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UGT1A1 Mediated Drug Interactions and its Clinical Relevance

[ Vol. 17 , Issue. 2 ]


Chong Ping Goon, Ling Zhi Wang, Fang Cheng Wong, Win Lwin Thuya, Paul Chi-Lui Ho and Boon Cher Goh   Pages 100 - 106 ( 7 )


Background: The administration of multiple drugs for the treatment of diseases is an integral aspect of modern medicine. Though its purpose is to create the intended therapeutic effect, the unintended consequences of drug interactions can cause severe side effects and subsequent economic losses. Likewise, herbal extracts and supplements with pharmacologically active moieties also have the potential to interact with medications. There are many possible mechanisms on how these moieties could potentially interact, one of which is mediated by modulation of the activity of metabolizing enzymes. One such enzyme of high clinical significance is uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1). Genetic polymorphism of UGT1A1 has been found to affect the plasma concentrations of many drugs, and may even be linked to treatment outcome.

Objective: This mini-review summarized the potential in vitro and in vivo interactions mediated by UGT1A1.

Method: Firstly, literature search was conducted using the Web of Knowledge database. No date limitation was applied to the search. Following which, the interactions were stratified into 3 main categories based on its clinical significance. Both herbal and pharmacological drug moieties are covered within the scope of this mini-review.

Results: Of 35 UGT1A1 induced drug interactions, likely and unlikely to be clinically significant interactions are 11 and 6 respectively. The rest of them are inconclusive.

Conclusion: We hope that this secondary literature can broaden and update the perspective of clinicians, pharmacists and academics on the interactions mediated by UGT1A1.


Clinical relevance, drugs, drug interactions, herbal supplements, Phase II, UGT1A1.


Cancer Science Institute of Singapore, National University of Singapore, P.O. Box: 117599, Singapore, Singapore.

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