Targeting tumor cells' fat synthesis, combined with cancer drug, cuts tumors by 87%

Salk Institute researchers and collaborators develop novel cancer treatment that halts fat synthesis in cells. Placebo-treated cells (left) have far more lipid (red) production compared with ND-646 treated cells (right).--Courtesy of Salk Institute

A group of researchers from the Salk Institute, joined by scientists from academic and industry collaborators, has demonstrated that an acetyl-CoA carboxylase, or ACC, inhibitor can shrink tumors when delivered to lung cancer cells. The inhibitor targets fat synthesis, essentially cutting off one of the tumor’s sources of growth.

Funded by the National Institutes of Health and the Department of Defense, among others, and using the ACC inhibitor program picked up by Gilead ($GILD) earlier this year, the team set out to test the hypothesis that interrupting a tumor’s lipid creation process could cause it to stop growing.

The team, led by Salk’s Reuben Shaw and working with Boston’s Nimbus Therapeutics, which originally developed the ACC inhibitor (called ND-646), tested human lung cancer cells in animals, showing that the tumor mass shrank by about two-thirds. And combined with the cancer treatment carboplatin, 87% of the tumors were suppressed.

It was this combination that performed the task of both killing tumor cells and halting their fat synthesis. The results, published in the journal Nature Medicine this week, also showed that dosing was well-tolerated.

“This is the first time anyone has shown that this enzyme, ACC, is required for the growth of tumors and this represents compelling data validating the concept of being able to target fat synthesis as a novel anticancer approach,” Shaw said. “The implications are that we have a very promising drug for clinical trials for subtypes of lung cancer as well as liver and other types of cancer. This represents a new weapon in the arsenal to fight cancer.”