Firm plans to develop OXY111A to treat cancer and chronic heart failure.

NormOxys raised $17.5 million in Series B financing for clinical development of its lead drug candidate, OXY111A, as a treatment for both chronic heart failure and cancer. NormOxys separately confirmed starting a dose-escalating Phase I trial with the compound.

The round was led by new investor, Care Capital LLC. Existing investor, Index Ventures, also participated.

NormOxys is focused on developing a drugs that enhance the body’s ability to deliver oxygen more efficiently to oxygen-deficient, diseased tissues. Such oxygen release enhancer compounds represent a new class of allosteric effectors of hemoglobin that, NormOxys claims, allow hemoglobin to release much more than the normal 25% of its bound oxygen. The molecules are being evaluated for a range of diseases including heart failure, cancer, and potentially as an alternative to erythropoietin for the treatment of anemia.

“We plan to initiate additional trials to evaluate the efficacy of OXY111A in chronic heart failure and cancer later this year and we are looking forward to advancing additional candidates within our pipeline,” comments Martin Tolar, M.D., Ph.D., CEO of NormOxys.

NormOxys claims that allosteric effectors of hemoglobin demonstrate significant effects on tumor growth. The drug increases hemoglobin’s oxygen-release capacity under tumor-related hypoxic conditions and so switches off the hypoxia-inducible factor HIF-1 alpha, which then down-regulates hypoxia-inducible genes, the company explains. The firm also reports that studies in mice with severe heart failure found that administration of OXY111A resulted in a dose-related increase in maximal exercise capacity of 63 ± 7%.

“In chronic heart failure patients OXY111A has tremendous potential to improve clinical outcome both in terms of morbidity and mortality and also improved exercise tolerance and therefore quality of life,” remarks David Clark, M.D., CMO. “This Phase I study builds on preclinical cardiovascular studies in which we have shown that OXY111A enhances the exercise capacity of normal mice as well as of mice with severe heart failure caused by dilated cardiomyopathy, and, additionally, OXY111A attenuates the left ventricular remodeling seen in mice post MI [myocardial infarction], with no apparent side effects in either model.”

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