Gomisin D

Gomisin D is an orally active lignan that binds to PDGFRβ with a K_d of 10 μM. By targeting PDGFRβ to regulate signaling pathways, Gomisin D inhibits the activation and proliferation of hepatic stellate cells and promotes their apoptosis, thereby ameliorating hepatic fibrosis. Gomisin D exhibits multiple activities such as photoprotection, antimelanogenesis, antioxidant effects, and hypoglycemic activity. Gomisin D can be used in studies related to diabetes, Alzheimer's disease, and hepatic fibrosis^[1][2][3]. IC50 & Target:UDP-Glucuronosyltransferases^[1] In Vitro:Gomisin D (10-80 μM; 25 h) enhances the viability and reduces the cytotoxicity of HaCaT keratinocytes irradiated with UVA and UVB, and inhibits intracellular ROS generation^[1].
Gomisin D (30 μM; 25 h) significantly inhibits apoptosis of UVA- and UVB-irradiated HaCaT keratinocytes^[1].
Gomisin D (10-80 μM; 49 h) dose-dependently inhibits α-MSH-induced tyrosinase activity^[1].
Gomisin D (30 μM; 49 h) significantly downregulates the mRNA and protein expression of α-MSH-induced melanogenesis-related factors MITF, tyrosinase, TRP-1 and TRP-2, as well as the phosphorylation of PKA and CREB, in B16F10 melanocytes^[1].
Gomisin D (20-80 μM; 48 h) inhibits the activation of T6, LX-2 and primary mouse hepatic stellate cells by targeting PDGFRβ^[3].
Gomisin D (40 μM) inhibits the downstream signaling pathways (p38, AKT, ERK pathways) of PDGFRβ in HSC-T6 cells by targeting PDGFRβ^[3].
Gomisin D (5-80 μM) dose-dependently inhibits PDGF-BB-induced activation, proliferation, and PDGF-BB/PDGFRβ pathway signaling in LX-2 cells^[3]. In Vivo:Gomisin D (25-50 mg/kg; i.g.; 4 weeks) alleviates CCl₄-induced hepatic fibrosis in male BALB/c mice^[3].
Gomisin D (50 mg/kg; p.o.; 30 days) causes no observable histotoxicity in male BALB/c mice^[3].