Elevated lipid metabolism in certain cancers such as in prostate cancer, and is required both for carcinogenesis and cancer cell survival. Cancer cells divide much more rapidly than healthy cells. To support this relentless proliferation, cancer cells must alter their metabolism to make large amounts of building blocks, such as fat molecules that form plasma membranes and other important structures. So lipid metabolism and biosynthetic activities is often up-regulated. A research team led by the Salk Institute has developed a method to target lipid synthesis in cancer cells, and therefore block cancer growth. The method, described in Nature Medicine, represents a new weapon to fight cancer. Since a cancer cell is more dependent on lipid synthesis compared to a healthy cell, medications that impair this metabolic process could have therapeutic effect on cancer, according to Reuben Shaw, professor at the Salk Institute and corresponding author of the study. This study was carried out in collaboration with academic and industry scientists. Using computational chemistry method, the research team found a molecule that inhibits Acetyl-CoA Carboxylase (ACC), an enzyme crucial for lipid synthesis. Trials on laboratory animals showed that the new ACC inhibitor, called ND-646, significantly reduced tumor mass. Moreover, ND-646 plus carboplatin was more effective in suppressing tumors than carboplatin alone. Carboplatin is a chemotherapy drug used to treat various types of cancer. By the way, CusAb offers proteins such as ACC and Recombinant HTR2C. The data showed that ACC mediates a metabolic liability of cancer and that ACC inhibition by ND-646 is detrimental to cancer growth. Prof. Shaw said that their study was the first to demonstrate that ACC is critical for tumor growth.