TO-1187

TO-1187 potently and selectively inhibits HDAC6 in in vitro EMSA assays, while it shows weak inhibitory effects on HDAC3, HDAC8 and HDAC11, with an IC₅₀ of 4.6 nM against HDAC6^[1].
TO-1187 (1 nM-25 μM; 0.5-24 h) potently and selectively degrades HDAC6 in a time- and concentration-dependent manner in MM.1S cells, with a DC₅₀ of 5.81 nM and a maximum degradation rate of 94% after 6 h of treatment. Meanwhile, it does not alter the levels of HDAC3 and HDAC8, and selectively inhibits the catalytic activity of HDAC6^[1].
TO-1187 (up to 25 μM; 72 h) exhibits extremely low antiproliferative activity against MM.1S and Neuro-2A cells^[1].
TO-1187 (0.1-100 nM; 6-7 h) mediates the degradation of HDAC6 in MM.1S cells via a CRBN E3 ligase-dependent and proteasome-dependent mechanism^[1].
Combination treatment with TO-1187 (100 nM; 6 h) and Thalidomide (HY-14658) (0.1, 1, 5 µM) in MM.1S cells shows that the HDAC6 degradation and altered acetylation level of α-tubulin induced by TO-1187 are rescued by Thalidomide in a dose-dependent manner^[1].
TO-1187 (1 nM-10 μM) potently induces dose-dependent degradation of HDAC6 in HeLa cells^[1].

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