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April 14, 2016

Bristol-Myers Squibb to add new space to advance immuno-oncology research

Bristol-Myers Squibb will add a new laboratory and office space at BioMed Realty's Woodside Technology Park life science campus in Redwood City, California, for research and development in the field of immuno-oncology.

Bristol-Myers Squibb will add a new laboratory and office space at BioMed Realty’s Woodside Technology Park life science campus in Redwood City, California, for research and development in the field of immuno-oncology.

Both the companies have signed a new lease agreement to this effect.

The 62,000ft2 expansion adds a third building to Bristol-Myers’ existing 194,000ft2 space at BioMed’s campus.

The new facility will be involved in the discovery of cancer therapies, including novel biologics therapeutics.

"We are thrilled to be able to provide cutting-edge spaces for the important cancer research conducted by Bristol-Myers Squibb."

BioMed Realty vice-president Scott Altick said: "We are thrilled to be able to provide cutting-edge spaces for the important cancer research conducted by Bristol-Myers Squibb.

"They are a global leader in the life science community known for scientific breadth and excellence and we look forward to supporting their science in the Bay Area for many years to come."

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As per the agreed terms, the leases for all the three buildings totalling 256,000ft2 extend through March 2027.

Bristol-Myers Squibb oncology biology discovery head Nils Lonberg said: "The expansion of our facilities in Redwood City is evidence of the value that Bristol-Myers Squibb sees in the Bay Area scientific community and our relationship with BioMed Realty."

Additionally, the US Food and Drug Administration (FDA) has granted priority review status to supplemental biologics license application (sBLA) submitted by Bristol-Myers Squibb for its Opdivo (nivolumab), as a treatment in classical hodgkin lymphoma.

Opdivo is a PD-1 immune checkpoint inhibitor that binds to the checkpoint receptor PD-1 expressed on activated T-cells, and blocks the binding of PD-L1 and PD-L2.

It prevents the PD-1 pathway’s suppressive signalling on the immune system, including the interference with an anti-tumour immune response.

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