Bristol-Myers hands over $100M in cash for a new fibrosis drug, beefing up NASH focus
It’s not all checkpoints all the time at Bristol-Myers Squibb. The big biotech has been ramping up an ambitious effort in fibrosis and NASH and this morning it’s taking the wraps off another deal in the field, paying $100 million to Japan’s Nitto Denko for an early-stage drug candidate that now becomes part of their portfolio.
The key drug in this package deal is ND-L02-s0201, a siRNA that is designed to inhibit heat shock protein 47. By hitting HSP47, their investigators believe that they can cut the production of collagen that plays a role in fibrosis and NASH, while helping correct at least some of the damage that has already been done to patients.
The drug is undergoing a 5-week Phase Ib study now to give them a better idea of how the drug works for fibrosis caused by NASH, an epidemic fatty liver disease, and hepatitis C. And Bristol-Myers gets the rights to Nitto Denko’s portfolio in the field, bagging exclusive rights for fibrosis in a variety of diseases.
The deal includes milestones, which weren’t discussed in their statement.
Nitto Denko is a century-old diversified materials manufacturer based in Osaka with a newfound interest in diversifying into biotech. Early this year the company established a biotech subsidiary called Nitto BioPharma, with facilities in San Diego and plans to continue to pursue R&D in IPF and other diseases.
Bristol-Myers execs have been putting a brave face on their recent debacle in frontline non-small cell lung cancer for their PD-1 pioneer Opdivo. The late-stage failure left a bad scar, but the company points to its R&D work in fibrosis/NASH and heart failure as examples of a more diversified pipeline.
Back in August, 2015, the ambitious R&D group struck a $1.25 billion deal — $150 million up front — to gain an option to acquire Promedior if its mid-stage fibrosis program comes through.
Bristol-Myers has its sights set on PRM-151, a recombinant form of human pentraxin-2 protein in development for idiopathic pulmonary fibrosis and myelofibrosis. The company scored another provisional buyout agreement for Denmark’s Galecto in 2014, agreeing to pay up to $444 million for the company. That deal centered on TD139, an inhibitor of galectin-3, which binds to carbohydrate structures, playing a role in IPF that can be derailed by this new drug. TD139 joined BMS-986020, a lysophosphatidic acid 1 (LPA1) receptor antagonist also in studies for fibrosis. Bristol-Myers also struck research deals with the California Institute for Biomedical Research (Calibr) and The Medical University of South Carolina.