Butyrolactone I

Butyrolactone I is an orally active and ATP-competitive inhibitor of CDK1. Butyrolactone I inhibits NF-κB, cdc2 kinase, Bax, ROS production, modulates the PERK/CHOP. Butyrolactone I mitigates heat-stress-induced Apoptosis. Butyrolactone I shows anti-inflammatory and intestinal protective activity. Butyrolactone I has antitumor effects against non-small cell lung, small cell lung, prostate cancer and leukemia. Butyrolactone I can be used in NASH research^{[1][2][3][4][5][6][7]}. In Vitro:Butyrolactone I (20 μg/mL, concentration equivalent to IC₅₀ value, 2 h) inhibits the cdc2 kinase activity in PC-14 cells^[1].
Butyrolactone I (35-100 μM) inhibits cell proliferation and causes an incomplete cell cycle arrest in G2/M, resulting in occasional skipping of mitosis and subsequent cell cycle progression in human prostate cell lines (DU145, PC-3, LNCaP)^[2].
Butyrolactone I (10-50 μM, 24 h) mitigates heat-stress-induced apoptosis in IPEC-J2 cells by modulating the ROS/PERK/CHOP signaling pathway^[3].
Butyrolactone I (63-1,000 μM, 2 h) induces morphological and sporulation changes in A. terreus and enhances secondary metabolite production^[4].
Butyrolactone I exhibits potent anti-cancer activity against HL-60 (human leukemia) cells and PC-3 cells with the IC₅₀s value of 13.2  μM and 41.7 μM, respectively^[5].
In Vivo:Butyrolactone-I (1-5 mg/kg, p.o., 14 days) ameliorates heat-stress-induced apoptosis in mice through the ROS/PERK/CHOP signaling pathway^[3].
Butyrolactone-I (1-5 mg/kg, p.o., 14 days) alleviates intestinal barrier damage caused by DSS through regulating lactobacillus johnsonii and its metabolites in mice^[6].
Butyrolactone I (10-40 mg/kg, p.o., from the 17th week to 24th week) attenuates inflammation in murine NASH by inhibiting the NF-κB signaling pathway^[7].