Good morning and thank you for joining us today. With us today from Compugen are, Martin Gerstel, Compugen's Chairman of the Board; Dr. Anat Cohen-Dayag, President and CEO; Mr. Ari Krashin, CFO; and Dr. John Hunter, Vice President, Antibody R&D and Site Head, Compugen USA Incorporated. Before we begin, I would like to read the following regarding forward-looking statements. During the course of this conference call, the Company may make projections or other forward-looking statements regarding future events or future business outlook, including statements relating to the potential of the CGEN-15029 program for the development of new cancer immunotherapy treatments for solid tumors, including the potential for drug combination with current immune checkpoint blockers, and the potential of COM701 as a new cancer immunotherapy treatment, anticipated progress on Compugen's pipeline program as well as commercialization efforts. We wish to caution you that such statements reflect only the Company's current expectations and that actual events or results may differ materially. You are kindly referred to the risk factors and cautionary language contained in the documents that the Company filed with Securities and Exchange Commission, including the Company's annual report on Form 20-F, filed March 7, 2016. The Company undertakes no obligation to update any projections or forward-looking statements in the future. I will now turn the call over to Dr. Anat Cohen-Dayag. Please go ahead.

On behalf of all of us at Compugen, welcome to our third quarter 2016 conference call and thank you for joining with us today. As we announced in our third quarter financial results press release last week, this quarterly conference call was postponed until today so that we would be able to include the discussion of the very exciting new results for our CGEN-15029 program and its clinical lead antibody COM701. These results were presented by the Company in a late breaking session at the Annual Meeting of the Society for Immunotherapy of Cancer (SITC), last Friday. Therefore, after my brief introductory remarks, John Hunter, the Site Head of our South San Francisco operation will view key data he presented at this leading Immuno-Oncology Conference. In doing so, John will be referring to a PowerPoint slide presentation which is available on our website. If possible, I encourage you to view this presentation during the call in order to be able to better follow the remark. Following John's prepared remarks, we will move to a Q&A session where Martin and Ari will be able together with John and myself to answer questions about either today's presentation or our quarterly financial results published last week. The call will end with closing remarks by Martin. Since John is participating from our facilities in South San Francisco, we hope that the difference in locations will not create any communication problem. In his prepared remarks today as was the case at the Citi Conference last week, John will focus solely on one of the programs in our immuno-oncology pipeline. However, we also announced last week that the Company will hold a R&D Day in New York City on December 7th, which will be webcasted. At this upcoming R&D Day, we will provide an overview of…

Thanks, Anat. Today, I'll be giving in a few of our lead therapeutic program CGEN-15029, including details on its discovery, functional data for COM701, our lead antibody targeting CGEN-15029, and supporting in vivo data for mouse study showing the utility of targeting CGEN-15029 in the tumor setting. All of this demonstrates the promising potential of COM701 as a first-in-class drug opportunity for cancer Immunotherapy. As previously mentioned, most of the results I will be showing were first disclosed last week, at the Annual Meeting for the Society for Immunotherapy of Cancer. Since I know that our audience today has varying degrees of scientific knowledge in this field, I will attempt to describe the key points on each of the slides with a minimum of scientific jargon. This will not in some cases captured all of the information presented last week and for those of you who want more of the science, I encourage you to join us for our R&D Day in December, where we will go into much greater detail on the program. I would like to refer to the slides on our webcast starting with Slide number 3. Six years ago, the first clinical data on ipilimumab commercially knows as Yervoy was published, demonstrating unprecedented responses in late stage melanoma patients. Since then, there has been a slew of new data, not only justifying the original excitement around and immune checkpoint inhibition, but also demonstrating the broader patient populations can be addressed by targeting additional immune checkpoints, and by using checkpoint inhibitors together in combination. However, even with these advances, the majority of patients don’t derive long-term benefit from current therapeutics; and there is still a substantial unmet medical need. The approach the Compugen has taken to address this unmet need and to generate a competitive edge in…

Thank you. Ladies and gentlemen, at this time, we'll begin the question-and-answer session. [Operator Instructions] The first question is from Mike King of JMP Securities. Please go ahead.

I just wanted to ask the question about -- just help me to understand the model, John, I am just trying to understand, if PVRIG is also -- are the T-cells that you are looking at also co-expressing PD-1? And if so, is there any either crosstalk or competitive action of PD-1 versus PVRIG when you do those experiments? Are they completely devoid of PD-1?

The T-cells that we are using do express PD-1 as well as TIGIT, so all of the relevant checkpoint inhibitors are present in the model system. We're starting to look at combination to see what the effects of co-inhibition with PD-1 and PVRIG are, but based on some recent data presented by Genentech where Ira Mellman has been showing that PD-1 when activated results in dephosphorylation of those CD28 by dNM. We do think that there is a tie end between the two pathways that we are further exploring right now.

Okay. So, we don’t know certain what the temporal relationship is between PD-1 engagement either by an inhibitory antibody or the ligand by PD-L1 versus?

No, we are kind of working through that now multiple assay systems.

Just another follow-up question, so then when you go to the animal experiments, I guess the working assumption or working hypothesis is that the tumors that are implanted at [Indiscernible] all of full compliments of checkpoints. Is that a fair statement?

Yes, in the early models that we have looked at, we do see all the relevant players present in the tumor microenvironment, which you would expect given the combination data that we generated in those models.

Right. Okay. And finally, the cartoon where you showed blockhead of PVRIG, TIGIT, or both, those are theoretical or do you actually -- have you actually done those in kind of what biology? Thank you.

Well, I mean the combination data that we showed in the presentation with the increased activation using dual blockhead would tend to validate that model. I do want to point out that’s a very simplified model.

Sure.

There is a lot of other players obviously that have to be accounted for, but at least in the assay system that we've set up to look at that the results do replicate our model.

The next question is from Ted Tenthoff of Piper Jaffray. Please go ahead.

I guess my question is looking forward a little bit with respect to [Indiscernible] the clinic. Obviously, we'll do sort of all kind of studies, monotherapy, but those studies to sort of tease up where you would do potential expansion still or do you have from the animal work and the preclinical work kind of some hypothesis in terms of where these interactions may best be applied either as monotherapy for combination?

Yes, I think we are going to use a combination of those datasets. We are doing a number of combinations studies in mice to try to get a better sense of what combinations we want to use and possibly what patient population we want to address. We are also doing a number of translation on medicine studies to look at expression of all of the relevant components within the given tumor, but that work is very early. So, we're not at a stage at where we know what indications we want to focus on. But ultimately, if you look at the history of other checkpoint inhibitors, it's really been in the clinic that people have generated the data they need to know what patient populations they want to do to expansion studies in.

That makes sense. And then just I might have missed this, but the IND on track next year then or what's the call?

Hi, Ted. Just before I am answering that I'd like just to add that in the planning for Phase 1 study, we would like to make sure that we keep our options open and that we target both for a PD-1 treated the patients and also those that do not respond to PD-1. Just in terms of a guidance to IND, with the data that we discussed today at the R&D Day that we are planning on December 7th, we plan to discuss in detail the path for COM701 to IND and to the clinic and will give much more details from this. So, I defer the question to the R&D Day.

Understood that makes a lot of sense. Thanks and I am looking forward to seeing at R&D Day in our conference.

The next question is from Thomas Yip of FBR. Please go ahead.

One question I have is regarding PVRL2, it was identified as a binding partner for PVRIG. What do you think about the potential of binding to PVRL2 alone? And as far as you know, are there other checkpoint targets that are related to PVRL2 as well? Thank you.

We decided in looking at it. I assume the question is whether we would consider targeting PVRL2.

Yes. Sorry, and if there're other existing shape on targets that also associated with PVRL2?

Yes, so we did consider PVRL2 as a legitimate target because it has an activating role when it binds to dNM. We felt that that would counteract what we were trying to accomplish. So, we really feel that targeting PVRIG is a much better way to go because you're very selectively inhibiting that negative signal and allowing the free PVRL2 to bind to and activate through dNM. With regards to other molecules that PVRL2 binds to, as I mentioned in the presentation, it has been reported to bind to TIGIT, although in the literature and in the studies, we've done in house we see that as a very affinity interaction that we're not sure whether it's theologically relevant, but again really one of the key activities for PVRL2 is to send the second stimulatory signal to T-cells through dNM for activation.

Okay, got it, I guess I've one follow-up. So in upcoming on the following, we reasonable to assume that it will include the mechanism of how COM701 the antibody binds to PVRIG and also effects as we discussed PVRL2 and other associated ligand as well?

Yes, the mechanism of action that we have for COM701 is that, it does bind to PVRIG and it completely disrupts the PVRL2 interaction. And studies that we've run which strongly suggest that to get the inhibitory signals through PVRIG, it does require binding to PVRL2. So, it's really just a blocking mechanism of action, and we are looking at effects of blocking that on downstream signaling from PVRIG.

The next question is from Steven Bayer [ph]. Please go ahead.

Hi, this question is more general. Could you give some details about timeframes or the range of timeframes that it takes to move some of the programs forward, and I guess the steps involved, I mean on your mechanism of action, validating in vivo, finding a binding partner et cetera. You know the bare deals over three years old, are there -- I mean I guess apparently given of this 15029 is moving along know. There is obviously a range of timeframes, but sort about the any particular steps that are slower than others, any information that we can maybe gauge what expectations going forward are for other programs or do you learn anything from what you are doing now that might speed up other programs?

Yes, there are couple of variables here, I would say that from the stage of lead selection to IND to Phase 1, Phase 2; in general, I would say that industry standards are relevant to everyone and of course also to Compugen. But I think the pre-lead selection there are different variables that would either shorten or extend the timelines, and it depends on the following. In general and I think that you know it by now, I am saying it and I relate it to almost every quarterly call, the fact that we are working on proteins that we discovered a drug target that do not have a lot of information in the public domain doesn’t have a lot of years of literature around them, is generating a situation for Compugen that we need to make sure that we have the understanding that other have on their known targets when we are moving ahead with the therapeutic program. This may vary as to what's the nature of the target. There are targets that we can get this information faster as compared to other targets. And it is really has to do, not with the potential of the target to become a good drug target for the development of therapeutics, but really about the mechanism affection how complicated this is, how new it is, do we have the systems, other industry standards, how much we think we can trust one or two systems or need to expand to 10 or 20 different systems. And this all has to be taken into consideration, both for our internal program. And also it applies you mentioned the two buyer programs without getting into details with respect to the bio programs that we cannot share, you know by now that’s one of them we already got through different preclinical milestones, and that the consol move to buy for this specific program that is more advanced. And there is another program that is less advanced and takes more time. So, it's really by the nature of the target and the amount of work that has to be on it. And this is the variable, and this is the variable within Compugen internally for each of our program and also with respect to Compugen as compared to the rest of the industry.

The next question is from Vernon Bernardino of FBR. Please go ahead.

Thanks for taking my question and congrats on the reveal of the targets and the candidate. I am just wondering if you could describe a little bit about the efforts and what activities have you already done as far as intellectual property of protection?

Yes, it’s a very sensitive question that I'll give you an answer that is broader than what you are asking because I think this is something that’s interest different shareholders. In general, we do not give any specific information about filings that we do. This is something that has to do with the competition and how we protect our IP, as you could probably see in the public domain, there are patents of Compugen and we always take care not to connect between the CGEN name and this specific target that is mentioned in the pattern, this is now for us, the first time that we have done that with PVRIG and CGEN-15029. And again, as I was mentioning while we feel comfortable with the IP strategy that we are applying, and with the different filings that we have done throughout the years, it is better for us to make sure that we control when is the right timing for us to speak and when is the right timing for us to connect to the CGEN name to the target. And in general, we preferred to avoid an unnecessary competition and risk that we may put our patterns to. So, in general, the short answer is that we are hearing at out of information on this for a reason.

No, I understand, thanks Anat. I was just wondering confirm, but you have already started the application process?

Yes, of course. We already have prior filings on this, yes.

The next question is a follow-up from Mike King. Please go ahead. Mike, are you with us?

John, I was just wondering if you could clarify for me some terminology because I know there is a paper from Colorado Group in February describing the interaction of PVRIG in the ligand. So, could you just sort of translate for us, if we see these turn up in other publications of CD226, CD112 and CD112R?

Sure, yes, like many other areas of the literature, there is a lot of different names for some of the same molecules. So, CD112 is just a CD designation for PVRL2, and when the Colorado Group realized that PVRIG bound what they renamed it CD112R. The original designation in the data base when we found, it was PVRIG which is why we stuck with that. DNM1 is also known as CD226.

Okay.

Yes, and then with regards to the findings in the Colorado paper, they actually matched quite well with a lot of the research we have been doing here. So, in terms of looking at effects on T-cell activations, they were more focused on CD-4 cell activation because of our focus on tumor biology, we really have been focusing on CD-8 activation. But we did see some of the same effects that they have reported in the paper.

There are no further questions at this time. Before I ask Martin Gerstel to go ahead with some closing statements, I would like to remind participants that a replay of this call is scheduled to begin in two hours for a period of 72 hours. In the U.S., please call 1-888-295-2634. In Israel, please call 03-925-5921. Internationally, please 972-3925-5921. Martin Gerstel would you like to make concluding statement?

Yes, thank you very much. Pioneering a paradigm shift in the underlying methodology used to create new products in a well established and already very profitable industry is never an easy task, and it becomes much more difficult when the underlying science required for the intended paradigm shift is not yet known. As was the case when Compugen began its efforts at using in silico science based predictive biology to discover novel drug targets. Today even though all of our programs and product candidates are still at very early stages, the compelling data discussed today for one of our novel checkpoint based immuno-oncology programs clearly demonstrate that in silico predictive science-based methodologies can in fact identify very promising novel drug targets, an important unmet need in the industry and something that few industry leaders would have believed possible prior to our demonstrated success. In closing today's call, I want to thank all of you for participating and for your interest in our company, and a very special thank you to our long-term shareholders who’ve provided us support and encouragement through the years, as we developed the unique and broadly applicable capabilities that have allowed us to now reach this critical point. And it is just the beginning, thank you very much.

Thank you, this concludes the Compugen Limited third quarter 2016 financial results conference call. Thank you for your participation you may go ahead and disconnect.