Abstract
Homology modeling and molecular docking of URAT1 with chemotherapeutic agents in hyperuricemia and gout
Highlights
In humans, hyperuricemia is caused by reduction in renal urate excretion, and leads to diseases such as gout, urolithiasis, hypertension and diabetes mellitus[1,2] as well as cardiovascular diseases and renal failure[3]
We have mainly focussed our investigation on uricosurics associated with uric acid transporter 1 (URAT1) due the high malignancy and high incidence of kidney dysfunction induced hyperuricemia
We have investigated chemotherapeutic drugs binding to URAT1 as experimental studies have shown these compounds interact with this protein
Summary
Hyperuricemia is caused by reduction in renal urate (the salt of uric acid) excretion, and leads to diseases such as gout, urolithiasis, hypertension and diabetes mellitus[1,2] as well as cardiovascular diseases and renal failure[3]. The underlying cause of gout is the elevated levels of plasma uric acid resulting from diet, genetic predisposition, or under excretion of urate[6] Given these considerations, the development of novel compounds that could lower serum uric acid levels could be therapeutically important. The cells lining the nephron contain specific transporters in contact with the urine, especially human uric acid transporter 1 (URAT1; SLC22A12)[10], which was mainly identified and demonstrated to mediate urate handling in the human kidney. It is a member of the organic anion transporter family and is expressed only in the kidney, where the protein is located
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