BCPyr

BCPyr (0.015-2.0 μM; 24 h) induces dose-dependent degradation of BTK in THP-1 cells with a DC₅₀ of 800 nM^[1].
BCPyr (0.4-1.0 μM; 150-200 s association, 300 s dissociation) binds directly to purified BTK^KD with a binary K_d of 692 nM^[1].
BCPyr (1 μM; 60 s binary complex formation) mediates formation of a ternary complex between cIAP1^BIRC[1] and BTK^KD with a ternary K_d of 262 nM and modest positive cooperativity (α = 2.6)^[1].
BCPyr mediates formation of a strongly cooperative ternary complex between cIAP1^BIR3 and BTK^KD with a ternary K_d of 23 nM and α = 30^[1].
BCPyr (0.313-2.5 μM; 15 min) promotes dose-dependent in vitro ubiquitination of BTK^KD by cIAP1^BUCR[1], with reduced potency relative to BC5P^[1].
BCPyr forms a more rigid ternary complex with cIAP1^BIR3 and BTK_KD, as evidenced by substantial global broadening of [¹⁵N,¹H]-HSQC NMR signals relative to the cIAP1^BIR3-BCPyr binary complex^[1].
BCPyr (180 μM; 30 min on ice) forms a stable, rigid ternary complex with cIAP1^BIR3 and BTK^KD, characterized by extensive protein-protein interactions and distinct from BC5P-mediated ternary complex poses, as visualized in a 2.2-Å resolution X-ray crystal structure^[1].
BCPyr promotes formation of a cIAP1^BURC dimer and subsequent dimerization of cIAP1^BURC-BCPyr-BTK^KD ternary complexes in vitro, as detected by SEC-MALS^[1].

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