The Clinical Pharmacology of Cladribine Tablets for the Treatment of Relapsing Multiple Sclerosis

Clin Pharmacokinet. 2019 Mar;58(3):283-297. doi: 10.1007/s40262-018-0695-9.

Abstract

Cladribine Tablets (MAVENCLAD®) are used to treat relapsing multiple sclerosis (MS). The recommended dose is 3.5 mg/kg, consisting of 2 annual courses, each comprising 2 treatment weeks 1 month apart. We reviewed the clinical pharmacology of Cladribine Tablets in patients with MS, including pharmacokinetic and pharmacometric data. Cladribine Tablets are rapidly absorbed, with a median time to reach maximum concentration (Tmax) of 0.5 h (range 0.5-1.5 h) in fasted patients. When administered with food, absorption is delayed (median Tmax 1.5 h, range 1-3 h), and maximum concentration (Cmax) is reduced by 29% (based on geometric mean). Area under the concentration-time curve (AUC) is essentially unchanged. Oral bioavailability of cladribine is approximately 40%, pharmacokinetics are linear and time-independent, and volume of distribution is 480-490 L. Plasma protein binding is 20%, independent of cladribine plasma concentration. Cladribine is rapidly distributed to lymphocytes and retained (either as parent drug or its phosphorylated metabolites), resulting in approximately 30- to 40-fold intracellular accumulation versus extracellular concentrations as early as 1 h after cladribine exposure. Cytochrome P450-mediated biotransformation of cladribine is of minor importance. Cladribine elimination is equally dependent on renal and non-renal routes. In vitro studies indicate that cladribine efflux is minimally P-glycoprotein (P-gp)-related, and clinically relevant interactions with P-gp inhibitors are not expected. Cladribine distribution across membranes is primarily facilitated by equilibrative nucleoside transporter (ENT) 1, concentrative nucleoside transporter (CNT) 3 and breast cancer resistance protein (BCRP), and there is no evidence of any cladribine-related effect on heart rate, atrioventricular conduction or cardiac repolarisation (QTc interval prolongation). Cladribine Tablets are associated with targeted lymphocyte reduction and durable efficacy, with the exposure-effect relationship showing the recommended dose is appropriate in reducing relapse risk.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B, Member 1 / antagonists & inhibitors
  • ATP Binding Cassette Transporter, Subfamily B, Member 1 / drug effects
  • ATP Binding Cassette Transporter, Subfamily B, Member 1 / metabolism
  • ATP Binding Cassette Transporter, Subfamily G, Member 2 / drug effects
  • ATP Binding Cassette Transporter, Subfamily G, Member 2 / metabolism
  • Administration, Oral
  • Adult
  • Aged
  • Biological Availability
  • Cladribine / administration & dosage
  • Cladribine / blood
  • Cladribine / pharmacokinetics*
  • Cladribine / therapeutic use
  • Cytochrome P-450 Enzyme System / metabolism
  • Equilibrative Nucleoside Transporter 1 / drug effects
  • Equilibrative Nucleoside Transporter 1 / metabolism
  • Female
  • Humans
  • Immunosuppressive Agents / administration & dosage
  • Immunosuppressive Agents / blood
  • Immunosuppressive Agents / pharmacokinetics*
  • Immunosuppressive Agents / therapeutic use
  • Lymphocytes / drug effects
  • Lymphocytes / metabolism
  • Male
  • Membrane Transport Proteins / drug effects
  • Membrane Transport Proteins / metabolism
  • Middle Aged
  • Multiple Sclerosis, Relapsing-Remitting / drug therapy*
  • Neoplasm Proteins / drug effects
  • Neoplasm Proteins / metabolism
  • Pharmacology, Clinical
  • Protein Binding / drug effects

Substances

  • ABCG2 protein, human
  • ATP Binding Cassette Transporter, Subfamily B, Member 1
  • ATP Binding Cassette Transporter, Subfamily G, Member 2
  • Equilibrative Nucleoside Transporter 1
  • Immunosuppressive Agents
  • Membrane Transport Proteins
  • Neoplasm Proteins
  • cif nucleoside transporter
  • Cladribine
  • Cytochrome P-450 Enzyme System