Thalidomide

E3 Ligase ,TNF-alpha

258.23

DMSO : 6.5 mg/mL (25 mM)

白色结晶性粉末

Thalidomide must be metabolized by the liver to form an epoxide that may be the active teratogenic metabolite. Thalidomide selectively inhibits the production of human monocyte tumor necrosis factor alpha (TNF-alpha) when human monocytes are triggered with lipopolysaccharide and other agonists in culture. Thalidomide exerts its inhibitory action on tumor necrosis factor alpha by enhancing mRNA degradation. Thalidomide acts directly, by inducing apoptosis or G1 growth arrest, in MM cell lines and in patient MM cells that are resistant to melphalan, doxorubicin, and dexamethasone (Dex). Thalidomide enhances the anti-MM activity of Dex and, conversely, are inhibited by interleukin 6. Thalidomide is a potent costimulator of primary human T cells in vitro, synergizing with stimulation via the T cell receptor complex to increase interleukin 2-mediated T cell proliferation and interferon gamma production. Thalidomide also increases the primary CD8+ cytotoxic T cell response induced by allogeneic dendritic cells in the absence of CD4+ T cells.

Thalidomide (200 mg/kg) results in an inhibition of the area of vascularized cornea of rabbits that ranged from 30% to 51% in three experiments with a median inhibition of 36%.

沙利度胺；酞胺哌啶酮

C₁₃H₁₀N₂O₄

50-35-1