Coompo Research Chemicals

Isoliquiritigenin have been shown to have a inhibition of xanthine oxidase activity in vitro and doserelated anti-allergic activities. In addition, isoliquiritigenin caused great interest after it was found to have effects in: inhibiting proliferation of the human non-small cell
lung cancer A549 cell line, inducing apoptosis and locking cell cycle progression in the G1 phase, suppressing azoxymethane (AOM)-induced colon carcinogenesis in ddY mice, and inhibiting the growth of prostate cancer. It had been suggested that isoliquiritigenin  merits investigation as a potential cancerchemopreventive agent in humans.

isoliquiritigenin showed selective H2 histamine receptor (H2R) antagonistic effect and remarkably reduced several H2R-mediated physiological responses. Preincubation of U937 and HL60 hematopoietic cells with isoliquiritigenin significantly inhibited H2R agonist-induced cAMP response in a concentration-dependent manner without affecting the viability of cells. Isoliquiritigenin also blocked the binding affinity of [3H]tiotidine to membrane receptors in HL-60 cells.

Isoliquiritigenin did not affect the elevation of cAMP levels induced by cholera toxin, forskolin, or isoproterenol, indicating that the action site of isoliquiritigenin is not Gs protein, effector enzyme, adenylyl cyclase, or β2-adrenoceptor. Isoliquiritigenin affected neither H1R-nor H3R-mediated signaling. In molecular docking studies, isoliquiritigenin exhibited more favorable interactions with H2R than histamine. Isoliquiritigenin prominently inhibited H2R selective agonist dimaprit-induced cAMP generation in MKN-45 gastric cancer cell. Moreover, isoliquiritigenin reduced gastric acid secretion and protected gastric mucosal lesion formation in pylorus-ligated rat model. Taken together, the results demonstrate that isoliquiritigenin is an effective H2R antagonist and provides the basis for designing novel H2R antagonist.
Isoliquiritigenin produces hypnotic effects by positive allosteric modulation of gamma-aminobutyric acid type A-benzodiazepine receptors.