Clopidogrel (Plavix)

Antiplateletprescriptionoral · predicted

Thienopyridine prodrug converted to active metabolite via two-step CYP450 oxidation (CYP2C19 key enzyme) followed by hydrolysis. Only ~15% of absorbed dose is bioactivated; 85% hydrolyzed to inactive metabolites by carboxylesterase-1. Active metabolite H4 irreversibly binds to P2Y12 ADP receptors on platelets, inhibiting aggregation. Significant CYP2C19 genetic polymorphism: poor metabolizers (~13-15%) show markedly reduced antiplatelet effect and higher cardiovascular event rates. Genetic testing increasingly recommended. FDA label includes CYP2C19 genotype-based dosing recommendation. High loading dose (300-600 mg) often used for acute coronary syndromes.

Projected serum levels — 75 mg, once daily

Clopidogrel (Plavix)
Clopidogrel (Plavix) modeled serum levels, 75 mg once daily over 15 days Population-based pharmacokinetic estimate. Steady state reached after approximately 2 days. 0 0.25 0.50 0.75 1 Day 0 Day 4 Day 8 Day 11 Day 15 Time on a regular schedule ≈ steady state · day 2
Clopidogrel (Plavix) modeled serum levels with a loading dose of 122 mg, then 75 mg once daily The first dose is larger so levels approach steady state faster. 0 0.25 0.50 0.75 1 Day 0 Day 4 Day 8 Day 11 Day 15 Time on a regular schedule

Maintenance schedule: 75 mg once daily (oral).

Loading schedule: 122 mg on day 1, then 75 mg once daily — reaching therapeutic levels sooner.

Modeled steady state after ~2 days: peak ≈ 0.33 mg, trough ≈ 0.14 mg body load. Population-based estimate over 15 days for a 75 mg dose at a 70 kg reference body mass — the interactive app scales curves to your doses, timing, and body mass.

Key facts

Category
Antiplatelet
Route modeled
Oral
Model confidence
predicted
Half-life
6 h
Common dose
75 mg
Suggested maximum
300 mg/day
Reference dose range
37.5–300 mg (single dose)
Suggested cadence
once daily
Validated against
75 mg oral — Cmax 0.003 mg/L at 0.75 h

Documented interactions

  • danger
    Fluvoxamine (Luvox) + Clopidogrel (Plavix) Depletion

    Fluvoxamine is a strong CYP2C19 inhibitor. Clopidogrel requires CYP2C19-mediated bioactivation to its active metabolite. Inhibition reduces active metabolite formation by up to 50%, increasing stent…

  • danger
    Levothyroxine (Synthroid) + Clopidogrel (Plavix) Protein binding

    Clopidogrel (Plavix) may displace Levothyroxine (Synthroid) from plasma protein binding sites, transiently raising free drug concentration. This drug has a narrow therapeutic index; free…

  • danger
    Montelukast (Singulair) + Clopidogrel (Plavix) CYP inhibition

    Clopidogrel (Plavix) reversible_inhibitor of CYP2C8 predicted to change Montelukast (Singulair) AUC by ~2.07x

  • danger
    Pioglitazone + Clopidogrel (Plavix) CYP inhibition

    Clopidogrel (Plavix) reversible_inhibitor of CYP2C8 predicted to change Pioglitazone AUC by ~2.07x

  • danger
    Tacrolimus (Prograf) + Clopidogrel (Plavix) Protein binding

    Clopidogrel (Plavix) may displace Tacrolimus (Prograf) from plasma protein binding sites, transiently raising free drug concentration. This drug has a narrow therapeutic index; free concentration…

  • danger
    Warfarin (Coumadin) + Clopidogrel (Plavix) Protein binding

    Clopidogrel (Plavix) may displace Warfarin (Coumadin) from plasma protein binding sites, transiently raising free drug concentration. This drug has a narrow therapeutic index; free concentration…

Serum checks 177 modeled interaction pairings for clopidogrel (plavix) across your whole stack — absorption conflicts, enzyme inhibition, and nutrient depletion included.

Research behind this entry

  1. Clinical Pharmacokinetics and Pharmacodynamics of Clopidogrel Sanofi-Aventis US LLC and Bristol-Myers Squibb Company · Clinical Pharmacokinetics, 2015 DOI

    Comprehensive review of clopidogrel prodrug activation, active metabolite pharmacokinetics, CYP2C19 polymorphism effects on bioactivation, and clinical consequences for antiplatelet response.

  2. Clinical Pharmacogenetics Implementation Consortium Guideline for CYP2C19 Genotype and Clopidogrel Therapy: 2022 Update Lee CR et al. · Clinical Pharmacology & Therapeutics, 2022 DOI

    Updated CPIC guidelines recommending CYP2C19 genotype-based clopidogrel dosing: alternatives for poor metabolizers, standard dosing for normal/rapid metabolizers.

  3. Carboxylesterase-mediated inactivation of the prodrug clopidogrel is enhanced by P2Y12 inhibition Teng R et al. · Journal of Thrombosis and Haemostasis, 2010 DOI

    Mechanism study showing carboxylesterase-1 hydrolysis of clopidogrel to inactive acid metabolite is major elimination pathway, accounting for 85% of absorbed drug.

3 published studies referenced in the app, each with a plain-language summary.