Occupies mortalin-2 (mot-2), a member of the Hsp70 family, at its p53 binding site and enables p53 translocation to the nucleus. Selectively cytotoxic; causes growth arrest of cancer cells in culture. Also inhibits telomerase activity and cross-links F-actin.

＞96%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

MKT077； MKT-077；FJ-776

orange to red powder

DMSO : 41.67 mg/mL (96.46 mM; Need ultrasonic)

HSP70

MKT-077 treatment (0.1-10 ?M) for 48 hours can effectively decrease TT cell viability. MKT-077 treatment results in the accumulation of cells in the G0/G1 phase in a dose-dependent manner, and also increases the sub-G0/G1 phase population in TT cell culture in a dose-dependent manner. MKT-077 also downregulates cellular levels of the proliferation marker, Ki67, and the S-phase transcription factor, E2F-1, in TT and MZ-CRC-1 cells. Moreover, TT cells can uptake and retain MKT-077 at significantly higher levels than MZ-CRC-1 cells. MKT-077 has EC50 values of 1.4±0.2 and 2.2±0.2 μM against MCF7 and MDA-MB-231 breast cancer cells, respectively.

Systemic administration of MKT-077 significantly delayed the growth of TT xenografts in mice throughout the treatment. At the end of the drug treatment, we found that tumor weights were about two-timed less in MKT-077-treated group than in the control group. These data are consistent with the growth inhibitory effects of MKT-077 observed in the in vitro setting above . The succinate-induced, ADP-stimulated respiratory rate in mitochondria isolated from the liver of rats treated with a bolus i.v. injection of 15 mg MKT-077 1kg body weight each day for 5 days is significantly lower than that of untreated controls.