In vitro activity: Tinoridine HCl (also known as Y-3642 HCl), the hydrochloride of tinoridine (Y-3642), is a nonsteroidal anti-inflammatory drug (NSAID) that also has potent radical scavenger and antiperoxidative activity. At concentrations from 5 μM to 100 μM, tinoridine can produce a concentration-dependent inhibition on the simultaneous increases in lipid peroxide formation and renin release induced by 50 μM ascorbic acid in the renin granule fraction. While other NSAIDs and steroids such as indomethacin, hydrocortisone and prednisolone do not inhibit the lipid peroxidation in the renin granule fraction, did not influence the release of renin from the granules, suggesting that tinoridine suppresses renin release by inhibiting the oxidative disintegration of membranes of renin granules.

Kinase Assay: CCl4 aministration produces a marked decrease in the concentrations of liver microsomal cytochrome P-450 and G6Pase, indicating that hepatic endoplasmic reticulum function is disrupted. Prior treatment of the animals with tinoridine (100 mg/kg) significantly reduces the CCl4-induced alterations in the enzyme activities, and a rapid recovery toward the normal values is observed.

Cell Assay: Tinoridine reduces a stable free radical, diphenyl-p-picrylhydrazyl, in the molar ratio of about 1:2, indicating its free radical scavenging ability. Tinoridine inhibits the lipid peroxidation in rat liver microsomes induced by xanthine-xanthine oxidase system in the presence of ADP and Fe2+, in which hydroxyl radical is formed. Tinoridine is demonstrated to be oxidized in the course of the lipid peroxidation by following the fluorescence derived from the oxidation product of tinoridine. It is also oxidized by the xanthine-xanthine oxidase system in the presence of Fe2+, but its oxidation is slow in the absence of Fe2+ and almost completely inhibited by catalase. Tinoridine is also oxidized by H2O2-Fe2+ system producing OH (Fenton reaction), but it does not affect the reduction of cytochrome c caused by superoxide radical