NCATS-SM0225

NCATS-SM0225 (0-12800 nM; 30 min) directly binds to recombinant human VDAC1 with a K_d of 3.13 μM.
NCATS-SM0225 (2 μM; 1 h) engages with all three VDAC1, VDAC2, VDAC3 in HeLa cells, as evidenced by enhanced thermal stability of the VDAC proteins^[1].
NCATS-SM0225 (100-400 nM) modulates VDAC1 channel function by promoting voltage-dependent closure at lower negative potentials, with a functional IC₅₀ of 140 nM^[1].
NCATS-SM0225 (0.625-5 μM; 6 h) potently inhibits ER dislocation in HeLa cells with an IC₅₀ of 1.02 μM, as measured by the NHK-drGFP reporter assay^[1].
NCATS-SM0225 (0.625-5 μM; 6-22 h) elevates calcium levels in mitochondria, cytosol, and ER in HeLa cells in a VDAC-dependent manner, with effects enhanced by higher concentrations and longer incubation times^[1].
NCATS-SM0225 (0-10 μM; 40-48 h) selectively induces apoptotic cell death in a subset of cancer cell lines while sparing normal cells, with selectivity correlating with its ability to disrupt calcium homeostasis and degrade ERAD complex proteins^[1].
NCATS-SM0225 (1.25-10 μM; 6-24 h) induces selective degradation of ERAD complex proteins (HERP1, OS9, FAM8A1) in HeLa cells in a dose- and time-dependent, Ca²⁺-dependent manner, while activating PERK signaling^[1].

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