Pharmacokinetics

The metabolism of PRISTIQ is independent of the CYP2D6 pathway in the liver¹

PRISTIQ 50 mg delivered predictable ODV concentrations regardless of CYP2D6 metabolizer status.^1,2

Data from an open-label, 2-period, parallel-group, crossover study evaluating single doses of PRISTIQ 50 mg in healthy subjects who are extensive or poor CYP2D6 substrate metabolizers (N=14). The primary objective was to determine the difference in the pharmacokinetics of PRISTIQ when influenced by CYP2D6 polymorphism. ²

• ODV levels after administration of PRISTIQ were largely unaffected by genetic variability in CYP2D6 metabolism¹
• Metabolizer status can vary based on genetics or on other drugs that patients may be taking to treat comorbid conditions⁶
  • The majority of patients being treated for MDD have been prescribed 3 or more medications to manage a variety of comorbid conditions.²

Clinical Pharmacology of PRISTIQ¹

Important Treatment Considerations

• PRISTIQ must not be used concomitantly with an MAOI or within 14 days of stopping an MAOI. Allow 7 days after stopping PRISTIQ before starting an MAOI.
• Development of a potentially life-threatening serotonin syndrome or Neuroleptic Malignant Syndrome-like reactions have been reported with SNRIs and SSRIs alone, including PRISTIQ treatment, but particularly with concomitant use of serotonergic drugs, including triptans, with drugs that impair the metabolism of serotonin (including MAOIs), or with antipsychotics or other dopamine antagonists. If concomitant use with a triptan is clinically warranted, careful observation of the patient is advised, particularly during treatment initiation and dose increases. Concomitant use of PRISTIQ with serotonin precursors is not recommended.
• SSRIs and SNRIs, including PRISTIQ, may increase the risk of bleeding events. Concomitant use of aspirin, NSAIDs, warfarin, and other anticoagulants may add to this risk.

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