Hsp90-IN-42

Hsp90-IN-42 (compound 13l) potently inhibits purified Hsp90α with an IC₅₀ of 15.65 nM by competitively binding to the ATP-binding pocket and forming stable interactions with key residues. It potently inhibits the proliferation of various human cancer cell lines, with the strongest activity against HT-29 colorectal cancer cells (IC₅₀ = 0.69 μM)^[1].
Hsp90-IN-42 (0.5-5.0 μM; initial treatment for 48 h, followed by 14 days of culture) potently inhibits colony formation of HT-29 colorectal cancer cells^[1].
Hsp90-IN-42 (0.5-5.0 μM; 24-48 h) effectively inhibits the migration of HT-29 colorectal cancer cells in a concentration-dependent manner^[1].
Hsp90-IN-42 (0.5-5.0 μM; 24 h) induces dose-dependent G0/G1 phase arrest in HT-29 colorectal cancer cells after 24 h of treatment, led to mild, dose-dependent apoptosis; it regulates the expression of cell cycle- and apoptosis-related proteins in HT-29 colorectal cancer cells, downregulates the expression of CDK12, CDK13 and Bcl-2, and upregulates the expression of p53 and Bax^[1].
Hsp90-IN-42 (0.5-5.0 μM; 24 h) destabilizes EGFR and inhibits the activation of the EGFR-Akt signaling pathway in HT-29 colon cancer cells by reducing the levels of EGFR, total Akt, and phosphorylated Akt in a dose-dependent manner. It induces a dose-dependent heat shock response in HT-29 colon cancer cells and upregulates the expression of Hsp70^[1].

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