Gomisin M2

Gomisin M2 ((+)-Gomisin M2) is a lignan isolated from the fruits of Schisandra chinensis with oral availability. Gomisin M2 inhibits STAT1 phosphorylation as well as NF-κB p65 phosphorylation and nuclear translocation. Gomisin M2 reduces inflammatory cell infiltration, cytokine and chemokine expression, and serum IgE and IgG_2a levels. Gomisin M2 inhibits MAPK phosphorylation, IκBα degradation, and NF-κB nuclear translocation in keratinocytes. Gomisin M2 induces apoptosis, mitochondrial membrane potential disruption, and cytochrome c release, and inhibits DNA synthesis and mammosphere formation through downregulation of Wnt/β-catenin. Gomisin M2 can be used for research on atopic dermatitis, psoriasis, breast cancer, liver injury, and multidrug-resistant mammary adenocarcinoma^{[1][2][3][4][5][6]}. In Vitro:Gomisin M2 (GM2) (0.1-10 μM; 1 h) inhibits the expression of inflammatory cytokines and chemokines in TNF-α/IFN-γ-stimulated HaCaT cells through the suppression of STAT1 phosphorylation and the nuclear translocation of NF-κB^[1].
Gomisin M2 (GM2) (0.1-10 µM; 1 h) reduces the secretion of CCL17 and IL-6 in TNF-α- and IFN-γ-stimulated HaCaT keratinocytes^[2].
Gomisin M2 (0.1-10 µM; 1 h) decreases inflammatory gene expression in TNF-α- and IFN-γ-stimulated HaCaT keratinocytes^[2].
Gomisin M2 (10 µM; 1 h) inhibits STAT1 phosphorylation and NF-κB translocation in TNF-α- and IFN-γ-activated HaCaT keratinocytes^[2].
Gomisin M2 (0.1-10 μM) possesses anti-inflammatory effects on TNF-α and IFN-γ stimulated HaCaT keratinocytes by alleviating PS-associated cytokines and inhibiting mitogen-activated protein kinase phosphorylation^[3].
Gomisin M2 (48 h) inhibits MDA-MB-231 and HCC1806 cell viability with IC₅₀ values of 60 and 57 μM respectively, and shows low cytotoxic activity against MCF10A non-cancer cells in vitro^[4].
Gomisin M2 (100 μM; 9 days) decreases the size of 3D spheroids formed by MDA-MB-231 and HCC1806 cells over 9 days in culture^[4].
Gomisin M2 (5-40 μM; 48 h) dose-dependently increases cytosolic cytochrome c release in MDA-MB-231 and HCC1806 cells after 48 h of treatment^[4].
Gomisin M₂ (20-80 μM; 48 h) inhibits DNA synthesis and cell proliferation in MDA-MB-231 and HCC1806 cells^[4].
Gomisin M2 (5-40 μM; 1-3 days) downregulates the Wnt/β-catenin self-renewal pathway in MDA-MB-231 and HCC1806 cells by decreasing CyclinD1, β-catenin, and p-GSK3β, and increasing p-β-catenin and GSK3-β in a dose- and time-dependent manner^[4].
Gomisin M2 (40 μM; 48 h) induces mitochondrial-initiated apoptotic events in MDA-MB-231 and HCC1806 tumor spheres, characterized by increased cell permeability and cytochrome c release, decreased mitochondrial membrane potential, and reduced nuclear intensity^[4].
Gomisin M2 (20-80 μM; 48 h) induces apoptosis in MDA-MB-231 and HCC1806 cells in a dose-dependent manner^[4].
Gomisin M2 (10-60 μM; 48 h) induces cleavage of caspase-3 and PARP in MDA-MB-231 and HCC1806 cells in a dose-dependent manner^[4].
Gomisin M2 (compound 5) (10 µM; 1 h) exhibits moderate hepatoprotective activity against APAP-induced damage in HepG2 cells, resulting in a 43.5% survival rate at 10 µM^[5]. In Vivo:Gomisin M2 (0.1-10 mg/kg; p.o.; five consecutive days per week; two weeks) ameliorates DNCB/DFE-induced atopic dermatitis-like skin lesions in BALB/c mice by inhibiting STAT1 and NF-κB activation and reducing inflammatory mediators and immunoglobulin levels^[1].
Gomisin M2 (0.1-10 mg/kg; p.o.; daily; 7 consecutive days) dose-dependently alleviates IMQ-induced psoriasis-like skin inflammation by reducing skin thickness, PASI scores, TEWL, inflammatory gene expression, serum inflammatory proteins, and Th1/Th17 cell populations^[2].
Gomisin M2 (0.1-10 mg/kg; p.o.) possesses anti-inflammatory effects on psoriasis-like skin inflammation, reducing symptoms and Th1/Th17-related cytokine production in a dose-dependent manner^[3].
Gomisin M2 (10 μM; water exposure; single treatment) effectively suppresses the growth and proliferation of CSC-enriched breast cancer cells in a zebrafish xenograft model, demonstrating in vivo anti-BCSC activity at a concentration two-fold lower than that required to suppress tumor sphere formation in vitro^[4].