Ubenimex competitively inhibits many aminopeptidases, including B, N and leucine aminopeptidases. Ubenimex is a microbial metabolite and dipeptide with potential immunomodulatory and antitumor activities. Aminopeptidases has been implicated in the process of cell adhesion and invasion of tumor cells. Therefore, inhibiting aminopeptidases may partially attribute to the antitumor effect of ubenimex. This agent also activates T lymphocyte, macrophage, and bone marrow stem cell as well as stimulates the release of interleukin-1 and -2, thus further enhances its antitumor activity.
Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.
DMSO : 6 mg/mL (19.46 mM; Need warming)
1eq. NaOH : 15.4 mg/mL (50 mM)
Bestatin inhibits proliferation of all the human leukemic cell lines except KG1. Bestatin induces DNA fragmentation quantitatively and DNA ladder and enhances caspase-3 activity in U937 cells. Bestatin dose-dependently induces DNA fragmentation in human leukemic cell lines. Bestatin dose-dependently inhibits the invasion of SN12M cells into reconstituted basement membrane (Matrigel). Bestatin inhibits the degradation of type IV collagen by tumor cells, but not by tumor-conditioned medium (TCM), in a concentration-dependent manner. Bestatin inhibits hydrolysing activities towards substrates of aminopeptidases in SN12M cells. Bestatin inhibits the tube-like formation of human umbilical vein endothelial cells (HUVECs) in vitro. Bestatin exerts a direct stimulating effect on lymphocytes (and monocytes) via its fixation on cell surface leucine-aminopeptidase, and an indirect effect on monocytes (and lymphocytes) via aminopeptidase B inhibition of tuftsin catabolism.
Bestatin significantly inhibits the melanoma cell-induced angiogenesis in a mouse dorsal air sac assay. Bestatin reduces the number of vessels oriented towards the established primary tumor mass on the dorsal side of mice implantated of B16-BL6 melanoma cells. Bestatin statistically significantly inhibits leukotriene B4 biosynthesis in the esophageal tissues of EGDA rats and reduces the incidence of EAC in the EGDA rats from 57.7% (15 of 26 rats) to 26.1% (6 of 23 rats).
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