}

Flurbiprofen

Pain Management

Drug Overview

Flurbiprofen is a nonsteroidal anti-inflammatory drug (NSAID) marketed under brand names such as Ansaid, Ocufen, and Strepfen. It is used to alleviate pain, reduce inflammation, and lower fever.

This medication is commonly prescribed for conditions including osteoarthritis, rheumatoid arthritis, musculoskeletal injuries, dental pain, and inflammatory eye disorders. Treatment goals typically focus on reducing discomfort and improving function.

Flurbiprofen works by inhibiting cyclooxygenase‐1 (COX-1) and cyclooxygenase-2 (COX-2) enzymes, which decreases the production of prostaglandins—lipid compounds that mediate pain, inflammation, and fever.

Relevant Genes and Their Roles

The primary gene affecting flurbiprofen metabolism is CYP2C9, a liver enzyme responsible for processing many NSAIDs. CYP2C9 variants can change how quickly the drug is broken down.

Genetic alterations that reduce CYP2C9 activity slow the metabolism of flurbiprofen, leading to higher drug exposure. Conversely, increased enzyme activity accelerates clearance. Understanding these terms helps guide personalized dosing: “metabolism” refers to how the body chemically modifies the drug for elimination.

Impact of Genetics on Drug Response

Individuals are categorized as normal, intermediate, or poor metabolizers based on CYP2C9 activity. Poor metabolizers clear flurbiprofen more slowly, resulting in higher plasma levels and greater risk of toxicity. Intermediate metabolizers have moderately elevated levels, while normal metabolizers process the drug as expected. If genotype is indeterminate or unavailable, standard dosing with clinical monitoring is recommended.

Expected Clinical Effects of Genetic Variation

Normal Metabolizer

  • Effect on drug levels: Flurbiprofen is metabolized at expected rates, resulting in normal plasma concentrations.
  • Clinical consequence: Standard efficacy and safety profile.
  • Side effects: Typical NSAID-related discomfort such as mild gastrointestinal irritation or transient renal changes; frequency similar to general population.

Intermediate Metabolizer

  • Effect on drug levels: Moderately slower metabolism leads to higher plasma concentrations.
  • Clinical consequence: Increased risk of adverse events due to elevated drug exposure.
  • Side effects: More frequent or pronounced gastrointestinal upset and renal stress; usually mild to moderate in severity.

Poor Metabolizer

  • Effect on drug levels: Significantly reduced metabolism causes substantially elevated plasma concentrations.
  • Clinical consequence: Higher likelihood of serious adverse events and toxicity.
  • Side effects: Increased risk of severe gastrointestinal bleeding and renal impairment; less common but potentially severe.

Indeterminate/Not Available

  • Effect: Unknown
  • Clinical consequence: No specific guidance; follow standard dosing with clinical monitoring.
  • Side effects: Cannot predict; monitor for typical NSAID-related effects.

Dosing Guidelines

The following dosing guidelines are based on CPIC recommendations for flurbiprofen and CYP2C9 genotype.

CYP2C9 Dosing Guideline

Phenotype Clinical Consequence Guideline Recommendation
Normal Metabolizer Normal metabolism Initiate therapy with recommended starting dose. In accordance with the prescribing information, use the lowest effective dosage for the shortest duration consistent with individual patient treatment goals.
Intermediate Metabolizer (AS 1.5) Mildly reduced metabolism Initiate therapy with recommended starting dose. In accordance with the prescribing information, use the lowest effective dosage for the shortest duration consistent with individual patient treatment goals.
Intermediate Metabolizer (AS 1.0) Moderately reduced metabolism; higher plasma concentrations may increase probability of toxicities Initiate therapy with lowest recommended starting dose. Titrate dose upward to clinical effect or maximum recommended dose with caution. In accordance with the prescribing information, use the lowest effective dosage for the shortest duration consistent with individual patient treatment goals. Carefully monitor adverse events, such as blood pressure and kidney function, during course of therapy.
Poor Metabolizer (AS 0.5–0) Significantly reduced metabolism and prolonged half-life; higher plasma concentrations may increase probability and/or severity of toxicities Initiate therapy with 25–50% of the lowest recommended starting dose. Titrate dose upward to clinical effect or 25–50% of the maximum recommended dose with caution. In accordance with the prescribing information, use the lowest effective dosage for the shortest duration consistent with individual patient treatment goals. Upward dose titration should not occur until after steady‐state is reached. Carefully monitor adverse events such as blood pressure and kidney function during course of therapy. Alternatively, consider an alternate therapy not metabolized by CYP2C9.
Indeterminate No CPIC guidance for this phenotype Initiate therapy with recommended starting dose.
Not available No CPIC guidance for this phenotype Initiate therapy with recommended starting dose.

Alternative Treatment Options

For CYP2C9 poor metabolizers, guidelines suggest considering NSAIDs that are less dependent on CYP2C9 for clearance (e.g., ketorolac, naproxen) or alternative analgesic approaches. These examples are for informational purposes and not medical advice.

Sources and References

Disclaimer: This document is for informational purposes only and is not a substitute for medical advice. Clinical decisions should be made by a qualified healthcare professional.

Interested in learning more about how your genetics may affect your response to medication? Get started with Gene2Rx today.

I'm Interested