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YM BioSciences licensee Pulmokine awarded NIH funding to develop small molecule drugs for pulmonary hypertension
Date:9/29/2010

e for other molecules from our library, with a view to potentially augmenting our clinical development pipeline in the future with internally-discovered compounds."

Pulmonary Arterial Hypertension (PAH) is characterized by constriction of the pulmonary arterioles, the small blood vessels that carry absorbed oxygen from the lungs into the circulation. The average survival after diagnosis of PAH is three years for untreated patients. The worldwide incidence of primary PAH is estimated to be 5-6 cases per million of population, while PAH secondary to other diseases has a higher incidence. For example, the incidence of PAH associated with systemic sclerosis is estimated to be 11-47 cases per million.

The SBIR Program is a US-federally funded grant program administered by the US NIH. The aims of the program are to support small business in the development of new technologies, specifically the generation of proof-of-concept data in relevant models.

About YM BioSciences

YM BioSciences Inc. is a drug development company advancing three clinical-stage products: CYT387, a small molecule, dual inhibitor of JAK1/JAK2 kinase; nimotuzumab, an EGFR-targeting monoclonal antibody; and CYT997, a potent vascular disrupting agent (VDA).

CYT387 is an orally administered inhibitor of both the JAK1 and JAK2 kinase enzymes, which have been implicated in a number of immune cell disorders including myeloproliferative neoplasms and inflammatory diseases as well as certain cancers. CYT387 is currently in a Phase II trial in myelofibrosis with detailed initial safety and activity data expected at the American Society of Hematology (ASH) meeting in December 2010. Nimotuzumab is a humanized monoclonal antibody targeting EGFR with a potential best-in-class side effect profile. Nimotuzumab is being evaluated in numerous Phase II and III trials worldwide by YM's licensees. CYT997 is a uniquely orally-available agent with dual mechanisms of vascular disruption and c
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