Midodrine shows relevant bioactivities related to liver enzyme activity, affecting markers such as alkaline phosphatase, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, lactate dehydrogenase, and gamma-glutamyl transferase, albeit with varying degrees of effect. Importantly, it demonstrates no liver toxicity or hepatic side effects, with all hepatic side effect scores—including bilirubinemia, cholecystitis, cirrhosis, hepatitis, and jaundice—recorded as 0.0 according to the Drug Induced Liver Injury Prediction System (DILIps). Pharmacokinetically, Midodrine has a pKa value of 7.59, a LogD7.4 of -0.71 indicating it is hydrophilic, and an intrinsic clearance of less than 3.0 uL.min-1.(10^6cells)-1 in human hepatocytes.
In antiviral testing, Midodrine exhibits activity against SARS-CoV-2 (USA-WA1/2020 strain) in HRCE cells, with a hit score of 0.1739 implying moderate efficacy, and an IC50 value greater than 20,000.0 nM in VERO-6 cells, indicating low potency in inhibiting virus-induced cytotoxicity. Additionally, it shows inhibitory activity against the human HDAC6 enzyme, with inhibition rates of 12.02% using a commercial peptide substrate and 16.07% using a custom peptide substrate, suggesting some potential as an HDAC6 inhibitor.
Despite extensive testing against various receptors and enzymes, Midodrine generally displayed limited bioactivity, with AC50 values exceeding 10000.0 nM across most targets, indicating weak or insignificant pharmacological effects on the evaluated receptors and enzymes..
Note: Summary generated by AI. Data source: ChEMBL 