RIGL- Rigel Pharma and Bristol-Myers Squibb collaboration

Discussion in 'In the Pipe' started by Anonymous, Feb 24, 2015 at 5:49 AM.

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  1. Anonymous

    Anonymous Guest

    Much more to come from this

    SOUTH SAN FRANCISCO, Calif. and NEW YORK, February 23, 2015 /PRNewswire/ -- Rigel Pharmaceuticals, Inc. (Nasdaq: RIGL) and Bristol-Myers Squibb Company (NYSE: BMY) today announced that they have entered into a collaboration agreement for the discovery, development and commercialization of cancer immunotherapies based on Rigel's extensive portfolio of small molecule TGF beta receptor kinase inhibitors. TGF beta can promote tumor growth, broadly suppress the immune system and increase the ability of tumors to spread in the body. The collaboration will focus on developing a new class of therapeutics aimed at increasing the immune system's activity against various cancers either as monotherapy or in combination with immune checkpoint inhibitors, including Bristol-Myers Squibb's Opdivo (nivolumab) and Yervoy (ipilimumab).

    Under the terms of the agreement, Bristol-Myers Squibb will obtain exclusive, worldwide rights to develop and commercialize small molecule therapeutics derived from Rigel's TGF beta library, including, but not limited to, those approved to treat cancer. Bristol-Myers Squibb will pay $30 million upfront and Rigel will be eligible to receive development and regulatory milestones that could total more than $309 million for a successful compound approved in multiple indications. Rigel will also be eligible to receive tiered royalties on the net sales of any products from the collaboration.

    "As a company dedicated to leading scientific advances in immuno-oncology, we are committed to exploring the utility of TGF beta inhibition as a potential therapeutic to fight certain cancers," said Carl Decicco, Ph.D., Head of Discovery, R&D, Bristol-Myers Squibb. "Working with Rigel and having access to their TGF beta receptor kinase inhibitors extends our existing portfolio of immunotherapeutic approaches to include this key mediator of immunosuppression in the tumor microenvironment."