Arvinas has been on a roll this year, starting with a Pfizer R&D deal worth potentially $830 million and bagging a $55 million series C in April to push its cancer drugs into the clinic. Now, the Yale spinout has filed to raise up to $100 million in its IPO, which will get its lead assets through the IND stage and into phase 1.
The New Haven, Connecticut-based biotech is working on an androgen receptor program, ARV-110, in castration-resistant prostate cancer, and an estrogen receptor program, ARV-471, in metastatic ER-positive breast cancer. The bulk of the IPO funds is earmarked to carry these assets into the clinic; what’s left will go toward expanding its protein degradation platform and conducting preclinical work for its earlier-stage programs, Arvinas said in its S-1, filed Thursday.
Arvinas drew its series C round from the likes of Deerfield, Sirona Capital, Canaan Partners and OrbiMed, saying at the time that it aimed to start clinical studies in the fourth quarter.
Arvinas’ drugs are based on its PROTACs (proteolysis targeting chimeras) platform, which grew out of the work of Craig Crews’ lab at Yale University. PROTACs work by activating the body’s protein disposal system. They recruit an enzyme to tag target proteins for ubiquitination and degradation.
Ubiquitination is a process whereby a damaged or unneeded protein is tagged with the protein ubiquitin and then sent to a protein complex called a proteasome, where it is degraded. The hope is that by degrading proteins instead of just blocking them, Arvinas’ drugs will surmount challenges that come with small-molecule protein inhibitors.
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The company’s pipeline focuses on cancer, but its multiyear deal with Pfizer centers on developing PROTACs for multiple disease areas. The pair didn’t disclose which indications they would be chasing, but protein degradation could have applications in central nervous system disorders and rare diseases.
Arvinas isn’t alone in the growing protein degradation field. Its Fierce 15 peer, C4 Therapeutics, is using small-molecule binders called degronimids that can target, destroy and clear proteins through the ubiquitin/proteasome system. And Cedilla Therapeutics, which launched in April, is studying protein stability in search of points in the protein degradation process it can intervene.
"Where we are looking is in pivotal events upstream of this machinery that govern the transition [of proteins] between an operational state to a susceptible state,” said Cedilla’s Chief Scientific Officer Brian Jones at the company’s launch.