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Related Concept Videos

Pharmacokinetics: Drug–Drug Interactions01:25

Pharmacokinetics: Drug–Drug Interactions

Drug interactions occur when the pharmacological effect of one drug is altered by another substance, either enhancing or diminishing its activity. The drug whose activity is altered is known as the object drug, and the substance causing the alteration is called the agent drug or the precipitant. The net effects of these interactions are mostly undesirable, leading to decreased effectiveness or increased adverse effects. In rare cases, interactions can be beneficial, such as the enhanced...
Drug toxicity: Drug–Drug Interaction01:30

Drug toxicity: Drug–Drug Interaction

Drug–drug interactions can precipitate toxicity through multiple mechanisms. Absorption interactions alter how drugs enter the body, exemplified when ranitidine increases the absorption of basic drugs, while cholestyramine decreases the levels of propranolol. Protein binding interactions occur when drugs share the same binding sites on plasma proteins. Drugs like aspirin and warfarin, when bound in excess, can lead to increased free drug concentrations, enhancing the potential for...
Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
Nonlinear Pharmacokinetics: Dependence of Elimination Half-Life and Dose Clearance01:23

Nonlinear Pharmacokinetics: Dependence of Elimination Half-Life and Dose Clearance

The elimination half-life and drug clearance of drugs following nonlinear kinetics can vary with dosage. The Michaelis-Menten parameters and drug concentration influence these factors. As the dose increases, the elimination half-life tends to lengthen, resulting in a reduction in clearance and a disproportionately larger area under the curve. The total clearance can be derived from the Michaelis-Menten equation for drugs following a one-compartment model.
A study on guinea pigs examined the...
Combined Effects of Drugs: Antagonism01:30

Combined Effects of Drugs: Antagonism

The combined effects of drugs can result in various interactions, of which an important type is antagonism. Antagonism is a mechanism where one drug inhibits or counteracts the effects of another drug. Antagonism can occur through various means, including receptor binding, allosteric modulation, functional interaction, chemical reactions, and pharmacokinetic processes.
The most common type is receptor antagonism, where one drug acts as an antagonist to block the effects of another drug by...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...

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Related Experiment Video

Updated: Jul 19, 2026

Mass Spectrometry and Luminogenic-based Approaches to Characterize Phase I Metabolic Competency of In Vitro Cell Cultures
10:44

Mass Spectrometry and Luminogenic-based Approaches to Characterize Phase I Metabolic Competency of In Vitro Cell Cultures

Published on: March 28, 2017

Valdecoxib does not interfere with the CYP2D6 substrate metoprolol.

U Werner1, C Lamprecht, D Werner

  • 1Department of Experimental and Clinical Pharmacology and Toxicology, Friedrich Alexander University of Erlangen-Nuremberg, Germany. ulrike-werner@arcor.de

International Journal of Clinical Pharmacology and Therapeutics
|September 26, 2006
PubMed
Summary

Valdecoxib and rofecoxib do not affect the metabolism of metoprolol, a substrate for cytochrome P450 2D6. This study found no significant pharmacokinetic or pharmacodynamic changes in volunteers receiving these COX-2 inhibitors alongside metoprolol.

Related Experiment Videos

Last Updated: Jul 19, 2026

Mass Spectrometry and Luminogenic-based Approaches to Characterize Phase I Metabolic Competency of In Vitro Cell Cultures
10:44

Mass Spectrometry and Luminogenic-based Approaches to Characterize Phase I Metabolic Competency of In Vitro Cell Cultures

Published on: March 28, 2017

Area of Science:

  • Pharmacology
  • Drug Metabolism
  • Clinical Pharmacology

Background:

  • Cytochrome P450 (CYP)2D6 plays a crucial role in drug metabolism.
  • Previous research indicated celecoxib inhibits CYP2D6 activity.
  • Valdecoxib, a metabolite of parecoxib, was also suspected to interact with CYP2D6 substrates, necessitating further investigation.

Purpose of the Study:

  • To evaluate the impact of valdecoxib on the pharmacokinetics of metoprolol, a CYP2D6 substrate.
  • To assess potential drug-drug interactions between COX-2 inhibitors and CYP2D6 substrates.

Main Methods:

  • A randomized, 3-period crossover study involving 15 healthy male volunteers.
  • Volunteers received metoprolol (50 mg) alone or after 7-day pre-treatment with valdecoxib (20 mg/day) or rofecoxib (25 mg/day).
  • Pharmacokinetic and pharmacodynamic parameters of metoprolol were analyzed.

Main Results:

  • Valdecoxib and rofecoxib did not significantly alter the area under the plasma concentration-time curve of metoprolol.
  • No significant changes in pharmacokinetic or pharmacodynamic parameters of metoprolol were observed.
  • Higher doses of metoprolol also showed no interaction.

Conclusions:

  • Therapeutic doses of valdecoxib and rofecoxib do not inhibit the CYP2D6-mediated metabolism of metoprolol.
  • These findings suggest a lack of significant drug-drug interaction between these COX-2 inhibitors and metoprolol.
  • Clinical implications for perioperative use of parecoxib regarding CYP2D6 substrate interactions are minimal at therapeutic doses.