Reprint

Drug—Drug Interactions

Edited by
September 2021
242 pages
  • ISBN978-3-0365-2035-3 (Hardback)
  • ISBN978-3-0365-2036-0 (PDF)

This book is a reprint of the Special Issue Drug–Drug Interactions that was published in

Biology & Life Sciences
Chemistry & Materials Science
Medicine & Pharmacology
Summary

Drug–drug interactions (DDIs) cause a drug to affect other drugs, leading to reduced drug efficacy or increased toxicity of the affected drug. Some well-known interactions are known to be the cause of adverse drug reactions (ADRs) that are life threatening to the patient. Traditionally, DDI have been evaluated around the selective action of drugs on specific CYP enzymes. The interaction of drugs with CYP remains very important in drug interactions but, recently, other important mechanisms have also been studied as contributing to drug interaction including transport- or UDP-glucuronyltransferase as a Phase II reaction-mediated DDI. In addition, novel mechanisms of regulating DDIs can also be suggested. In the case of the substance targeted for interaction, not only the DDIs but also the herb–drug or food–drug interactions have been reported to be clinically relevant in terms of adverse side effects. Reporting examples of drug interactions on a marketed drug or studies on new mechanisms will be very helpful for preventing the side effects of the patient taking these drugs. This Special Issue aims to highlight current progress in understanding both the clinical and nonclinical interactions of commercial drugs and the elucidation of the mechanisms of drug interactions.

Format
  • Hardback
License
© 2022 by the authors; CC BY-NC-ND license
Keywords
tadalafil; ticagrelor; drug-drug interaction; pharmacokinetics; plasma concentration; CYP3A4; Loxoprofen; drug-drug interaction; CYP3A; Dexamethasone; Ketoconazole; CYP2D6; O-desmethyltramadol; pharmacokinetics; physiologically-based pharmacokinetics; tramadol; (‒)-sophoranone; CYP2C9; potent inhibition; in vitro; in vivo; drug interaction; low permeability; high plasma protein binding; biflavonoid; cytochrome P450; drug interactions; selamariscina A; uridine 5′-diphosphoglucuronosyl transferase; drug interaction; pharmacokinetics; tissue-specific; systemic exposure; P-glycoprotein (P-gp); organic anion transporting polypeptide 1A2 (OATP1A2); Rumex acetosa; pharmacokinetics; fexofenadine; drug interaction; chronic kidney disease; drug–drug interactions; polypharmacy; adverse drug reactions; Lexicomp; subset analysis; signal detection algorithms; drug-drug interaction; spontaneous reporting systems; drug–drug interactions; mechanism-based inhibition; competitive inhibition; non-competitive inhibition; substrate; inhibitor; cytochromes P450; OATP1B1; OATP1B3; tyrosine kinase inhibitors; drug-drug interactions; migraine; lasmiditan; gepants; monoclonal antibodies; drug–drug interactions; cytochrome P450; CYP1A1; CYP1A2; drug–drug interaction; expression; metabolism; regulation; drug transporter; ubiquitination; ixazomib; regulation; drug interaction; DDI; computational prediction; in silico; QSAR; drug metabolism; ADME; pharmacokinetics; CYP; polypharmacy; metabolic DDI; P450; 1A2; 2B6; 2C19; 2C8; 2C9; 2D6; 3A4