Drug development relies on a few key principles, with one being that, to work, medicines must interact with the right molecules in the body.
But that requirement is difficult to meet. The helpful ingredients in most pharmaceuticals are microscopic. So, too, are their targets. In the relatively enormous spaces that are tissues or the blood, it’s rarely guaranteed the pieces needed for a therapeutic reaction will come together.
As such, there’s a growing pocket of research focused on designing drugs to overcome this challenge. Vicinitas Therapeutics, a biotechnology company that launched Thursday, is built around this type of research.
Vicinitas wants to stop cells from breaking down beneficial proteins by removing a molecular tag called an ubiquitin chain, which tells them to do just that. Vicinitas has a technology it claims can recruit a special enzyme to remove the tag, thereby stabilizing the protein.
Protein degradation research has “become incredibly hot in biotech and pharma in recent years,” said Daniel Nomura, a professor of chemical biology at the University of California, Berkeley, and the founder of Vicinitas. Conversely, Nomura argues there hasn’t been as much attention on technologies meant to safeguard or restore proteins.
“There are tons and tons of proteins and diseases where the pathology of the disease is driven by aberrantly degraded proteins, where the protein is lost from the cell,” he said. “And if you can stabilize the levels of those proteins and restore their function, then that would enable disease treatment.”
Vicinitas is a byproduct of a partnership that began in 2017 between University of California, Berkeley and the Novartis Institutes for BioMedical Research, with the goal of tackling “undruggable” proteins. In February, the company’s technology was featured in the journal Nature Chemical Biology, in an article detailing how researchers had discovered a recruiter molecule that, when linked to a drug developed by Vertex Pharmaceuticals, was able to stabilize — among other kinds of proteins — the mutated one that causes cystic fibrosis.
Nomura said that soon after the publication, there was “tremendous venture capital interest” to invest in a company with this protein-stabilizing technology.
Vicinitas has since raised $65 million in a Series A funding round co-led by the venture firm a16z and the crossover firm Deerfield Management. Also participating in the round were Droia Ventures, The Mark Foundation for Cancer Research, the Berkeley Catalyst Fund and Alphabet’s venture arm, GV.
Nomura expects the new funds will keep Vicinitas running long enough to hit “value inflection points,” when the company will be able to build a “robust” slate of drug programs and expand its technology platform.
He added that Vicinitas is “always looking” for business development deals. “I think that there are plenty of strategic partnerships that could potentially be made,” Nomura said, “and we're certainly interested in figuring out what interest there might be.”
Initially, Vicinitas will focus on developing therapies for cancer, as well as genetic disorders tied to changes in a single gene. Cystic fibrosis, for example, is a disease the company is “definitely pursuing” following the recent study results published in Nature, Nomura said.
Another area of interest, according to Nomura, is “haploinsufficiency diseases,” which arise when there’s only one working copy of a gene, leading to inadequate production of a necessary protein.
Vicinitas isn’t yet disclosing how many programs it’s working on or when the most advanced of them could enter human testing.
Nomura will be part of the Vicinitas leadership team and hold a seat on the company’s board. Joining him there are Jorge Conde, a general partner at a16z, Cameron Wheeler, a partner at Deerfield, and George Golumbeski, a partner at Droia Ventures who’s well known in the biotech industry for his time at Celgene, where he led dealmaking activities for nearly a decade before the company’s eventual $74 billion sale to Bristol Myers Squibb.