SAN DIEGO — January 28, 2015 — San Diego-based Crinetics Pharmaceuticals announced today that it has been awarded a $1.5 MM Phase II Small Business Innovation Research (SBIR) grant from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) of the National Institutes of Health (NIH) for the development of orally-available, small molecule kisspeptin receptor antagonists to treat polycystic ovary syndrome (PCOS) and other women’s health disorders.

“PCOS is so prevalent, yet inadequately treated in most patients. As an industry we haven’t done enough to develop new therapeutic strategies to help these patients,” said Stephen Betz, Ph.D., Crinetics’ Vice President of Biology and principal investigator on this grant. “Kisspeptin receptor antagonists could provide a real opportunity to treat PCOS at the root cause rather than simply trying to mitigate downstream symptoms.”

“This program represents a significant extension of Crinetics’ efforts to develop drugs that target endocrine diseases and endocrine related cancers. With this program our goal is to give physicians an important new tool to help the millions of women suffering with PCOS,” said Scott Struthers Ph.D., Founder and CEO of Crinetics. “This award is also another important step forward in our strategy to build a pipeline of important new drug candidates with support from the NIH and other patient focused groups,” continued Struthers.

About Polycystic Ovary Syndrome: PCOS is the most common endocrine disorder in women, and current estimates suggest that it affects up to 10% of women ages 18 to 44. It is usually first identified during a woman’s early reproductive years. Symptoms can vary and in addition to polycystic ovaries often include irregular menstruation, which can lead to infertility. Hyperandrogenism, which can manifest as acne and hirsutism is also frequently observed. Another hallmark of PCOS is the development of insulin resistance and obesity. At the neuroendocrine level, PCOS is characterized by the presence of persistently rapid pulses of the hormone GnRH. This hyperpulsatility results in unbalanced gonadotropin levels that in turn lead to ovarian dysfunction. Because the kisspeptin system controls the pulsatility of GnRH and gonadotropins, its modulation by small molecule antagonists presents a new opportunity to treat the underlying defect driving the disorder.