Utilizing in vitro and PBPK tools to link ADME characteristics to plasma profiles: case example nifedipine immediate release formulation

J Pharm Sci. 2013 Sep;102(9):3205-19. doi: 10.1002/jps.23611. Epub 2013 May 20.

Abstract

One of the most prominent food-drug interactions is the inhibition of intestinal cytochrome P450 (CYP) 3A enzymes by grapefruit juice ingredients, and, as many drugs are metabolized via CYP 3A, this interaction can be of clinical importance. Calcium channel-blocking agents of the dihydropyridine type, such as felodipine and nifedipine, are subject to extensive intestinal first pass metabolism via CYP 3A, thus resulting in significantly enhanced in vivo exposure of the drug when administered together with grapefruit juice. Physiologically based pharmacokinetic (PBPK) modeling was used to simulate pharmacokinetics of a nifedipine immediate release formulation following concomitant grapefruit juice ingestion, that is, after inhibition of small intestinal CYP 3A enzymes. For this purpose, detailed data about CYP 3A levels were collected from the literature and implemented into commercial PBPK software. As literature reports show that grapefruit juice (i) leads to a marked delay in gastric emptying, and (ii) rapidly lowers the levels of intestinal CYP 3A enzymes, inhibition of intestinal first pass metabolism following ingestion of grapefruit juice was simulated by altering the intestinal CYP 3A enzyme levels and simultaneously decelerating the gastric emptying rate. To estimate the in vivo dispersion and dissolution behavior of the formulation, dissolution tests in several media simulating both the fasted and fed state stomach and small intestine were conducted, and the results from the in vitro dissolution tests were used as input function to describe the in vivo dissolution of the drug. Plasma concentration-time profiles of the nifedipine immediate release formulation both with and without simultaneous CYP 3A inhibition were simulated, and the results were compared with data gathered from the literature. Using this approach, nifedipine plasma profiles could be simulated well both with and without enzyme inhibition. A reduction in small intestinal CYP 3A levels by 60% was found to yield the best results, with simulated nifedipine concentration-time profiles within 20% of the in vivo observed results. By additionally varying the dissolution input of the PBPK model, a link between the dissolution characteristics of the formulation and its in vivo performance could be established.

Keywords: absorption; bioavailability; computational ADME; cytochrome P450; dissolution; drug metabolizing enzymes; first-pass metabolism; pharmacokinetics; quality by design (QbD).

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Beverages / analysis
  • Calcium Channel Blockers / administration & dosage
  • Calcium Channel Blockers / blood*
  • Calcium Channel Blockers / chemistry
  • Calcium Channel Blockers / metabolism*
  • Citrus paradisi* / metabolism
  • Computer Simulation
  • Cytochrome P-450 CYP3A / metabolism
  • Cytochrome P-450 CYP3A Inhibitors
  • Food-Drug Interactions*
  • Humans
  • Models, Biological
  • Nifedipine / administration & dosage
  • Nifedipine / blood*
  • Nifedipine / chemistry
  • Nifedipine / metabolism*
  • Solubility

Substances

  • Calcium Channel Blockers
  • Cytochrome P-450 CYP3A Inhibitors
  • Cytochrome P-450 CYP3A
  • Nifedipine