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Solute carrier family 22 member 6 (OAT1) and member 8 (OAT3) are essential multispecific transporters primarily expressed on the basolateral membrane of renal proximal tubule cells [5, 10, 14]. They facilitate the uptake of a diverse range of organic anions from the systemic circulation into the kidney for subsequent excretion into the urine [5, 15]. These transporters handle critical endogenous substrates, including uric acid, prostaglandins, and uremic toxins, as well as numerous pharmaceutical agents such as beta-lactam antibiotics, antivirals, and diuretics [5, 10, 11]. Due to their broad substrate specificity, OAT1 and OAT3 are major sites for clinically significant drug-drug interactions, where competitive inhibition can prolong the half-life of co-administered drugs or protect against nephrotoxicity [10, 15, 16]. They are recognized as therapeutic targets in the management of hyperuricemia and gout, and their dysfunction is linked to the progression of chronic kidney disease and acute kidney injury [1, 3, 17]. Understanding their activity is vital for predicting drug pharmacokinetics and ensuring therapeutic safety [9, 12].
Inhibition of basolateral uptake to modulate drug clearance or reduce intracellular toxicity
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