression of GITR on intratumoral Treg cells from human tumor samples. And that these intratumoral Treg cells could be depleted by 1876 through the process of antibody-dependent cellular cytotoxicity or ADCC. These data support the idea that 1876 may have the potential to enhance T-cell responsiveness to weakly-immunogenic tumor antigens, while attenuating the immune suppressive function of intratumoral…

Bob, thank you very much. For the first quarter ended March 31, 2016 Agenus reported a net loss attributable to common stockholders of $31.8 million or about $0.37 per share, basic and diluted, including $9.6 million in non-cash expense. This compares to a net loss attributable to common shareholders for the first quarter of 2015 of $18.8 million or $0.28 per share, basic and diluted. The increase in net loss attributable to common stockholders for the three months ended March 31, 2016 compared to the net loss attributable to common stockholders for the same period in 2015 was primarily due to the advancement of our checkpoint programs. Cash and cash equivalents, and short-term investments were $148.2 million as of March 31, 2016. This concludes the financial portion of our call. I would like to now turn the call over to Garo for closing comments.

Thank you, Evan, and thank you, Bob. What you have heard from Dr. Stein is a glimpse at the broad and deep efforts that are going on in our research in the field of immuno-oncology and immunology. Looking ahead to the rest of the year, some of the key anticipated milestones will include: initiation of one or more additional clinical trials for our checkpoint antibody programs; filing our first IND for an ASV neoantigen vaccine candidate, while advancing our phosphopeptide-based vaccine efforts; advancing our lead vaccine program, Prophage, into a clinical trial in newly diagnosed GBM in combination with a checkpoint antibody; advancing our earlier-stage pipeline of checkpoint agents to IND enabling studies; and securing additional strategic alliances and/or partnerships. With that, I would like to thank you for joining us on this call today. We hope that you found this update informative. And we look forward to providing you with additional updates. And with that, I will turn the call back to Michelle.

Thank you, Garo. Operator, you can now open the call for questions.

Thank you. [Operator Instructions] The first question is from Jason McCarthy of Maxim Group. Your line is open.

Hi, guys. Congratulations on getting over back into the clinic with first checkpoint. I just have two questions for Bob and one for Evan. Bob, the OX40, can you give us some background on some of the preclinical work. If you’re knocking down Tregs significantly, and you’re also up regulating NKs and macrophages as well as T-cells, have you seen any adverse events in the form of any hyperimmune activation in your animal model?

So the OX40 agonist is not active in the current form. 1949 doesn’t interact with the murine receptors, so it’s not possible to assess its actual activity. OX40 agonist have been relatively well tolerated in mice, though based surrogate antibodies. And the toxicity that we’ve seen in the IND enabling studies with our compound looks very manageable and we’re not concerned about that. It does have interesting properties in that - for cells that are partially activated. It can help them get fully activated, but it doesn’t indiscriminately activate. And then for the Tregs, based on animal models, the depletion of Tregs is restricted to intratumoral settings. It’s not seen in the periphery. It’s not seen even in the tumor-draining lymph nodes. So the likelihood you have widespread dysregulation on that basis is very small. So it’s a really attractive point of intervention we believe. It’s very similar to GITR.

Great. Now that actually leads me right into my next question. Could you give us an update on LAG-3, because LAG-3 hasn’t been talked about too much from Agenus and it has these similar properties to OX40 where it seems to be not too active in the periphery, but you can hit the receptor in the tumor microenvironment or in the case of autoimmune? You can actually deplete T-cells that are just causing damage. Can you give us an update on the LAG-3 program?

I’ll make one general comment, and then I’ll point out that that is a partnered program with Incyte for oncology and we don’t generally speak about the programs that are in process. We’re very pleased with how it’s progressing. With LAG-3 it seems to be a marker of deeply exhausted T-cells. It comes up after PD-1. And what we see in all likelihood is in the tumor setting where we can identify T-cells that have the potential to recognize tumor antigens but have been driven to a state of exhaustion. They’re often being driven there by activation through PD-1 and LAG-3. So combinations of PD-1 and LAG-3 or PD-1 and TIM-3 blockers are expected to be helpful in patients that you can hope to pre-identify in part by the presence of these more deeply exhausted T-cells.

Great, thank you. And just, Evan, can you walk us through the expenses for the quarter? There were $25 million in R&D. And what you guys are projecting for 2016, as you are ramping up all of these new studies now?

Yes, but we haven’t given overall guidance on what we expect. But we have said that we expect to have cash into the second-half or middle of 2017. Our primary expense - and I should point out we are actually on budget, but our primary spend, as Bob and Garo both indicated, is associated with the checkpoint antibody programs and advancing several of those into the clinic, and the ASV, advancing that into the clinic as well.

Okay, great. Thanks, guys.

Thank you, Jason.

Thank you. The next question is from Mike King of JMP Securities. Your line is open.

Thanks for taking my call. And also I’ll add the congratulatory remarks about your progress last 18 months or so. I wanted to maybe just follow-up on the previous questions, sort of ask the inverse of those questions, which has to do with the combination therapies. I was kind of struck at AACR by, I guess, what I - not to be cynical here, but I thought some of the agonist antibodies and some of the combination checkpoint inhibitors, the data were less than impressive. And I am just wondering, is that because we don’t understand sort of the chronology of the immune response? And I am just wondering, before you guys begin combination therapies either with checkpoints, agonists or vaccines, if you will undertake further preclinical studies to be sure, when you go into humans you elicit the kind of response that you’re hopeful for.

Mike, I just want to make sure that it’s clear, that what you’re referring to is not our agents, it’s…

No, that’s - yes, yes.

…make sure that, but, Bob.

I think that part of that is that if there is a need to identify the right patients in whom to test different combinations. And part of that you can learn some, maybe guiding information from animal models. But part of it is to be able employ the latest approaches to understanding in a given patient how mutant a particular tumor is, what the potential neoepitopes are, whether in that patient immune system has already recognized the tumor as non-self, and to have the tools to monitor what the state of the patient is at the time of presentation. If it’s a patient with a moderate mutational burden who hasn’t recognized the tumor as non-self, then that’s a place to think about applying a vaccine. And if you have the ability to monitor the baseline and post-vaccination response to the specific neoepitopes then you can look for the impact of adding different things like GITR or OX40 agonist, or CTLA-4 blocker or PD-1 blocker, on the ability to supercharge some of the responses. I think that largely when you look at what’s going on right now, a lot of it is very large studies that aren’t deeply mined for information. And I think that the opportunity to do smaller studies that are more intensively investigated is a very real way for us to be able to compete in a world where other people are just blanketing the clinical trials in an expensive, but not in necessarily a highly guided way.

Right, exactly. It seems like it’s - there is not a lot of a priority thought. And it’s just, add A plus B and see what happens or it’s very much of an empiric approach rather than a scientifically guided approach as you point out.

I appreciate you’re bringing it up, because I do think that is a place where Agenus has long history in the immuno-education aspect of it. And the ways in which we’ve augmented that with the addition of next-gen sequencing in the neoepitopes prediction, is not only useful in the vaccine space, but also in doing intelligent navigation through the checkpoint modulator space.

Right.

And finding how to make the combinations are most appropriate to the patients and how to get the right patients in the studies you design. And then use…

Yes.

Determine whether you’re on track or not. And that’s a key part of a, I think, successful concentrated efforts in this area, not just blanketing in a less effective way.

Yes. I’m just wondering if I could ask a quick follow-up. One of the questions we get asked just a fair bit, when talking to investors about Agenus, what differentiates your neoantigen identification process from some of the recent startup companies like Gritstone or Neon. I don’t know if you can spend a minute with sort of comparing and contrasting.

And I think it’s a very important question, and I will point out that Agenus really is the original neoepitope, because by harvesting tumors and pulling out the heat-shock protein peptide complexes, that was an agnostic way to sample the neoantigen space. And what we’ve been able to leverage that into is using the bioinformatic tools to allow us to predict the neoepitopes. I would like to point out that although there’s a lot of interest in the algorithms for predicting neoepitopes there far from perfect, if you lever the work that John Castle has been doing for over a decade at the mice TRON institute to try to be able to take next generation sequencing data and turn that into accurate predictions of neoepitopes. In 2012, he published the first real study using B-16 [ph] in animal model to show that that was doable and that vaccinating with those peptides was capable of providing anti-tumor protection, and in a treatment mode as well. So we’ve continued to refine the work that John and his 20 scientists had been doing. And we’ve added into it the structural biology and computational biology considerations. And we in the context of the recent acquisition of PhosImmune have added the Ligendome [ph] capabilities that Don Hunt and his colleagues have been building over the last two decades. In addition to the mutationally-based neoepitopes that have been the focus of most of the other efforts including Neon and Gritstone and some of what we’ve been doing here, PhosImmune has identified a very exciting new class of neoepitopes that don’t come from abnormal protein sequences. So you don’t detect them by looking at next generation sequencing of DNA. But represent abnormal sites of phosphorylation on intracellular proteins that get processed and presented on the surface of tumor cells as a basis for high-affinity TCR recognition and conform the basis for very exciting vaccines. It could be highly patient-relevant, but not have to be made differently for every single patient, because those phosphopeptide neoepitopes tend to be characteristic of different tumor types. And Don Hunt and Vic Engelhard, Mark Cobbold at PhosImmune have cataloged over a thousand of these and characterized them for their recurrence on different types of tumors, and then the context of different MHC genotypes.

Great. Thanks for the thoughtful answer as always.

Thank you, Mike. And one other point, I would like to make is that, while there is a lot of interest in neoepitopes, we really are the only company that has a demonstrated way to produce good CDA responses against peptides. And that comes from the success we have with our HerpV vaccine trial, which is a Phase 2 controlled trial, showing that when we complex a mix of peptides with heat-shock protein-70, and mix that with QS-21 and inject that to patients we can generate very good T-cells responses, CDA positive responses over a half of patients. And in then those patients we had a 70% reduction in viral load, which shows that they’re biologically meaningful as well. So we think we can leverage that into the AutoSynVax base quickly.

Thanks again.

Thank you. The next question is from Swayampakula Ramakanth of H.C. Wainwright. Your line is open.

Thank you. Good morning, gentlemen. Thanks for taking my questions. I got on the call a little bit late. And I was just wondering, if you had provided anything - any update on the Prophage program, especially the Phase 2 study in the newly diagnosed glioblastoma. And also with regarding glioblastoma, I was wondering how you think about your program now, that one of your competitors could not get through their program and how do you view your position in the market within the GBM space?

Thank you, RK. With regard to Prophage we did cover in our comments earlier. So we are slated to start randomized combination trials in newly diagnosed glioma. And the agents would be immuno-oncology agents in combination with Prophage. With regard to a registrational trial, we said that we will provide an update on this in the third quarter based on our regulatory deliberations and business considerations as well as the rapidly moving market in this field. So the rest of your question I will ask Bob to address.

Yes, hi, RK. So just a little bit of follow-up on the Phase 2 trial that was reported - presented by Orin Bloch at ASCO. We’re now out more than four years in all the patients in the less elevated PDL-1 group. And we have 5 out of 17 patients alive for four more years, looks like we were heading towards about a 29% four year survival on that half of the patients in which PDL-1 was measured at baseline. And then, with regard to the Celldex concerns that was sort of an interesting trial, because it suggests that maybe you can make a immunologic impact on glioblastoma in patients with the EGF receptor variant III, but putting all that selective pressure on that one antigen leads to escape by antigen loss. Which isn’t very surprising and so we’re encouraged by the hint that immunologic mechanisms can do something in brain cancer. And we also believe that our approach is very distinct, because we have multiple neoepitopes which are much more difficult for the cells to get rid of all of them, so that they don’t have that way of getting around the vaccine effect. And we also have with our vaccine, the stimulation of NK cells. So they - if the cells try to get around it by down-regulating class 1 and they’re penalized for starting to express class I by NK killing. So we think it’s an unfortunate result, but we don’t think it reached directly on our product.

Okay. It was great. And actually it leads me to my next question about the AutoSynVax program. So could you highlight to us, some of the developments that you have been achieving which gives you the confidence and be optimistic that you can get this into the clinic over the next 12 months?

While we as - a lot of it is predicated on what we’ve done with the HerpV product, which is heat shock protein complex 70 expressed in bacteria mixed with 32 different - 35 more peptides and QS-21. And we know how that performed. We have a lot of work ongoing to be able to predict appropriate neoepitopes from patients next generation sequencing of their tumors. We’re working to optimize peptide design, because we want to ensure that each peptide that we put in is well complex to Hsc70. And that’s part of the ongoing optimization. But we know what path we had to take to get the IND filed for HerpV. We are in some discussions upcoming with the FDA to clarify the path exactly. But we believe that we have pretty good clarity about that and it should be accomplishable in the timeframe of within the next 12 months.

Great. And, Bob, the last question is - the company acquired a couple of interesting assets over the last year, especially the CEACAM on the PhosImmune molecule. Can you provide us with some insight into how this programs are moving forward? And what gives you the confidence that we should see them in clinic soon?

Well, we remain very enthusiastic about CEACAM, that program is progressing well. We don’t in general give details about our internal programs, but we are enamored with that as a target. As you probably know, a number of tumors over-express the shorter-form of CEACAM1 which can inhibit lymphocyte function by interacting with the longer-form. So we think there is a very good rationale for that as a target. That program is progressing well. We really fine-tuned our ability to generate useful antibodies and characterized them quickly and get them through cell-line development and scale up in our new GMP pilot plant that used to belong to XOMA at Berkeley. So we are very enthusiastic about that. And I think, the - stay tuned for later developments on that. You asked me one other second part of that question, could you repeat it, please?

That’s just on the PhosImmune assets.

So on the PhosImmune piece, so that is a really out-of-the-box and orthogonal observation, because everybody has been focused on trying to predict the tumor neoantigens based on mutational sequences - mutated sequences in proteins. And what Don Hunt, Vic Engelhard, Mark Cobbold really pioneered was the observation that just on the basis of being malignantly transformed cell, there is enough disordered biochemical regulation that new phosphopeptides show up in the context of MHC molecules on the surface of cancer cells. And interestingly, if you look at a bunch of leukemias. Leukemias of certain type tend to present the same phosphopeptide neoepitopes if you have the same MHC genotype, so B7 or AO201. And so they are different from self. They don’t seem to be present on any normal tissues, and they seem to be shared across people with a particular kind of cancer. So they really represent extremely interesting ways to generate new immunity that will have high impact on particular types of tumors, that has all the advantage of mutationally based neoepitopes. But it doesn’t have the disadvantage that you have to make an absolutely different product for every patient. So we are very excited about to getting that moved forward and we are heavily at work in incorporating that type of immunogen into some of our synthetic vaccine approaches.

Thank you very much, Bob. And thanks for taking all my questions.

Thanks, RK.

Thank you. And the next question is from Biren Amin of Jefferies. Your line is open.

Yes, hey, guys. Thanks for taking my questions. Maybe I’ll start with recent AACR meeting. What were your impressions of the Roche [Amox R916] [ph] OX40 program. They presented some early Phase 1 data. How do you think - first of all, what were your impression of the data and how do you think it differentiates from you program?

I don’t want to comment specifically on their data, but I will say that in conducting our research programs and selecting our candidates, we in our cases make all the competitor antibodies that we can and test them head-to-head with ours. We believe that 1949 has some very interesting differencing features, which we believe will make it better behaved and potentially more efficacious clinically. We’ll have to wait until later in the year to start to verify that in the clinic.

When do we start to getting clinical data from the some of the Phase 1 assets. Should we expect that this year?

We are in a Phase 1 that was as the FDA is doing all of these immuno modulatory antibodies, constrained to start at a pretty low dose and they have a fairly standard Phase 1 single ascending dose escalation. So we expect to get to efficacious doses as quickly as possible. And we’ll heavily monitor the studies to try to derive useful information and when we have that we’ll be able to talk about it. I would expect to have at the somewhat second-half of the year or beyond.

And then, Evan, I think you talked about cash with cash proceeds to [last or mid] [ph] to second half of 2017. So given you have about five or six quarters of cash, which targets are on the table from a partnership standpoint?

Oh, we can’t comment on the potential partnerships as Garo said earlier, he is evaluating various options.

Okay, great. Thank you.

Thanks, Biren.

Thank you. [Operator Instructions] There are no further questions in queue at this time.

Thank you, operator. I’d like to remind listeners that a replay of this call will be available approximately two hours after the call and that the call will also be accessible from the company’s website at www.agenusbio.com. On behalf of the management team at Agenus, I would like to thank everyone for joining us on today’s call. We will be available to receive any further inquiries following the call. With that, operator, please conclude the call.

Thank you. Ladies and gentlemen, this concludes today’s conference. You may now disconnect. Good day.