Sierra Oncology to Host KOL Call with Dr. Thomas Helleday presenting "DNA Damage Response (DDR) Targets Beyond PARP"

VANCOUVER, Sept. 14, 2017 /CNW/ - Sierra Oncology, Inc. (SRRA), a clinical stage drug development company focused on advancing next generation DNA Damage Response (DDR) therapeutics for the treatment of patients with cancer, today announced that it will host a Key Opinion Leader call on the topic of "DNA Damage Response Targets Beyond PARP" on Tuesday, September 19 at 10:30 am Eastern Time.

The call will feature a presentation by distinguished scientist Thomas Helleday, PhD, the Torsten and Ragnar Söderberg Professor of Translational Medicine and Chemical Biology at Karolinska Institutet, Stockholm, Sweden, who will examine emerging data and current mechanistic understandings of the next generation of clinical stage DDR targets in oncology, including Chk1. In addition, he will review which drug targets are synergistic in combination with Chk1 inhibition, and also will discuss certain preclinical DDR targets currently generating interest in the field. Dr. Helleday will be available to answer questions at the conclusion of the presentation.

Sierra Oncology's Senior Vice President of Research, Christian Hassig, PhD, will provide a brief overview on the company's research and development strategy for SRA737, a potent, highly selective, orally bioavailable small molecule inhibitor of the DDR target, Chk1. SRA737 has best-in-class potential and is currently in two Phase 1 clinical trials focused on enrolling patients with tumors identified to have genetic aberrations hypothesized to confer sensitivity to Chk1 inhibition via synthetic lethality, as a monotherapy or in combination.

Professor Helleday heads a large multidisciplinary translational research group at Karolinska Institute focusing on understanding basic DNA repair and DNA-damage and developing novel drugs for anti-cancer treatments. His group was the first to demonstrate a novel concept for treating cancer called "synthetic lethality" established by the selective killing of BRCA1 or BRCA2 mutated breast and ovarian cancers by PARP inhibitors (now EMA/FDA approved). Dr. Helleday has published extensively on the ATR/Chk1 pathway, and has established a cancer specific synthetic lethal relationship between ATR and Chk1 inhibition. Professor Helleday has been awarded numerous eminent international grants and awards in recognition of his research accomplishments including the Eppendorf-Nature Young European Investigator Award (2005) for outstanding contributions within the field of biomedical science by the journal Nature and two prestigious European Research Council Advanced Grants (2010 and 2016).

Dial-In & Webcast Information
Domestic:	800-289-0496
International:	719-325-4826
Conference ID:	8310106
Webcast:	www.sierraoncology.com
	direct link: http://public.viavid.com/index.php?id=126208

If you would like to ask a question during the live Q&A, please submit your request via email at [email protected]

About Sierra Oncology
Sierra Oncology is a clinical stage drug development company advancing next generation DNA Damage Response (DDR) therapeutics for the treatment of patients with cancer. Our lead drug candidate, SRA737, is a potent, highly selective, orally bioavailable small molecule inhibitor of Checkpoint kinase 1 (Chk1), a key regulator of important cell cycle checkpoints and central mediator of the DDR network. SRA737 is currently being investigated in two Phase 1 clinical trials in patients with advanced cancer:

• SRA737-01, a Monotherapy dose ranging trial evaluating SRA737 in cancer patients including prospectively enrolling subjects with tumors identified to have genetic aberrations hypothesized to confer sensitivity to Chk1 inhibition via synthetic lethality into five indication-specific cohorts: colorectal, ovarian, non-small cell lung, prostate, and head and neck cancers. In cancer cells, replication stress induced by oncogenes (e.g., MYC or RAS) or genetic mutations in DNA repair machinery (e.g., BRCA1 or FA) combined with loss of function in tumor suppressors (e.g., TP53 or ATM) results in persistent DNA damage and genomic instability leading to an increased dependency on Chk1 for survival. Targeted inhibition by SRA737 may therefore be synthetically lethal to these cancer cells and have utility as a monotherapy in a range of tumor indications.
  
• SRA737-02, a Chemotherapy Combination dose ranging trial evaluating SRA737 in combination with low-dose gemcitabine in cancer patients including an indication-specific cohort of prospectively-selected, genetically-defined subjects. Profound mechanistic potentiation has been reported when Chk1 inhibition is combined with DNA damaging cytotoxic agents or radiation. The widely-used chemotherapy gemcitabine is a strong exogenous inducer of replication stress and preclinical modeling demonstrates robust synergistic anti-tumor activity for SRA737 potentiated by gemcitabine.

Sierra Oncology is also advancing SRA141, a potent, selective, orally bioavailable small molecule inhibitor of Cell division cycle 7 kinase (Cdc7) undergoing preclinical development. Cdc7 is a key regulator of DNA replication and is involved in the DDR network, making it a compelling emerging target for the potential treatment of a broad range of tumor types. For more information, please visit www.sierraoncology.com.

Cautionary Note on Forward-Looking Statements
This press release contains forward-looking statements within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995, including, but not limited to, statements regarding Sierra Oncology's market and industry position, expectations from current data, anticipated clinical development and potential benefits of Sierra Oncology's product candidates. All statements other than statements of historical fact are statements that could be deemed forward-looking statements. These statements are based on management's current expectations and beliefs and are subject to a number of risks, uncertainties and assumptions that could cause actual results to differ materially from those described in the forward-looking statements. Such forward-looking statements are subject to risks and uncertainties, including, among others, the risk that Sierra Oncology may be unable to successfully develop and commercialize product candidates, SRA737 and SRA141 are at early stages of development and may not demonstrate safety and efficacy or otherwise produce positive results, Sierra Oncology may experience delays in the preclinical and anticipated clinical development of SRA737 or SRA141, Sierra Oncology may be unable to acquire additional assets to build a pipeline of additional product candidates, Sierra Oncology's third-party manufacturers may cause its supply of materials to become limited or interrupted or fail to be of satisfactory quantity or quality, Sierra Oncology's cash resources may be insufficient to fund its current operating plans and it may be unable to raise additional capital when needed, Sierra Oncology may be unable to obtain and enforce intellectual property protection for its technologies and product candidates and the other factors described under the heading "Risk Factors" set forth in Sierra Oncology's filings with the Securities and Exchange Commission from time to time. Sierra Oncology undertakes no obligation to update the forward-looking statements contained herein or to reflect events or circumstances occurring after the date hereof, other than as may be required by applicable law.

SOURCE Sierra Oncology

James Smith, Vice President of Corporate Affairs, Sierra Oncology, 604.558.6536, [email protected]; Andrew McDonald, LifeSci Advisors, LLC, 646-597-6987, [email protected]