09 May 2011
Heptares Grants Shire an Exclusive Option to License Novel Adenosine A2A Antagonist
Welwyn Garden City, UK. 9 May 2011 - Heptares Therapeutics today announced it has signed an exclusive option agreement with Shire Pharmaceuticals for a novel adenosine A2A antagonist discovered by Heptares and currently in preclinical development. Adenosine A2A is a G-protein coupled receptor (GPCR) involved in the regulation of dopaminergic pathways in the brain. Recently, inhibition of the A2A receptor has been proved to be clinically effective in treating symptoms of Parkinson’s disease and may offer benefits in additional CNS diseases.
The Heptares A2A programme reflects a new approach to this GPCR target. Heptares stabilised the A2A receptor using its proprietary StaR® technology, determined the receptor’s binding characteristics through Biophysical Mapping™, and resolved its 3D crystal structure using x-ray crystallography. This advanced knowledge of the target enabled Heptares scientists to discover entirely new types of chemical structures for inhibiting the A2A receptor.
Under the terms of the agreement, Heptares has granted Shire an exclusive option, upon completion of certain preclinical studies, to license worldwide development and commercial rights to the Heptares A2A programme. Heptares has received an upfront payment and is eligible, upon exercise of the option by Shire, to an option exercise payment, future milestone payments, plus royalties on product sales. Further terms of the agreement are not being disclosed.
"We are excited to sign this option agreement with Shire for the development of our novel A2A antagonist, a potentially best-in-class new agent for treating patients suffering from debilitating CNS diseases," said Malcolm Weir, CEO of Heptares. "A2A is an important and clinically validated GPCR drug target, yet it has never been adequately addressed by the available older chemistries. Heptares has discovered fundamentally novel chemotypes as the basis for a new and, we believe, superior approach to A2A receptor pharmacology."