Pharmacogenetic influences on mycophenolate therapy

Barraclough, Katherine A., Lee, Katie J. and Staatz, Christine E. (2010) Pharmacogenetic influences on mycophenolate therapy. Pharmacogenomics, 11 3: 369-390. doi:10.2217/PGS.10.9

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Author Barraclough, Katherine A.
Lee, Katie J.
Staatz, Christine E.
Title Pharmacogenetic influences on mycophenolate therapy
Journal name Pharmacogenomics   Check publisher's open access policy
ISSN 1462-2416
1744-8042
Publication date 2010-03-01
Year available 2010
Sub-type Critical review of research, literature review, critical commentary
DOI 10.2217/PGS.10.9
Open Access Status Not yet assessed
Volume 11
Issue 3
Start page 369
End page 390
Total pages 22
Editor David Gurwitz
Howard McLeod
Munir Pirmohamed
Place of publication London, U.K.
Publisher Future Medicine
Language eng
Abstract Mycophenolic acid (MPA) is a cornerstone immunosuppressant therapy in solid organ transplantation. MPA is metabolized by uridine diphosphate glucuronosyltransferase to inactive 7-O-MPA-glucuronide (MPAG). At least three minor metabolites are also formed, including a pharmacologically active acylglucuronide. MPA and MPAG are subject to enterohepatic recirculation. Biliary excretion of MPA/MPAG involves several transporters, including organic anion transporting polypeptides and multidrug resistant protein-2 (MRP-2). MPA metabolites are also excreted via the kidney, at least in part by MRP-2. MPA exerts its immunosuppressive effect through the inhibition of inosine-5-monophosphate dehydrogenase. Several SNPs have been identified in the genes encoding for uridine diphosphate glucuronosyltransferase, organic anion transporting polypeptides, MRP-2 and inosine-5-monophosphate dehydrogenase. This article provides an extensive overview of the known effects of these SNPs on the pharmacokinetics and pharmacodynamics of MPA.
Formatted abstract
Mycophenolic acid (MPA) is a cornerstone immunosuppressant therapy in solid organ transplantation. MPA is metabolized by uridine diphosphate glucuronosyltransferase to inactive 7-O-MPA-glucuronide (MPAG). At least three minor metabolites are also formed, including a pharmacologically active acyl-glucuronide. MPA and MPAG are subject to enterohepatic recirculation. Biliary excretion of MPA/MPAG involves several transporters, including organic anion transporting polypeptides and multidrug resistant protein-2 (MRP-2). MPA metabolites are also excreted via the kidney, at least in part by MRP-2. MPA exerts its immunosuppressive effect through the inhibition of inosine-5-monophosphate dehydrogenase. Several SNPs have been identified in the genes encoding for uridine diphosphate glucuronosyltransferase, organic anion transporting polypeptides, MRP-2 and inosine-5-monophosphate dehydrogenase. This article provides an extensive overview of the known effects of these SNPs on the pharmacokinetics and pharmacodynamics of MPA.
© 2010 Future Medicine Ltd
Keyword Mycophenolate
Mycophenolic acid
Pharmacodynamics
Pharmacogenetics
Pharmacogenomics
Pharmacokinetics
Polymorphism
Renal-transplant recipients
Uridine diphosphate-glucuronosyltransferase
Single-nucleotide polymorphisms
Monophosphate dehydrogenase-activity
Resistance-associated protein-2
UGT2B7 genetic polymorphisms
Messenger-RNA expression
Drug-drug interactions
Acute rejection
UDP-glucuronosyltransferase
Q-Index Code C1
Q-Index Status Confirmed Code
Grant ID 511109
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Official 2011 Collection
School of Medicine Publications
School of Pharmacy Publications
 
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Citation counts: TR Web of Science Citation Count  Cited 23 times in Thomson Reuters Web of Science Article | Citations
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Created: Sun, 18 Apr 2010, 10:01:37 EST