acetyl-coa carboxylase 1 (acc1)

CIL56 (CA3) is a small molecule that induces cellular ferroptosis through the production of iron-dependent reactive oxygen species (ROS). It also induces accumulation of long-chain saturated, monounsaturated, and polyunsaturated fatty acids in HT-1080 cells in vitro.HT-1080 cells lacking acetyl-CoA carboxylase 1 (ACC1), the rate-limiting enzyme in fatty acid synthesis, exhibit 5-fold resistance to CIL56 treatment, indicating ACC1 activity sensitizes cells to CIL56-induced cell death.

CMS-121, a quinolone derivative, is an orally active acetyl-CoA carboxylase 1 (ACC1) inhibitor. CMS-121 protects HT22 cells against ischemia and oxidative damage (EC50: 7 nM and 200 nM). CMS-121 shows strong neuroprotective, antioxidative, anti-inflammatory, and renoprotective activities.

PF 05175157 is an inhibitor of acetyl-CoA carboxylase 1 (ACC1) and ACC2 (IC50s = 27, 33, 23.5, and 50.4 nM for human ACC1, human ACC2, rat ACC1, and rat ACC2, respectively

Soraphen A ((-)-Soraphen A; Soraphen A1α), a polyketide fungal inhibitor, actively targets acetyl-CoA carboxylase (ACC1) in vivo. It can be isolated from Myxobacter cellulosum [1].