DBt-10

DBt-10 (0.625-10 μM; 6 h) also reduces BTK in a concentration-dependent manner and induces significant degradation at 2.5 μM^[1].
DBt-10 (1 μM; 1-24 h) reduces endogenous BTK protein in TMD8 cells, with obvious degradation occurring at approximately 6 h^[1].
DBt-10 (5 µM; 6 h) selectively degrades BTK in TMD8 cells, and global proteomic analysis detects that it only causes extremely mild off-target downregulation of LIMK1^[1].
The TR-FRET IC₅₀ of DBt-10 binding to DCAF1 is 0.136 μM, and the IC₅₀ decreases to 0.082 μM after the addition of BTK^[1].
The SPR K_D of the DBt-10/DCAF1 binary complex is 0.147 μM with a complex half-life of 175 s, whereas the apparent K_D of the DCAF1/DBt-10/BTK ternary complex is 0.033 μM with a half-life of 429 s^[1].
DBt-10 (24 h) degrades BTK-GFP in TMD8 BTK-GFP/mCherry cells, with a DC₅₀ of 0.137 μM and a maximum BTK reduction level of 94%. Its cell viability GI₅₀ is >25 μM, and the GI₅₀/DC₅₀ ratio is >182.6^[1].
DBt-10 (1 µM; 24 h) effectively degrades BTK and inhibits the proliferation of CRBN-resistant TMD8 cells, thereby overcoming acquired resistance to CRBN-based BTK PROTACs^[1].

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