HSP90-IN-11

HSP90-IN-11 (compound 12c) (2-3 h) potently inhibits recombinant HSP90α with an IC₅₀ of 27.8 nM^[1].
HSP90-IN-11 binds to the HSP90 (PDB ID: 5GGZ) binding pocket via four distinct sites, forming multiple hydrogen bonds and hydrophobic interactions that align with the binding mode of AUY-922, with additional stable interactions at Site 4 that support its potent inhibitory activity^[1].
HSP90-IN-11 (48 h) potently inhibits the proliferation of colorectal cancer HCT116 cells with a GI₅₀ of 0.010 μM^[1].
HSP90-IN-11 (48 h) potently inhibits the proliferation of NSCLC A549, H460, and H1975 cells with GI₅₀ values of 0.07 μM, 0.06 μM, and 0.04 μM, respectively, with greatest activity against EGFR-mutant H1975 cells^[1].
HSP90-IN-11 (0.004-0.15 μM; 24 h initial treatment; followed by 10 days of drug-free growth) inhibits colony formation in colorectal cancer HCT116 cells and NSCLC A549, H1975 cells in a concentration-dependent manner, with greater activity against the NSCLC cell lines at 0.009 and 0.018 μM^[1].
HSP90-IN-11 (0.075-1.25 μM; 24 h) activates HSP70 expression and downregulates HSP90 client proteins EGFR and Akt in a concentration-dependent manner in NSCLC A549 and H1975 cells after 24 h of treatment^[1].
HSP90-IN-11 (0.15-2.5 μM (A549); 0.075-1.25 μM (H1975); 48 h) induces concentration-dependent sub-G1 phase accumulation (apoptotic cell death) in NSCLC A549 and H1975 cells after 48 h of treatment^[1].
HSP90-IN-11 (0.15-2.5 μM; 48 h) induces concentration-dependent activation of caspase-3, -8, -9, PARP, and γH2AX, markers of apoptosis and DNA damage, in NSCLC A549 and H1975 cells after 48 h of treatment^[1].

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