Research ArticlesPharmacokinetics of Probenecid Following Oral Doses to Human Volunteers
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Solubility of probenecid in supercritical carbon dioxide and composite particles prepared using supercritical antisolvent process
2023, Journal of Supercritical FluidsPharmacological urate-lowering approaches in chronic kidney disease
2019, European Journal of Medicinal ChemistryCitation Excerpt :Probenecid undergoes the extensive metabolism, including glucuronide conjugation and alkyl side chain oxidation, after which only 5–11% of unchanged Probenecid is excreted in urine. The metabolites are mainly eliminated through kidney [67–69]. The American College of Rheumatology guidelines recommend Probenecid as the first choice of uricosuric for urate-lowering treatment (ULT) but recommend against using Probenecid in cases where the GFR is less than 50 ml/min [39].
Emodin-induced hepatotoxicity was exacerbated by probenecid through inhibiting UGTs and MRP2
2018, Toxicology and Applied PharmacologyCitation Excerpt :The aggravating hepatotoxicity of combination group was highly possible caused by the bidirectional interactions between emodin and probenecid. Pharmacokinetic experiment showed that the serum concentration of probenecid is highly dose-dependent in human (Selen et al., 1982; Wu et al., 2010), and thus aggravating hepatotoxicity might attribute to the increased accumulation of probenecid induced by emodin. Therefore, further studies will be needed to clarify the effect of emodin on the toxicokinetics of probenecid.
Transport of 3-fluoro-L-α-methyl-tyrosine (FAMT) by organic ion transporters explains renal background in [<sup>18</sup>F]FAMT positron emission tomography
2016, Journal of Pharmacological SciencesCitation Excerpt :The accumulation of [125I]IMT in S2-like region let us speculate that OAT1 present in S2 segment (38) at least contributes to the renal accumulation of [125I]IMT, while, at the moment, the detailed tubular distribution is not determined for OAT10 and OCTN2. As shown in Fig. 5, [14C]FAMT transports by OAT1, OAT10 and OCTN2 are mostly inhibited by probenecid, furosemide and ethacrynic acid, suggesting that particularly probenecid with relatively higher plasma concentration at clinical dosage (40) could suppress the renal accumulation of [18F]FAMT in PET when administered at appropriate doses. It was furthermore reported for IMT that, in cultured human renal proximal tubule epithelial cells in vitro, the small portion of [125I]IMT uptake is inhibited by BCH, an inhibitor of amino acid transport systems L, B0 and B0,+ (34), in a Na+-dependent manner (28).
Urate-Lowering Therapy
2016, Kelley and Firestein's Textbook of Rheumatology: Volumes 1-2, Tenth EditionDevelopment of 4-Pyridoxic Acid PBPK Model to Support Biomarker-Informed Evaluation of OAT1/3 Inhibition and Effect of Chronic Kidney Disease
2023, Clinical Pharmacology and Therapeutics