SMTIN-P01

SMTIN-P01 (1-6 μM; 30 min preincubation, 3 h ATP incubation) inhibits the ATPase activity of purified recombinant human TRAP1 in a concentration-dependent manner, with greater activity than gamitrinib^[1].
SMTIN-P01 (10 μM; 30 min at 37 °C) induces mitochondrial membrane depolarization in human cervical cancer HeLa cells, indicating disruption of mitochondrial function^[1].
SMTIN-P01 (2 μM; 24 h at 37 °C) does not induce canonical Hsp90 inhibition responses (Hsp70 upregulation, client protein depletion) in human 22Rv1, HeLa, or H460 cancer cells, indicating a mitochondria-specific mode of action distinct from non-targeted Hsp90 inhibitors^[1].
SMTIN-P01 (5-20 μM; 24 h at 37 °C) potently reduces viability of multiple human cancer cell lines (ACHN, HeLa, SK-OV3, 22Rv1, SK-HEP-1, A172, H460, MDA-MB-231) in a concentration-dependent manner, with greater cytotoxicity than PU-H71 and improved activity over gamitrinib in several cancer cell lines, while showing minimal toxicity to normal human corneal cells^[1].
SMTIN-P01 is a mitochondria-targeted TRAP1 inhibitor that binds the TRAP1 N-terminal domain ATP binding site, induces TRAP1 client protein degradation in cancer cells, and does not elicit Hsp90-related off-target effects or heat shock responses^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.