TRAP1-IN-2

TRAP1-IN-2 (compound 36) (72 h) inhibits the proliferation of 22Rv1, HeLa and PC3 human cancer cells, with IC₅₀ values of 10.1 μM, 16.4 μM and 23.9 μM, respectively^[1].
TRAP1-IN-2 (24 h) binds to purified human TRAP1 with a K_d value of 0.04 μM, exhibiting over 250-fold selectivity over Grp94^[1].
TRAP1-IN-2 (1-50 μM; 6 h) selectively induces the degradation of the TRAP1 client proteins NDUFS1, glutaminase-1, and Sirt3 in a dose-dependent manner in HeLa and 22Rv1 cells, without altering the levels of cytosolic Hsp90 client proteins or inducing Hsp70 expression^[1].
TRAP1-IN-2 (5-50 μM; 6 h) significantly inhibits oxidative phosphorylation (OXPHOS) in HeLa and 22Rv1 cells in a dose-dependent manner, including basal respiration, proton leak, maximal respiration, non-mitochondrial O₂ consumption, and spare respiratory capacity^[1].
TRAP1-IN-2 (5-50 μM; 6 h) disrupts the mitochondrial membrane potential in HeLa cells, as evidenced by a dose-dependent reduction in TMRM fluorescence^[1].
TRAP1-IN-2 (5-50 μM; 6 h) alters the cellular metabolism of HeLa cells by reducing mitochondrial ATP production and increasing glycolytic ATP production in a dose-dependent manner^[1].

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