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GlaxoSmithKline and Astex Pharmaceuticals Terminate Cancer Therapeutics Collaboration

On January 17, 2012 Astex Pharmaceuticals reported that the multi-year collaboration to discover cancer therapeutics based on epigenetic targets entered into by SuperGen and GlaxoSmithKline (GSK) in November 2009 is terminating and existing research work and assets generated under the CLIMB epigenetic collaboration will be transferred to GSK (Press release, GlaxoSmithKline, JAN 17, 2012, View Source [SID1234563941]). Astex will have no further obligation to conduct additional research work on the program. This decision follows on from the review and rationalization of Astex’s internal pipeline and drug discovery programs as part of the recent merger of Astex Therapeutics Limited and SuperGen, Inc. to form Astex Pharmaceuticals, Inc., and discussions with GSK. As a result of the transfer, Astex will continue to be eligible to receive milestones and royalties under an asset transfer agreement. A separate Research and Development Collaboration and License Agreement which includes a multi-target drug discovery collaboration, entered into by Astex’s UK subsidiary, Astex Therapeutics Limited and GSK in November 2009 will continue as previously announced.
"The decision to transfer the CLIMB epigenetic program to GSK was based on our assessment of internal resources and discussions with GSK," said Harren Jhoti, PhD, president of Astex Pharmaceuticals. "We continue to work closely with GSK on the discovery of molecules using our PyramidTM fragment platform as part of our successful and ongoing collaboration against multiple targets of interest to GSK entered into in November 2009."

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(Press release, Hoffmann-La Roche , JAN 17, 2012, View Source [SID:1234504440])

SFJ Pharma announced a collaborative development agreement with Pfizer Inc. to conduct a Phase 3 clinical trial in Asia of Pfizer’s investigational agent axitinib for the adjuvant treatment of patients at high risk of recurrent renal cell carcinoma(RCC) following nephrectomy.

On January 9, 2012 SFJ Pharmaceuticals reported that it has entered into a collaborative agreement with Pfizer to conduct a Phase III clinical trial in Asia for Pfizer’s investigational agent axitinib for the adjuvant treatment of patients at high risk of recurrent renal cell carcinoma (RCC) following nephrectomy (Press release Pfizer, JAN 9, 2012, View Source [SID:1234500285]).
Under the terms of ageement, SFJ will provide the funding and clinical development supervision to generate the clinical data necessary to submit axitinib for review by regulatory authorities for the adjuvant treatment of patients at high ris of recurrent RCC following nephrectomy. SFJ will be eligible to recieve milestone payments under the agreement.
In addition, if approved, Pfizer intends to commercialize axitinib for this indication and SFJ will receive earn-out payments under the agreement.

(Company Web Page, Niiki Pharma, JAN 8, 2012, View Source;a=NKP-1339Mechanism&a=NKP-1339ClinicalTrial&a=NKP-1339Companion&a=NKP-1339Projected&a=NKP-1339Commercial&a=NKP-1339Intellectual&a=NKP-1339ScientificPresentations&a=NKP-2235Compound&a=NKP-2235Mechanism&a=NKP-2235ClinicalTrial&a=NKP-2235Companion&a=NKP-2235Projected&a=NKP-2235Commercial&a=NKP-2235Intellectual [SID:1234506957])

GSK Exercises Option to License ChemoCentryx’s CCR1 Inhibitor, CCX354, for theTreatment of Rheumatoid Arthritis

On January 5, 2012 ChemoCentryx, Inc.reported that GlaxoSmithKline (GSK) has exercised its option to obtain an exclusive license for further development and worldwide commercialization of the investigational medicine CCX354, a potent and selective inhibitor of CCR1, a chemokine receptor that drives the recruitment of inflammatory cells into the joints of patients with rheumatoid arthritis (RA) (Press release, ChemoCentryx, JAN 5, 2012, View Source [SID:SID1234515181]). ChemoCentryx recently reported positive results from a Phase II clinical trial with CCX354 which investigated the safety, tolerability, clinical and biological activity of this compound in patients with RA.
Under the terms of the collaboration, ChemoCentryx will receive an option exercise fee of $25 million and will be eligible for further regulatory and sales milestone payments. Subject to successful development and commercialization of CCX354, ChemoCentryx will also receive double-digit royalties on net sales. GSK will now be solely responsible for funding further clinical development and commercialization for CCX354 worldwide.

"This announcement is a key milestone for ChemoCentryx that further validates our ability to advance new medicines from drug discovery through clinical development," said Thomas J. Schall, Ph.D., President and Chief Executive Officer of ChemoCentryx. "Furthermore, the exercise fee associated with this agreement provides additional financial flexibility to our already strong balance sheet. GSK’s continued enthusiasm and interest in our programs expands our relationship and highlights our belief in the tremendous potential of our innovative products. GSK’s global reach and financial commitment will be invaluable to the advancement of CCX354 through the rest of its development."

This transaction represents the second product licensing opportunity resulting from the original collaboration with ChemoCentryx through GSK’s Centre of Excellence for External Drug Discovery (CEEDD). GSK previously exercised its option to license ChemoCentryx’s CCX282-B (Traficet-EN), now designated GSK1605786 (also called GSK’786), a novel, orally active CCR9 inhibitor, for the treatment of inflammatory bowel disease, in January 2010.

About CCX354 and Rheumatoid Arthritis (RA)
CCX354 is a potent and selective antagonist of CCR1, a chemokine receptor that drives the recruitment of certain inflammatory cells including populations of monocytes, macrophages and T cells into the joints of patients with RA. By selectively blocking the CCR1 receptor, CCX354 is designed to reduce the infiltration of inflammatory cells into the joints of RA patients, thus inhibiting the inflammation, swelling, pain and associated joint destruction while minimizing the potential for off-target effects. RA is estimated to affect more than two million people in the U.S. and is a leading cause of morbidity, disability and reduced work ability. The exact cause of RA is unknown, but is believed to reflect the body’s immune system attack on the synovium, the tissue that lines the joints. Despite available treatments, there remains a significant unmet medical need for better therapies for RA.