Compugen Ltd.

Ladies and gentlemen, thank you for standing by. Welcome to Compugen's second quarter 2020 results conference call. At this time, all participants are in a listen-only mode. An audio webcast of this call is available in the investor section of Compugen's website, www.cgen.com. As a reminder, today's call is being recorded. I would now like to introduce Joanna Holtzman. Compugen's Director of Investor Relations and Corporate Communications. Please go ahead.

Thank you, Operator, and thank you all for joining us today. With me from Compugen are Dr. Anat Cohen-Dayag, President and CEO, Dr. Henry Attaway, Chief Medical Officer, Ali Krashen, CFO and COO, and Dr. Eran Ophir, VP Research and Drug Discovery. 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, our development efforts and their outcome, our discovery platform, anticipated progress and timelines for our programs, financial and accounting related matters, as well as statements regarding our cash position. 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 in cautionary language contained in the documents the company filed with the Securities and Exchange Commission, including the company's most recent annual report on Form 20F filed on February 24, 2020. The company undertakes no obligation to update projections or forward-looking statements in the future. I will now turn the call over to Anat.

Thank you, Ilana. Good morning and good afternoon, everyone, and welcome to our second quarter 2020 corporate and financial update. As Ilana mentioned, with me today are Dr. Henry Adewoy, our Chief Medical Officer, Ari Krushing, our CFO and COO, and Dr. Eran Ophir, our VP Research and Drug Discovery. After my prepared comments, Henry will review the progress across our clinical programs and Ari will review our financial statements and position. We will all be available for the Q&A session. We have reached an exciting new phase of development at Compugen. Today, there are three clinical programs, COM701, COM902, and Bay 190-5254 addressing drug targets we discovered computationally. COM701 and COM902, developed internally, are designed to strategically evaluate the genome axis as a potentially transformative checkpoint axis for cancer immunotherapy treatment. Henry will provide detailed updates across these programs later in the call, but first, I want to share what we believe are important developments for COMPIGEN and the broader immunoncology space that leave us increasingly optimistic about our drug candidates and distinctive clinical development path. As a reminder, COMPIGEN's internal computational discovery platform has enabled the discovery of two important new checkpoints in the DINAM axis, PDR-AG discovered by COMPIGEN and TIGIT, discovered by CompleGen and at the same time also by others. Our lead program, COM701, targets PVRIG, while COM902, now also in the clinic, targets TIGIT. It is important to note that we identified that PVRIG and TIGIT are part of a parallel and complementary inhibitory pathway in the denim axis. and we have preclinical data demonstrating that blocking PVRIG together with PIDGIT may be required in certain tumor types in order to generate or enhance an anti-tumor immune response. In addition, our preclinical work, supported also by others, provides the foundation of our hypothesis that there is an intersection between the two pathways on the denim axis , and the PD-1 pathway. Specifically, our findings suggest that the simultaneous blockade of these three pathways has the potential to synergistically enhance anti-tumor immune responses in certain patients' populations where the genome axis plays a role and who therefore are probably not responsive to PD-1 inhibitors alone. As such, the blockade of these two denim axis pathways have the potential to expand immune oncology treatment options to cancer patients who are not responsive to currently available drugs. It is quite remarkable to think that just a few quarters ago, of these three targets, only PD-1 was clinically validated. We have come a long way in a very short time, and are thrilled to now have initial signs of clinical activity by PVRIG and TGIT validated in the clinic by others. Taken together, these data increase our confidence in our hypothesis that in certain patient populations where these three pathways are dominant, blocking the denim axis and specifically the addition of PVRIG blockade to TIGIT and PD-1 blockers may be a critical component in driving cancer immunotherapy treatment responses. I want to dive in a bit more into PVRIG and TIGIT. It is important to recognize that while these are important complementary checkpoints in the same genome axis, they are in fact distinct. First, PVRIG and TIGIT bind preferentially to different ligands. PVRL2 and PVR respectively. In addition, and highly relevant to our clinical programs, PVRL2 and PVR are differentially expressed on different tumor types. Importantly, PVRL2 expression is more dominant compared to PVR in certain cancers such as breast, endometrial, and ovarian. This is significant because in these PVRL2 dominant indications, we expect that PVRLG must be blocked in order to drive antitumor immune responses. Furthermore, PVRL2 is more expressed on various myeloid populations, mainly DC subsets. These immune cell types have been shown recently to be important in the PD-1 pathway. In addition, PVRLG antigens are not necessarily expressed on same immune cell types. While both expressed on T cells and NK cells, TGIT is highly expressed on Tregs relative to PVRIG. These findings, with the totality of our functional data, suggest that PVRIG blockade should support synergistic effects with PD-1 and or TGIT inhibitors and that these pathways are not redundant. Therefore, as the only company with wholly owned clinical assets targeting both PBRG and TGIT, we believe we're uniquely positioned to evaluate the blockade of the denim axis within without PD-1 blockade and assess its potential to drive robust immune responses in patients. In line with our preclinical work, our initial clinical data suggests Thank you very much. as well as in dual and triple combination regimens that we believe will allow us to comprehensively extract the value of our drug candidates addressing these new checkpoints. So starting first with our COM701 clinical studies. In April, we presented at AACR the dose escalation data from both the COM701 monotherapy and combination arm with Bristol-Merrick squids of Devo. These data included all eight monotherapy dose escalation cohorts and four of a total of five cohorts from the dual combination arm. We were thrilled to observe two partial responses, one from each arm, with both having presented very encouraging durable responses of more than six months as of the data cutoff date. We were also highly encouraged with both safety and tolerability and disease control rates in both arms. We believe the notable durability of responses observed with COM701 is particularly significant given that these results were achieved in a dose escalation setting and in heavily pre-treated patients. These data serve as an important initial clinical validation of PVRIG as a new immune checkpoint with a role in cancer immunotherapy. And we're excited to continue advancing this program for the many patients who currently do not respond to available treatments, potentially because the dominant inhibitory checkpoints in their tumors were not being targeted. So what is next for COM701? This quarter, we initiated enrollment for the monotherapy expansion cohort, which is designed to evaluate the safety and tolerability of COM701 as a recommended dose for expansion. This study utilizes a biomarker-informed strategy to focus on tumor types where we believe the PGRHG pathway may play a role based on our preclinical genome access expression data and those escalation clinical results. We were excited to start this study which was also met with strong interest from our principal investigators and we're excited to share that the enrollment is progressing as planned. We remain on track to complete enrollment in 2020 and report initial data from this trial as previously indicated in the first half of 2021. We recently completed enrollment in fifth and last cohort of the combination dose escalation study of COM7-1 with Optivo and intend to provide the additional cohort data most likely at the same time as the initial monotherapy expansion cohort data in the first half of 2021. Finally, moving to our triple combination study. We remain on track to begin the Phase 1-2 study to evaluate COM701 in combination with Obdivon and Bristol-Mers Squibb's anti-tigit antibody in the second half of this year, following the recent clearance of the IND by the FDA. We're working closely with Bristol-Mers Squibb on this study and are very pleased with their continued support and involvement in our collaboration. This program allows us to directly test our hypothesis of an intersection between the PDRG, TGIT, and PD-1 pathways, and that the simultaneous blockade of these three pathways has the potential to synergistically enhance anti-tumor immune responses in selected patient populations not responsive or refractory to PD-1 blockers alone. As I have reviewed today, We believe there is now significant data, both clinical and preclinical, that support this strategy and we look forward to leveraging our position with our wholly owned clinical candidates against both PGRG and TIGIT. We're highly enthusiastic about this targeted, science-driven, clinical development program of COM701, which we believe has the potential to broaden the therapeutic benefit of checkpoint inhibitors to tumor types where they have previously not been successful. Moving next to COMP902, our anti-TGT therapeutic antibody. As I mentioned earlier in the call, new data presented by others over the past few months provided important clinical validation of TGT as an immunotherapy checkpoint. We're thrilled to see this data, which we believe further supports our triple pathway hypothesis, and we're excited to initiate this quarter the dose escalation study of COM902. We anticipate disclosing initial data from this study next year. I would like to reiterate that while PDIS is now a clinically validated target being evaluated by us and others in biopharma, Compugen is the only company with clinical assets targeting both PDRG and TGIT in its portfolio, allowing us to fully exploit the potential of blocking these parallel and complementary members of the genome axis to drive robust immune responses. Before I turn the call over to Henry, I would like to briefly touch upon the continued challenges associated with COVID-19. We're fortunate in that we're not experiencing significant impact on our activities for 2020. In fact, as indicated in our last call in May, we anticipate meeting our upcoming milestones and data readouts, including completing enrollment in the COM-701 monotherapy expansion cohort this year, and disclosing initial data from the study in the first half of 2021, Together with the data from the additional cohort of the dose escalation of COM701 in combination with Obdivo, as well as disclosing initial data from the COM902 dose escalation study in 2021. COVID-19 has introduced challenges in our work, and I am enormously proud of our team having watched them rise to overcome the extraordinary circumstances we are facing. Their dedication allows us to continue to advance our programs with the ultimate hope of broadly expanding the reach of cancer immunotherapy. We're grateful to our partners, investigators, and shareholders and look forward to continued progress. With that, I will turn the call over to Henry to review our clinical programs.