THNAN69

THNAN69 (compound 22b) (20 h protein expression, 2 h equilibration) potently engages with LIMK2 in intact and permeabilized HEK293T cells with an IC₅₀ of 80 nM, demonstrating good cell permeability^[1].
THNAN69 (100 nM-1 μM; 6 h) induces isoform-specific degradation of endogenous LIMK2 in HuCCT1 cells, achieving near-complete depletion at 10 nM, while leaving LIMK1 and phosphorylated cofilin levels unchanged^[1].
THNAN69 (0.01 nM-10000 nM; 72 h monitoring period) potently degrades ectopically expressed EGFP-LIMK2 in live HuCCT1 cells with a DC₅₀ of 1 nM, reaching up to 98.5% maximum degradation at 1000 nM within 60 h^[1].
THNAN69 (10 nM-1000 nM; 72 h monitoring period) mediated LIMK2 degradation in HuCCT1 cells is dependent on CRL activity via CRBN, as degradation is completely blocked by cotreatment with MLN4924^[1].
THNAN69 (500 nM; 6 h) shows proteome-wide isoform selectivity for LIMK2 degradation in HuCCT1 cells, with only transient, warhead-related off-target effects on CYBA and DGUOK^[1].
THNAN69 (20 h protein expression, 20 h ligand labeling, 4 h MG132 incubation, 3 h incubation) forms stronger ternary complexes with LIMK2 and CRBN in HEK293T cells (TC₅₀ = 77 nM) compared to LIMK1 and CRBN (TC₅₀ = 300 nM), contributing to isoform-specific degradation^[1].
THNAN69 (10 μM; 60 min) exhibits high metabolic stability in rat liver microsomes, with 85% of the parent compound remaining after 60 min of incubation^[1].
THNAN69 (24 h) has no cytotoxic effects on HEK293T cells^[1].

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