}

Tenoxicam

Pain Management

Drug Overview

Tenoxicam (brand name Mobiflex) is a nonsteroidal anti-inflammatory drug (NSAID) used to relieve pain, inflammation, and stiffness associated with conditions such as osteoarthritis, rheumatoid arthritis, and ankylosing spondylitis.

It is commonly prescribed for both chronic and acute musculoskeletal disorders, including postoperative pain. Tenoxicam works by inhibiting the cyclooxygenase (COX-1 and COX-2) enzymes, which reduces the production of prostaglandins that mediate inflammation and pain.

Due to its long half-life, tenoxicam provides sustained pain relief, allowing for once-daily dosing while helping to maintain consistent symptom control.

Relevant Genes and Their Roles

The primary gene influencing tenoxicam response is CYP2C9. CYP2C9 encodes an enzyme in the liver responsible for metabolizing tenoxicam into inactive forms that can be excreted. Variations in this gene can change how efficiently the enzyme works.

These genetic differences categorize individuals as normal, intermediate, or poor metabolizers based on their CYP2C9 activity. Metabolizer status refers to the rate at which the body breaks down and clears the drug, affecting both efficacy and risk of side effects.

Impact of Genetics on Drug Response

CYP2C9 genetic variations can lead to reduced or enhanced metabolic activity. Poor metabolizers clear tenoxicam more slowly, which can increase drug levels and risk of adverse effects, while normal metabolizers clear the drug at expected rates. When genotype information is indeterminate or unavailable, standard dosing with careful clinical monitoring is recommended.

Expected Clinical Effects of Genetic Variation

Ultra-rapid/Rapid Metabolizers

  • Effect on drug levels: Increased clearance leading to lower plasma concentrations
  • Clinical consequence: Potentially reduced pain relief due to faster elimination
  • Side effects: Fewer side effects; generally mild and infrequent

Normal Metabolizers

  • Effect on drug levels: Expected clearance and normal plasma concentrations
  • Clinical consequence: Therapeutic pain relief as anticipated
  • Side effects: Typical NSAID-related effects such as gastrointestinal discomfort; mild to moderate; common

Intermediate Metabolizers

  • Effect on drug levels: Moderately reduced clearance leading to slightly higher drug exposure
  • Clinical consequence: Adequate pain relief with a slight increase in exposure
  • Side effects: Mild increase in risk for NSAID side effects (e.g., GI irritation); mild to moderate; occasional

Poor Metabolizers

  • Effect on drug levels: Significantly reduced clearance and prolonged drug half-life
  • Clinical consequence: Higher plasma concentrations may increase probability and severity of side effects
  • Side effects: Increased risk of toxicity (e.g., gastrointestinal bleeding, renal impairment); moderate to severe; relatively common

Indeterminate/Not Available

  • Effect on drug levels: Unknown
  • Clinical consequence: No specific guidance; follow standard dosing with clinical monitoring
  • Side effects: As per general population; unknown severity and frequency

Dosing Guidelines

The following dosing guidelines are based on the available guidelines for CYP2C9 genotype and tenoxicam from CPIC.

CYP2C9 Dosing Guideline

Phenotype Clinical Consequence Guideline Recommendation
Normal Metabolizer (activity score 2) Normal metabolism Initiate therapy with recommended starting dose. Use the lowest effective dosage for the shortest duration consistent with individual patient treatment goals.
Intermediate Metabolizer (activity score 1.5) Mildly reduced metabolism Initiate therapy with recommended starting dose. Use the lowest effective dosage for the shortest duration consistent with individual patient treatment goals.
Intermediate Metabolizer (activity score 1) Moderately reduced metabolism; higher plasma concentrations may increase probability of toxicities Choose an alternative therapy not metabolized by CYP2C9 or not significantly impacted by CYP2C9 genetic variants, or select an NSAID with a shorter half-life.
Poor Metabolizer (activity score 0.5) Significantly reduced metabolism and prolonged half-life Choose an alternative therapy not metabolized by CYP2C9 or not significantly impacted by CYP2C9 genetic variants, or select an NSAID with a shorter half-life.
Poor Metabolizer (activity score 0) Significantly reduced metabolism and prolonged half-life Choose an alternative therapy not metabolized by CYP2C9 or not significantly impacted by CYP2C9 genetic variants, or select an NSAID with a shorter half-life.
Indeterminate No guidance available; unknown metabolism Initiate therapy with recommended starting dose.
Not available No guidance available; unknown metabolism Initiate therapy with recommended starting dose.

Alternative Treatment Options

For patients identified as intermediate or poor metabolizers of CYP2C9, guidelines suggest selecting an alternative NSAID not significantly metabolized by CYP2C9 (e.g., ibuprofen, celecoxib) or choosing an NSAID with a shorter half-life. These examples are drawn from the CPIC guideline and should not be interpreted as 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.

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