CD36-mediated lipid uptake drives steatosis, inflammation, and fibrosis

CD36, a fatty acid transporter, is upregulated across hepatocytes and liver-resident immune and stromal cells in metabolic dysfunction–associated steatohepatitis, enabling adaptation to a lipid-rich hepatic microenvironment. CD36-driven lipid uptake promotes hepatocellular stress, inflammatory macrophage activation, endothelial dysfunction, and fibrogenic signaling, collectively reinforcing a pro-inflammatory and pro-fibrotic state.

PLT012: Reprogramming Lipid-Driven Disease Biology

PLT012 is designed to block CD36-mediated lipid uptake and interrupt a central driver of MASH progression. By limiting pathologic lipid influx into hepatocytes, PLT012 reduces steatosis and hepatocellular stress, helping prevent the cycle of lipotoxic injury that drives liver damage. In parallel, CD36 inhibition suppresses chronic inflammation by reducing endothelial activation and downstream immune cell recruitment into the liver. PLT012 also attenuates pro-fibrotic signaling by reshaping macrophage-driven inflammatory responses, reducing the signals that promote stellate cell activation and collagen deposition. Through this integrated mechanism, PLT012 is designed to address the core pathological drivers of MASH-steatosis, inflammation, and fibrosis—with the goal of slowing or preventing disease progression.