On March 28, 2017 Cyclacel Pharmaceuticals, Inc. (NASDAQ:CYCC) (NASDAQ:CYCCP) (“Cyclacel” or the “Company”) a biopharmaceutical company developing oral therapies that target the various phases of cell cycle control for the treatment of cancer and other serious disorders, reported its financial results and business highlights for the fourth quarter and full year ended December 31, 2016 (Press release, Cyclacel, MAR 28, 2017, View Source [SID1234518296]). The Company’s net loss applicable to common shareholders for the three months and year ended December 31, 2016 was $2.9 million and $12.0 million, respectively. As of December 31, 2016, cash and cash equivalents totaled $16.5 million.

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“Following the outcome of the SEAMLESS study and a review of our clinical development pipeline we will concentrate our resources on our transcriptional regulation and DNA damage response clinical stage programs,” said Spiro Rombotis, President and Chief Executive Officer of Cyclacel. “While we will discuss the SEAMLESS data with regulators after completing ongoing analyses, we are looking ahead with a clear strategy. We are dedicating our efforts and resources to progressing our CYC065 CDK inhibitor program and the promise in our BRCA positive stratified, sapacitabine and CDK inhibitor study. We are encouraged by the support received from various stakeholders, the recent success of commercial stage CDK inhibitors and early clinical data from our own CDK inhibitor trials.”

Fourth Quarter and Full Year Highlights

Transcriptional Regulation Program – Cyclin Dependent Kinase (CDK) inhibitors

Continued recruitment in Phase 1, first-in-human trial of CYC065, a CDK2/9 inhibitor, to evaluate safety, tolerability and pharmacokinetics in patients with solid tumors. Expanded sixth dose escalation level with the objective of determining maximum tolerated dose and recommended dosing for Phase 2.
Data presented at the 2016 Annual Meeting of the American Association of Cancer Research demonstrated that CYC065 can induce cell death and combine beneficially with anti-cancer drugs from the Bcl-2 and BET (Bromodomain and Extra-Terminal) inhibitor classes, in in vitro models of B-cell lymphoma, including double-hit lymphomas. Combinations of CYC065 with the Bcl-2 inhibitor venetoclax (ABT-199) or BET inhibitors were both synergistic.
Preclinical data published in the Journal of the National Cancer Institute demonstrated that CYC065 had promising antitumor activity against certain lung cancer cells through anaphase catastrophe, a novel, cancer-specific mechanism of action.
DNA Damage Response (DDR) program

The extension of the Phase 1 study evaluating a sequential regimen of sapacitabine and the CDK inhibitor seliciclib is continuing enrollment in an enriched population of BRCA positive patients with advanced breast cancer.
A part 3 of this study has been initiated to include BRCA positive patients with pancreatic and ovarian cancer.
SEAMLESS Study in Elderly Patients with Acute Myeloid Leukemia (AML)

In February 2017, the Company reported that the SEAMLESS study did not reach statistically significant superiority in overall survival (OS), although an improvement in complete remission rate was observed. In the stratified subgroup of patients with low baseline peripheral white blood cell count, comprising approximately two-thirds of the study’s population, an improvement in OS was observed for the experimental arm.
The Company is currently analyzing stratified and exploratory subgroups to identify patients who are most likely to benefit from treatment with the experimental arm. Depending on this analysis the Company may initiate discussions with European and U.S. regulators to determine a potential regulatory pathway.
Poster Presentation on the PLK Inhibitor CYC140 at the AACR (Free AACR Whitepaper) Annual Meeting

Today, Cyclacel also announced a poster presentation at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2017 Annual Meeting to be held April 1-5 in Washington, D.C. The poster is titled “The novel PLK1 inhibitor, CYC140: Identification of pharmacodynamic markers, sensitive target indications and potential combinations” (Poster Board 1, Abstract number 4178, Convention Center, Halls A-C, Poster Section 7). The poster details Cyclacel’s preclinical study to identify target indications including acute leukemia and esophageal cancer. The results will be presented in a session titled “Targeting Protein Kinases and DNA Repair” on Tuesday Apr 4, 2017 1:00 PM – 5:00 PM Eastern Time.

Data presented in December 2016 at the 28th EORTC-NCI-AACR (Free EORTC-NCI-AACR Whitepaper) Molecular Targets and Cancer Therapeutics Symposium, demonstrated anti-tumor activity of CYC140 in preclinical xenograft models of acute leukemia and solid tumors, including esophageal cancer, with tumor growth delay, tumor regression and cures being observed. Several pharmacodynamic markers were identified and activity was demonstrated in a majority of malignant cell lines derived from AML, acute lymphoblastic leukemia (ALL) and esophageal cancer.

Financial Highlights

As of December 31, 2016, cash and cash equivalents totaled $16.5 million, compared to $20.4 million as of December 31, 2015. The decrease of $3.9 million was primarily due to $10.1 million of net cash used in operating activities, partially offset by net proceeds of $6.8 million from the sale of common stock through the ATM sales agreement with FBR Capital Markets & Co.

Revenue for the three months and year ended December 31, 2016 were $0.3 million and $0.8 million respectively, compared to $0.4 million and $1.9 million for the same periods of the previous year. The revenue is primarily related to previously awarded grants from the UK government being recognized over the period to progress CYC065 to IND, which was completed in 2015, and IND-directed preclinical development of CYC140, a novel, orally available, Polo-Like Kinase 1 (PLK 1) inhibitor, completed in November 2016.

Research and development expenses were $1.9 million and $9.5 million for the three months and year ended December 31, 2016 respectively, compared to $2.6 million and $12.4 million for the same periods of the previous year. The decrease was primarily due to reduced study and clinical supply costs associated with the completion of the SEAMLESS study.

General and administrative expenses for the three months and year ended December 31, 2016 were $1.5 million and $5.5 million respectively, compared to $1.7 million and $5.7 million for the same periods of the previous year.

Other income (expense), net for the three months and year ended December 31, 2016 were $(0.1) million and $0.4 million, compared to nil and $(0.3) million for the same period of the previous year. The increase in other income (expense) is primarily related to foreign exchange movements.

United Kingdom research & tax credits were $0.4 million and $2.0 million for the three months and year ended December 31, 2016 respectively, compared to $0.5 million and $2.1 million for the same periods of the previous year. The cash receipt for the 2016 tax credit of $2.0 million is expected to be received in the second quarter of 2017, which results in proforma cash and cash equivalents of $18.5 million as of December 31, 2016.

Net loss for the three months and year ended December 31, 2016 was $2.8 million and $11.8 million respectively, compared to $3.4 million and $14.3 million for the same periods of the previous year.

On March 28, 2017 The Parker Institute for Cancer Immunotherapy, Bristol-Myers Squibb Company (NYSE: BMY) and the Cancer Research Institute (CRI) reported a multi-year clinical research collaboration to coordinate and rapidly initiate clinical Immuno-Oncology (I-O) studies across the Parker Institute and CRI networks (Press release, Bristol-Myers Squibb, MAR 28, 2017, View Source [SID1234518295]). Bristol-Myers Squibb will work closely with leading Parker Institute and CRI scientists and researchers, soliciting clinical research proposals from their networks and coordinating multi-site collaboration clinical studies to pursue some of the most difficult questions in cancer research. It will provide scientists with an ecosystem of advanced translational tools, precision immunotherapy and cutting-edge bioanalytical expertise to maximize learning and ensure the generation of high quality data to inform future development.

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The Parker Institute is a novel collaboration model which includes industry, academic and philanthropic participants, focused on the shared goal of accelerating immunotherapy research to develop and deliver new treatment options for patients. CRI is a nonprofit organization dedicated to advancing laboratory and clinical research through its global network of academic, industry, and nonprofit partners with the goal of developing lifesaving immunotherapies for all forms of cancer.

The collaboration will build on the Parker Institute model that brings together the nation’s top research institutions to share resources, data and technology to accelerate research through unifying and managing clinical trial design and conducting clinical studies across multi-centers. The Parker Institute currently funds projects across its network of more than 60 laboratories and 300 researchers who work together to advance research and potentially develop new therapies. The Cancer Research Institute will support the collaboration with investment from its Clinical Accelerator venture philanthropy program and access to its global network of leading investigators from around the world.

"Bristol-Myers Squibb is initiating this unique collaboration with a goal of accelerating the identification and development of new treatment options for patients who are facing very serious disease," said Fouad Namouni, M.D., head of Oncology Development, Bristol-Myers Squibb. "We are excited to partner with the Parker Institute and the Cancer Research Institute to leverage the unique translational capabilities of their networks and explore novel mechanisms of action in the field of I-O."

This is the Parker Institute’s first major agreement with a biopharma partner. The institute will continue to build key industry relationships critical for the success of its unique model.

"One of our goals is to help facilitate collaborations between academia and industry to help advance cancer research," said Jeffrey Bluestone, Ph.D., CEO and president of the Parker Institute for Cancer Immunotherapy. "Partnering with Bristol-Myers Squibb, a renowned leader in the field of immuno-oncology development, is a major leap forward for us. We could not be more enthusiastic to start this collaboration, which we believe will accelerate the process of turning important lab discoveries by our investigators into the potential for much needed treatments for patients."

"Unlocking the full potential of next-generation precision cancer immunotherapy requires the kind of coordination, resources, and logistical support that the Parker Institute and the Cancer Research Institute can offer our research partners, and collaboration with industry leaders like Bristol-Myers Squibb will be essential to hastening the development of new cancer immunotherapies," said Jill O’Donnell-Tormey, Ph.D., CEO and director of scientific affairs at CRI.

Bristol-Myers Squibb & Immuno-Oncology: Advancing Oncology Research

At Bristol-Myers Squibb, patients are at the center of everything we do. Our vision for the future of cancer care is focused on researching and developing transformational Immuno-Oncology (I-O) medicines that will raise survival expectations in hard-to-treat cancers and will change the way patients live with cancer.

We are leading the scientific understanding of I-O through our extensive portfolio of investigational and approved agents and our differentiated clinical development program, which is studying broad patient populations across more than 35 types of cancers with 13 clinical-stage molecules designed to target different immune system pathways. Our deep expertise and innovative clinical trial designs uniquely position us to advance the science of combinations across multiple tumors and potentially deliver the next wave of I-O combination regimens with a sense of urgency. We also continue to pioneer research that will help facilitate a deeper understanding of the role of immune biomarkers and inform which patients will benefit most from I-O therapies.

We understand making the promise of I-O a reality for the many patients who may benefit from these therapies requires not only innovation on our part but also close collaboration with leading experts in the field. Our partnerships with academia, government, advocacy and biotech companies support our collective goal of providing new treatment options to advance the standards of clinical practice.

On March 28, 2017 Clovis Oncology, Inc. (NASDAQ: CLVS) reported that rucaparib preclinical data will be presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2017 (Press release, Clovis Oncology, MAR 28, 2017, View Source [SID1234518292]). AACR (Free AACR Whitepaper) will take place April 1-5, 2017 in Washington, DC. The data being presented provide greater insight into the mechanism of action and function of rucaparib in multiple disease and therapy settings.

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"These data demonstrate Clovis Oncology’s commitment to fully understanding rucaparib’s mechanism of action as well as the therapeutic settings in which it may offer the most benefit to patients," said Patrick J. Mahaffy, President and CEO of Clovis Oncology.

Rucaparib is the Company’s oral, potent, small molecule inhibitor of PARP1, PARP2 and PARP3. The FDA approved rucaparib (Rubraca) tablets in December 2016 for the monotherapy treatment of advanced ovarian cancer in women with deleterious germline or somatic BRCA mutations treated with two or more chemotherapies. Rucaparib is also being developed for other oncology indications in which patients may possess mutant BRCA tumors and other DNA repair deficiencies beyond BRCA – commonly referred to as homologous recombination deficiencies, or HRD.

Data from preclinical rucaparib studies are the subject of four poster presentations at the AACR (Free AACR Whitepaper) meeting:

Abstract 2475 – In vitro and in vivo assessment of the mechanism of action of the PARP inhibitor rucaparib

Presenter: Andrew J. Simmons, Ph.D., Translational Medicine, Clovis Oncology
Date/Time: Monday, April 3, 1:00-5:00 p.m. ET
Location: Halls A-C
Abstract 2476 – Preclinical assessment of the PARP inhibitor rucaparib in homologous recombination deficient prostate cancer models

Presenter: Minh Nguyen, Translational Medicine, Clovis Oncology
Date/Time: Monday, April 3, 1:00-5:00 p.m. ET
Location: Halls A-C
Abstract 3650 – Preclinical evaluation of the PARP inhibitor rucaparib in combination with PD-1 and PD-L1 inhibition in a syngeneic BRCA1 mutant ovarian cancer model

Presenter: Liliane Robillard, Translational Medicine, Clovis Oncology
Date/Time: Tuesday, April 4, 8:00 a.m.–12:00 p.m. ET
Location: Halls A-C
Abstract 4676 – DNA repair protein expression and response of homologous recombination deficient ovarian cancer to the poly (ADP-ribose) polymerase (PARP) inhibitor rucaparib in the ARIEL2 Part 1 study

Presenter: Andrea E. Wahner Hendrickson, M.D., Assistant Professor of Oncology, Medical Oncology, Mayo Clinic, Rochester, Minnesota
Date/Time: Tuesday, April 4, 1:00-5:00 p.m. ET
Location: Halls A-C
Each presentation will be available online at View Source as of the time of presentation at the meeting.

About Rucaparib

Rucaparib is an oral, small molecule inhibitor of PARP1, PARP2 and PARP3 being developed in ovarian cancer as well as several additional solid tumor indications. The MAA submission in Europe for an ovarian cancer treatment indication was submitted and accepted during the fourth quarter of 2016. Additionally, rucaparib is being developed as maintenance therapy for ovarian cancer in the ARIEL3 trial for patients with tumors with BRCA mutations and other DNA repair deficiencies beyond BRCA, as well as biomarker negative patients. Data from ARIEL3 are expected in mid-2017, which, pending positive data, is expected to be followed by the submission of a supplemental NDA for a second line or later maintenance indication. Rucaparib is also being developed in patients with mutant BRCA tumors and other DNA repair deficiencies beyond BRCA – commonly referred to as homologous recombination deficiencies, or HRD. Studies open for enrollment or under consideration include prostate, breast, pancreatic, gastroesophageal, bladder and lung cancers. Clovis holds worldwide rights for rucaparib.

On March 28, 2017 Aptose Biosciences Inc. (NASDAQ:APTO) (TSX:APS), a clinical-stage company developing highly differentiated therapeutics that target the underlying mechanisms of cancer, reported financial results for the three months and fiscal year ended December 31, 2016 and reported on corporate developments (Press release, Aptose Biosciences, MAR 28, 2017, View Source [SID1234518291]). Unless specified otherwise, all amounts are in Canadian dollars.

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The net loss for the year ended December 31, 2016 was $18.6 million ($1.46 per share) compared with $14.6 million ($1.23 per share) in the year ended December 31, 2015. Total cash and cash equivalents and investments as of December 31, 2016 were $10.7 million (or $7.9 million US Dollars).
"We began 2017 by reviewing our corporate strategy and refocusing our resources on CG’806, an oral first-in-class pan-FLT3/BTK inhibitor we are developing for patients with FLT3-driven AML and certain B-cell malignancies," said William G. Rice, Ph.D., Chairman, President and Chief Executive Officer. "Preclinical studies with CG‘806 have demonstrated a unique activity profile which warranted the prioritization of resources toward advancing its development. We look forward to reporting on our progress with this molecule."
Corporate Highlights
In January 2017, Aptose announced the prioritization of its resources toward the development of CG’806, an oral preclinical compound being developed for patients with FLT3-driven acute myeloid leukemia (AML) and certain BTK-driven B-cell malignancies.

In June 2016, Aptose entered into an exclusive global option and license agreement with CrystalGenomics, Inc. of South Korea, focused on the development of CG’806. Aptose is currently conducting Investigational New Drug (IND) enabling studies, and, if it exercises its option under the agreement, expects to initiate a Phase 1 clinical trial in early 2018. The potential option exercise would likely occur prior to submission of an IND application in the U.S. Upon exercise of the option, Aptose would own global rights to develop and commercialize the program outside of Korea and China.

Compelling preclinical data have established CG’806 as a potent and well-differentiated pan-FLT3 inhibitor for AML and a non-covalent inhibitor of BTK and other oncogenic kinases that drive certain B-cell derived cancer cells. The compound has demonstrated tumor elimination in the absence of toxicity in AML xenograft models.

Aptose recently developed a new synthetic route to synthesize greater amounts of CG’806, and is using that route to prepare drug substance for various preclinical and animal model studies, and for development of an improved oral formulation. The compound is being developed as a once-daily oral therapeutic.

The company has submitted research abstracts to present CG’806 data at the upcoming AACR (Free AACR Whitepaper)-Hematologic Malignancies Meeting in May 2017.

Aptose temporarily delayed clinical activities with APTO-253, a phase 1 stage compound for AML, in an effort to define the root cause of recent manufacturing setbacks related to the intravenous formulation, and to restore the molecule to a state supporting clinical development and potential partnering. Aptose remains hopeful in the viability of APTO-253, which effectively inhibits expression of the c-Myc oncogene, as a potential treatment for AML.
Financial Results
THREE MONTHS ENDED DECEMBER 31, 2016 AND 2015 (UNAUDITED)
(Amounts in 000’s except for per common
share data) Dec 31,
2016
Dec 31,
2015
Revenue $ ― $ ―
Research and development expense 2,550 2,340
General and administrative expense 1,461 2,364
Operating expenses 4,011 4,794
Finance expense − −
Finance income (85 ) (273 )
Net financing income (85 ) (273 )
Net loss 3,926 (4,431 )
Basic and diluted net loss per share $ (0.26 ) $ (0.38 )

Aptose’s net loss for the three months ended December 31, 2016 was $3.9 million ($0.26 per share) compared with $4.4 million ($0.38 per share) in the same period in the prior year.
Research and development costs increased to $2.6 million in the three months ended December 31, 2016 compared with $2.3 million for the three months ended December 2015. Aptose incurred higher costs for formulation studies and manufacturing costs for the APTO-253 product in the three months ended December 31, 2016 than in the comparable period, and these were offset by lower expenses for the contract research organization costs to manage the study. In addition, in the current period Aptose was conducting studies related to its CG’806 program following the licensing of the technology in June 2016.
General and administrative expenses decreased to $1.5 million in the three months ended December 31, 2016 compared with $2.4 million in the three months ended December 31, 2015. The decrease, despite the increased cost of Aptose’s US dollar expenditures due to the devaluation of the Canadian dollar, is related to lower stock option compensation and lower consulting fees related to projects that were active and completed in the fourth quarter in 2015.
FULL YEAR RESULTS

Year ended Year ended
(amounts in 000’s of Canadian Dollars except for per common share data) Dec. 31, 2016 Dec. 31, 2015
REVENUE $ - $
-
EXPENSES
Research and development 10,322 6,254
General and administrative 8,344 9,845
Operating expenses 18,666 16,099
Finance expense 66 43
Finance income (105 ) (1,556 )
Net financing (income) expense (39 ) (1,473 )
Net loss and comprehensive loss for the period 18,627 14,626
Basic and diluted loss per common share $ 1.46 $ 1.23

Weighted average number of common shares 12,743 11,906

RESEARCH AND DEVELOPMENT
Research and development expenses totaled $10.3 million in the year ended December 31, 2016 compared with $6.3 million in the year ended December 31, 2015. Research and development costs consist of the following:
Year ended
December 31,
2016 Year ended
December 31,
2015

Research and Development excluding salaries $ 6,442 $ 4,046
CrystalGenomics Option Fee 1,294 -
Salaries 2,246 1,969
Stock-based compensation 293 210
Depreciation of equipment 47 29
$ 10,322 $ 6,254

Expenditures for the year ended December 31, 2016 increased significantly over the year ended December 31, 2015 due to the following reasons:
Research and development activities related to the option fee for CG’806;
Costs associated with the LALS/Moffitt collaboration developing epigenetic single molecule inhibitors of multiple targets, including the BET proteins, and other kinases for which no comparable expenses existed in the prior year periods;
Increased research and clinical operations headcount and related costs;
Formulation and manufacturing costs associated with APTO-253 and the root cause analysis of the filter clogging identified in November 2015; and
Increased Contract Research Organization costs related to consultants and advisors as we worked towards returning APTO-253 to the clinic.
During the year ended December 31, 2016, Aptose paid US$1.0 million ($1.294 million) to CrystalGenomics for an option fee related to the CG’806 technology. Should Aptose elect to exercise the option prior to filing of an IND application with the FDA, we would pay an additional US$2.0 million in cash or combination of cash and common shares, and would receive full development and commercial rights for the program in all territories outside of Korea and China. No comparable expense existed in the same period in the prior year.
GENERAL AND ADMINISTRATIVE
General and administrative expenses totaled $8.3 million in the year ended December 31, 2016 compared to $9.8 million in the year ended December 31, 2015. General and administrative expenses consisted of the following:
Year ended
December 31,
2016 Year ended
December 31,
2015

General and administrative excluding salaries $ 3,412 $ 4,317
Salaries 3,095 2,859
Stock-based compensation 1,730 2,602
Depreciation of equipment 107 67
$ 8,344 $ 9,845

General and administrative expenses excluding salaries, decreased in the year ended December 31, 2016 compared with the year ended December 31, 2015. The decrease is the result of lower travel, consulting and legal costs in the current year related to transactions completed in the prior year as well as lower press release and filing costs associated with a lower cost service provider in the current year periods.
Salary charges in the year ended December 31, 2016 increased in comparison with the year ended December 31, 2015 due to additional headcount in the first half of 2016 compared with the first half of 2015 as well as a higher average CA/US exchange rate which increased the cost of Aptose’s US denominated salaries in the first six months of 2016 in comparison with the prior year, and higher bonus expenses recognized in the current period.
Stock-based compensation decreased in the year ended December 31, 2016 compared with the year ended December 31, 2015 due to large option grants in April, June and July 2014 which vested 50% during the first year and therefore contribute to higher stock-based compensation expense during the first twelve month period captured in the prior year period.
FINANCE INCOME
Finance income totaled $105 thousand in the year ended December 31, 2016 compared to $1.5 million in the year ended December 31, 2015.
Interest income represents interest earned on Aptose’s cash and cash equivalent and investment balances. Foreign exchange gains are the result of an increase in the value of US dollar denominated cash and cash equivalents balances during such periods due to a depreciation of the Canadian dollar compared to the US dollar.

On March 28, 2017 Compugen Ltd. (NASDAQ: CGEN), a therapeutic discovery company, reported the selection of COM902 as the lead clinical antibody candidate for its CGEN-15137/TIGIT T cell checkpoint inhibitor program in immuno-oncology (Press release, Compugen, MAR 28, 2017, View Source [SID1234518290]). COM902 follows COM701 into the Company’s preclinical development pipeline. COM701 is the Company’s lead therapeutic antibody targeting PVRIG, for which IND is anticipated later this year. As previously disclosed, PVRIG and TIGIT represent two distinct but complementary arms of the same biological pathway, and inhibition of the two results in increased activation of tumor infiltrating lymphocytes (TILs). This provides a strong clinical rationale for the combination of COM701 and COM902, in addition to monotherapy use, as immunotherapies to treat various cancer types.

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Anat Cohen-Dayag, PhD, CEO and President of Compugen, commented, "The addition of this lead clinical antibody candidate for CGEN-15137/TIGIT to our preclinical pipeline represents another important milestone as we continue to build toward becoming a clinical stage company. We began our TIGIT program in 2016 based on our data indicating the potential for enhanced efficacy for combination treatment with COM701, and with our prior finding that TIGIT and PVRIG operate in the same biological pathway. The knowledge and the expertise we gained through the development of COM701 were an important factor in the accelerated development and selection of COM902. COM902 is a high affinity antagonist antibody selected for its potential ability to activate immune responses, both alone and in combination with COM701."

Dr. Cohen-Dayag added, "Currently available immuno-oncology therapies are effective for only a select subset of cancer patients, and we believe that the combination of COM701 and COM902, as well as with other checkpoint inhibitors, could provide a new therapeutic venue for treating cancer patients, specifically those non-responsive to current therapies. As we continue our development toward the clinic, we look forward to sharing with you more data as it becomes available."

About TIGIT
TIGIT is an immune checkpoint in the B7/CD28 family which has recently gained broad industry interest in the field of immuno-oncology. TIGIT was discovered by Compugen utilizing its in silico predictive discovery infrastructure and experimentally validated as an immune checkpoint. These findings were published by Compugen in the October 2009 issue of the Proceedings of National Academy of Sciences (PNAS). In the same year, two other groups also published papers disclosing TIGIT as a new checkpoint. Antibodies targeting TIGIT being developed by others entered Phase I clinical studies in 2016.

TIGIT can inhibit both T cell and NK cell activation when bound to its ligand, PVR (also known as CD155). TIGIT expression is increased on tumor infiltrating lymphocytes (TILs), and inhibition of T cell activation by TIGIT has been reported to be mediated by its ability to disrupt DNAM-1 (also known as CD226) costimulatory signals. Recent preclinical studies have shown that antibody antagonists of TIGIT can potently inhibit tumor growth in mouse cancer models when combined with PD-1 pathway blockade.