INTRODUCTION: Hyperuricemia (chronically elevated serum uric acid) is the main 
pathology underlying the development of gout, the most common inflammatory 
arthropathy. Management of these conditions therefore relies on controlling 
serum uric acid levels. ATP-binding cassette transporter, sub-family G, member 2 
(ABCG2/BCRP) is a well-studied urate transporter expressed on apical membranes 
in several tissues, including the intestine, liver, and kidney. Here, we discuss 
the potential of future gout therapies targeting ABCG2. Areas covered: ABCG2 
regulates serum uric acid via physiologically important roles in both renal and 
extra-renal urate excretion. ABCG2 dysfunction, which promotes onset of 
hyperuricemia, often results in decreased urate excretion through the 
extra-renal (principally intestinal), rather than the renal pathway. This review 
covers recent attempts to establish the basis of ABCG2 function according to 
genetic diathesis, its molecular structure, and the effects of medication. 
Furthermore, the possibility of treating gout and hyperuricemia by upregulating 
intestinal ABCG2 expression is examined. Expert opinion: ABCG2 holds great 
promise as a therapeutic target for these conditions, particularly considering 
its involvement in extra-renal urate excretion. Manipulation of ABCG2, including 
controlling the level and location of its expression, has the potential to 
prevent gout by promoting uric acid excretion as effectively as general 
uricosuric drugs.
ABBREVIATIONS: ATP-binding cassette (ABC), transmembrane domain (TMD), 
nucleotide binding domain (NBD), single nucleotide polymorphism (SNP), single 
nucleotide polymorphisms (SNPs).