Start-up C4 Therapeutics of Cambridge, Massachusetts, in January raised $73 million in series A funding to develop therapeutics that target disease-causing proteins and facilitate their degradation through the ubiquitin/proteasome system. C4 was founded by a group from Boston's Dana-Farber Cancer Institute, including Jay Bradner, whose laboratory invented C4's targeted protein degradation (TPD) platform, which links drug-like small molecules to the cellular ubiquitin/proteasome system to eliminate designated proteins by tagging them with ubiquitin for destruction by the proteasome. Announcement of the funding coincided with news that C4 has entered into a strategic collaboration with the Basel-based pharma Roche to identify TPD drugs against a set of prespecified protein targets. Celgene, in Summit, New Jersey, has also inked proteasome-oriented collaborations with startups, including San Francisco's Nurix and Forma Therapeutics in Watertown, Massachusetts. Cleave Biosciences in Burlingame, California is currently in a phase 1 trial for myeloma with CB-5083, an inhibitor of p97, a AAA ATPase that regulates the ubiquitin/proteasome system. Proteasome inhibition is a core strategy in treating multiple myeloma: sales of the leading myeloma drug, Celgene's proteasome inhibitor Revlimid (lenalidomide), are projected to rise above $6 billion in 2016. In November, the US Food and Drug Administration approved Ninlaro, a proteasome inhibitor directed at the subunit beta type-5, from Takeda Pharma in Osaka, Japan (p. 126).