Human contains 49 ATP-binding cassette (ABC) transporter genes and the multidrug 
resistance associated proteins (MRP1/ABCC1, MRP2/ABCC2, MRP3/ABCC3, MRP4/ABCC4, 
MRP5/ABCC5, MRP6/ABCC6, MRP7/ABCC10, MRP8/ABCC11 and MRP9/ABCC12) belong to the 
ABCC family which contains 13 members. ABCC7 is cystic fibrosis transmembrane 
conductance regulator; ABCC8 and ABCC9 are the sulfonylurea receptors which 
constitute the ATP-sensing subunits of a complex potassium channel. MRP10/ABCC13 
is clearly a pseudo-gene which encodes a truncated protein that is highly 
expressed in fetal human liver with the highest similarity to MRP2/ABCC2 but 
without transporting activity. These transporters are localized to the apical 
and/or basolateral membrane of the hepatocytes, enterocytes, renal proximal 
tubule cells and endothelial cells of the blood-brain barrier. MRP/ABCC members 
transport a structurally diverse array of important endogenous substances and 
xenobiotics and their metabolites (in particular conjugates) with different 
substrate specificity and transport kinetics. The human MRP/ABCC transporters 
except MRP9/ABCC12 are all able to transport organic anions, such as drugs 
conjugated to glutathione, sulphate or glucuronate. In addition, selected 
MRP/ABCC members may transport a variety of endogenous compounds, such as 
leukotriene C(4) (LTC(4) by MRP1/ABCC1), bilirubin glucuronides (MRP2/ABCC2, and 
MRP3/ABCC3), prostaglandins E1 and E2 (MRP4/ABCC4), cGMP (MRP4/ABCC4, 
MRP5/ABCC5, and MRP8/ABCC11), and several glucuronosyl-, or sulfatidyl steroids. 
In vitro, the MRP/ABCC transporters can collectively confer resistance to 
natural product anticancer drugs and their conjugated metabolites, platinum 
compounds, folate antimetabolites, nucleoside and nucleotide analogs, arsenical 
and antimonial oxyanions, peptide-based agents, and in concert with alterations 
in phase II conjugating or biosynthetic enzymes, classical alkylating agents, 
alkylating agents. Several MRP/ABCC members (MRPs 1-3) are associated with tumor 
resistance which is often caused by an increased efflux and decreased 
intracellular accumulation of natural product anticancer drugs and other 
anticancer agents. Drug targeting of these transporters to overcome 
MRP/ABCC-mediated multidrug resistance may play a role in cancer chemotherapy. 
Most MRP/ABCC transporters are subject to inhibition by a variety of compounds. 
Based on currently available preclinical and limited clinical data, it can be 
expected that modulation of MRP members may represent a useful approach in the 
management of anticancer and antimicrobial drug resistance and possibly of 
inflammatory diseases and other diseases. A better understanding of their 
substrates and inhibitors has important implications in development of drugs for 
treatment of cancer and inflammation.