http://rdf.ncbi.nlm.nih.gov/pubchem/patent/KR-102490204-B1

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filingDate 2019-01-04-04:00^^<http://www.w3.org/2001/XMLSchema#date>
grantDate 2023-01-19-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationDate 2023-01-19-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber KR-102490204-B1
titleOfInvention Method for reducing ischemia-reperfusion-induced apoptosis with novel aminothiols
abstract In two preclinical models involving renal transplantation and myocardial infarction, members of the PrC-210 aminothiol family, including PrC-211 and PrC-252, are highly effective at reducing ischemia-reperfusion injury. PrC-210 has good resistance, the efficacy reaches 100% at a dose of 0.5 MTD, and there is no significant rodent toxicity when administered orally or systemically via IP route. In what may be the most important aspect of ischemia-reperfusion injury, when the concentration of PrC-210 in vitro is 2-3 mM, the same PrC-210 concentration in rodents treated with IP or oral administration of PrC-210 When is measured, PrC-210 can effectively prevent 100% of DNA damage in the ROS removal assay. In a standard mouse kidney clamping/unclamping model of IR kidney injury, all three aminothiols were able to significantly inhibit (>80%) the levels of renal caspases in the non-drug control group; PrC-210 and its analogues also reduce BUN levels in I-R renal mice. In a mouse myocardial infarction model, when PrC-210 was systemically administered, and the coronary artery was ligated and the anterior artery was released for 40 minutes, it was observed that myocardial death was significantly reduced. Further in vitro studies using primary neonatal mouse cardiomyocytes showed that concomitant administration of PrC-210 family aminothiols can significantly reduce hydrogen peroxide-induced cardiomyocyte apoptosis. PrC-210 family aminothiols inhibit cell and organ toxic effects induced by ischemia-reperfusion in various situations including organ transplantation and myocardial infarction.
priorityDate 2018-03-01-04:00^^<http://www.w3.org/2001/XMLSchema#date>
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