Summary of clinical studies using sulfasalazine as the intestinal BCRP probe

Dose/FormulationaSubject Race and GenderBCRP c.421C>A Number of subjects per GenotypeNAT2 PhenotypeSulfasalazine AUC VariabilityEffect of c.421C>A SNP or BCRP Inhibitor on PKReference
2000-mg IR tabletAsian men12 C/C, 16 C/A, 9 A/A13 RA, 16 IA, 8 SA1.9-fold (95% CI; genotype controlled)1.9-fold AUC increase in 421C/A; 3.5-fold AUC increase in 421A/A; clear gene-dose effectYamasaki et al., 2008
1000-mg suspension (also tested IR tablet)Caucasian men and women9 C/C, 5 C/A, 0 A/ANot genotyped; sulfapyridine PK not studied20.5-fold (maximum/minimum; genotype controlled)2.4-fold AUC increase in 421C/A genotypeUrquhart et al., 2008
500-mg enteric-coated tabletAsian men12 C/C, 12 C/A, 12 A/A4 RA, 20 IA, 12 SA21- to 81-fold (maximum/minimum; genotype controlled)None (trend for 2-fold AUC increase in A/A genotype; N.S.); no clear gene-dose effect; no significant effect of BCRP inhibitor (40 mg pantoprazole)Adkison et al., 2010
IR tablet/suspensionAsian men8 C/CNot genotyped; sulfapyridine PK not studiedAUC CV = 24%–40%Curcumin (2 ga) increased AUC 3.2-fold (therapeutic dose) and 2-fold (microdose)Kusuhara et al., 2012
  • CI, confidence interval; CV, coefficient of variation; IA, intermediate acetylator; RA, rapid acetylator; SA, slow acetylator.

  • a The route of administration was oral in all cases.