TH-407a

TH-407a potently inhibits the enzymatic activity of purified USP15 protein with an IC₅₀ of 0.76 μM via Ub-AMC hydrolysis inhibition^[1].
TH-407a (0.31-20 μM; 30 min) dose-dependently inhibits recombinant USP15-mediated hydrolysis of K48-linked diubiquitin^[1].
TH-407a inhibits the interaction between USP15 protein and the covalent-binding ubiquitin analog Ub-PA in vitro^[1].
TH-407a is selective for USP15, showing negligible inhibition of purified USP1, USP2, and USP7 proteins at 10 μM^[1].
TH-407a (10× IC₅₀; 30, 60, or 90 min) reversibly inhibits purified USP15 protein, with time-dependent recovery of enzymatic activity after dilution^[1].
TH-407a (1.5625-12.5 μM) directly binds to immobilized USP15 protein with strong affinity, as demonstrated by a K_d of 4.26 μM via SPR^[1].
TH-407a dose-dependently inhibits the proliferation of MCF-7, HCC70, MDA-MB-231, and MDA-MB-436 breast cancer cells, with IC₅₀ values of 19.57 μM for MCF-7 and 38.66 μM for MDA-MB-436^[1].
TH-407a (5-10 μM) inhibits clonal growth of MCF-7, HCC70, MDA-MB-231, and MDA-MB-436 breast cancer cells^[1].
TH-407a (10 μM (HCC70, MDA-MB-231); 20 μM (MCF-7, MDA-MB-436); 12 or 24 h) impairs the migratory capacity of MCF-7, HCC70, MDA-MB-231, and MDA-MB-436 breast cancer cells^[1].
TH-407a (5-40 μM (immunoblotting); 20 μM (MDM2 ubiquitination assessment)) modulates the p53 signaling pathway in MCF-7 breast cancer cells by downregulating MDM2, stabilizing p53, and increasing MDM2 ubiquitination^[1].
TH-407a (5-40 μM (immunoblotting); 10 μM (CHX stability assay); 4 or 12 h (pre-treatment); 0-12 h (monitoring)) reduces PARP1 protein stability and expression in MCF-7, HCC70, MDA-MB-231, and MDA-MB-436 breast cancer cells by increasing PARP1 ubiquitination and accelerating its degradation^[1].

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