KKL 顾客使用本产品发表的 6 篇科研文献

SM-164 is a cell-permeable Smac mimetic compound. SM-164 binds to XIAP protein containing both the BIR2 and BIR3 domains with an IC₅₀ value of 1.39 nM and functions as an extremely potent antagonist of XIAP.

SM-164 is a non-peptide, cell-permeable, bivalent small-molecule, which mimics Smac protein for targeting XIAP. SM-164 binds to XIAP containing both BIR domains with an IC₅₀ value of 1.39 nM, being 300 and 7000-times more potent than its monovalent counterparts and the natural Smac AVPI peptide, respectively. SM-164 concurrently interacts with both BIR domains in XIAP and functions as an ultra-potent antagonist of XIAP in both cell-free functional and cell-based assays. SM-164 targets cellular XIAP and effectively induces apoptosis at concentrations as low as 1 nM in leukemia cancer cells, while having a minimal toxicity to normal human primary cells at 10,000 nM. The binding affinities of SM-164 to XIAP, cIAP-1, and cIAP-2 proteins are determined using fluorescence-polarization based assays. SM-164 has a K_i value of 0.56 nM to XIAP protein containing both BIR2 and BIR3 domains. SM-164 has a K_i value of 0.31 nM to cIAP-1 protein containing both BIR2 and BIR3 domains. SM-164 binds to cIAP-2 BIR3 protein with K_i values of 1.1 nM. Addition of exogenous TNFα can significantly enhance the activity of these Smac mimetics, especially for SM-164, in resistant cancer cell lines such as HCT116 and MDA-MB-453.

SM-164 is evaluated for its ability to inhibit tumor growth. SM-164 is highly effective in inhibition of tumor growth and capable of achieving tumor regression in the MDA-MB-231 xenograft model. Treatment with SM-164 at 1 mg/kg completely inhibits tumor growth during the treatment. Treatment with SM-164 at 5 mg/kg reduces the tumor volume from 147±54 mm at the beginning of the treatment (day 25) to 54±32 mm at the end of the treatment (day 36), a reduction of 65%. The strong antitumor activity by SM-164 is long lasting and not transient. SM-164 at 5 mg/kg is statistically more effective than Taxotere at the end of the treatment (P<0.01) or when the tumor size in the control group reached 750 mm (P<0.02).

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