BMS-986020 sodium (AM152 sodium) is a high-affinity LPA1 (Lysophosphatidic Acid Receptor 1) antagonist for investigating idiopathic pulmonary fibrosis, slowing the rate of decline in forced vital capacity (FVC) and pulmonary function. BMS-986020 inhibits bile acid and phospholipid transporters (BSEP, MRP4, MDR3), altering bile homeostasis.

BSEP:4.8 μM, MDR3:7.5 μM, MRP4:6.2 μM

BMS-986020 sodium can inhibit the efflux transporters of bile acids in the liver, including BSEP (half-maximal inhibitory concentration IC₅₀ of 1.8μM), MRP3 (IC₅₀ of 22μM), and MRP4 (IC₅₀ of 6.2μM). At a concentration of 10μM, it suppresses the canalicular efflux of bile acids in Homo sapiens hepatocytes (inhibition rate of 68%). When the concentration reaches ≥10μM, BMS-986020 sodium impairs mitochondrial function in both Homo sapiens hepatocytes and cholangiocytes, including basal respiration, maximal respiration, adenosine triphosphate (ATP) production, and reserve capacity. Additionally, it inhibits phospholipid efflux in Homo sapiens hepatocytes (IC₅₀ for MDR3 is 7.5μM)[1].

BMS-986020 sodium (0.5, 2, 5, and 10 mg/kg, administered via gavage immediately or 3 hours after reperfusion) significantly reduced the cerebral infarction volume and neurological deficit scores induced by transient middle cerebral artery occlusion (tMCAO) in mice, with the most pronounced effects observed at doses of 5 and 10 mg/kg. Moreover, administration 3 hours after reperfusion provided equivalent protective efficacy[2].