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Related Concept Videos

Pharmacogenetics of Phase I Enzymes: Cytochrome P450 Isozymes01:28

Pharmacogenetics of Phase I Enzymes: Cytochrome P450 Isozymes

Cytochrome P450 (CYP450) enzymes are a superfamily of heme-containing monooxygenases that play a pivotal role in Phase I drug metabolism by catalyzing oxidation and reduction reactions.These enzymes transform lipophilic xenobiotics into more hydrophilic metabolites, facilitating subsequent Phase II conjugation and eventual excretion. The CYP450 family is classified into families (e.g., CYP1–CYP3) and subfamilies (e.g., CYP2A, CYP2C), based on amino acid sequence homology.CYP450 isoenzymes,...
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase01:27

Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase

Phase II biotransformation reactions are essential for detoxifying and eliminating xenobiotics, including many pharmaceutical compounds. These reactions typically involve conjugation, the covalent attachment of polar endogenous groups such as glucuronic acid, sulfate, methyl, or acetyl moieties to functional groups introduced during Phase I metabolism. The resulting conjugates are more water-soluble, enabling efficient renal or biliary excretion.The major classes of Phase II enzymes include...
Pharmacogenetics of Drug Metabolism: Overview01:27

Pharmacogenetics of Drug Metabolism: Overview

Genetic polymorphism in drug metabolism is crucial to the inter-individual variability observed in drug responses. Drug metabolism primarily involves the chemical modification of drugs and other xenobiotics to enhance their elimination by increasing their polarity. Two main classes of enzymes mediate this biotransformation process: Phase I enzymes, primarily cytochrome P450s, catalyze oxidation and reduction reactions, while other enzymes, such as esterases, mediate hydrolysis, and Phase II...
Drug toxicity: Idiosyncratic Reactions01:16

Drug toxicity: Idiosyncratic Reactions

Idiosyncratic drug reactions represent abnormal chemical responses that vary significantly among individuals, ranging from extreme sensitivity to low doses to insensitivity to high doses. These reactions often occur due to the drug's covalent binding with serum proteins, forming a foreign hapten that triggers an immunotoxicological response. The variability in drug reactions has a strong pharmacogenetic foundation, with genetic differences crucial in how individuals metabolize drugs. For...

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Related Experiment Video

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Riluzole metabolism and CYP1A1/2 polymorphisms in patients with ALS.

Senda Ajroud-Driss1, Mohammad Saeed, Humaira Khan

  • 1Davee Department of Neurology and Clinical Neurosciences, Northwestern University Institute of Neuroscience, Chicago, Illinois 60611, USA. s-ajroud@md.northwestern.edu

Amyotrophic Lateral Sclerosis : Official Publication of the World Federation of Neurology Research Group on Motor Neuron Diseases
|September 14, 2007
PubMed
Summary

Genetic variations in CYP1A1 and CYP1A2 genes do not appear to affect riluzole metabolism in patients with amyotrophic lateral sclerosis. Further research is needed to understand the genetic regulation of CYP1A enzymes in riluzole metabolism.

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Published on: April 4, 2018

Area of Science:

  • Pharmacogenomics
  • Neuroscience
  • Drug Metabolism

Background:

  • Riluzole is the sole FDA-approved medication for amyotrophic lateral sclerosis (ALS).
  • Riluzole metabolism is primarily attributed to hepatic CYP1A2 and extra-hepatic CYP1A1 enzymes.
  • Genetic polymorphisms in CYP1A2 and CYP1A1 are known, but their impact on riluzole metabolism in ALS patients remains unexamined.

Purpose of the Study:

  • To investigate the association between CYP1A1 and CYP1A2 gene polymorphisms and riluzole metabolic profiles in ALS patients.
  • To determine if specific genetic variations influence riluzole plasma levels.

Main Methods:

  • Study included 32 patients diagnosed with probable or definite ALS receiving riluzole.
  • Plasma riluzole trough and peak levels were quantified using liquid chromatography-mass spectrometry.
  • Genotypes for single nucleotide polymorphisms (SNPs) in CYP1A1 and CYP1A2 genes were analyzed.
  • Statistical analysis (ANOVA, Tukey's HSD) assessed the relationship between genotypes and riluzole levels.

Main Results:

  • The average peak plasma riluzole level was 202 ± 111 ng/ml, and the mean trough level was 54.3 ± 37.5 ng/ml.
  • No significant association was found between the studied CYP1A1 and CYP1A2 polymorphisms and the measured riluzole metabolic profiles.
  • The investigated genetic variations in CYP1A1 and CYP1A2 did not appear to influence riluzole levels in this ALS patient cohort.

Conclusions:

  • Genetic variations within the CYP1A1 and CYP1A2 genes do not seem to significantly impact riluzole levels in patients with amyotrophic lateral sclerosis.
  • Further investigation is warranted to elucidate the genetic regulation of CYP1A enzymes and their precise role in riluzole metabolism.
  • Understanding these genetic factors could potentially optimize riluzole therapy for ALS patients.