Clinical pharmacology studies with indobufen (K 3920): inhibitor of platelet aggregation

J Clin Pharmacol. 1980 May-Jun;20(5-6 Pt 1):316-25. doi: 10.1177/009127008002000502.

Abstract

When given to 12 subjects at single oral doses of 100 and 300 mg, indobufen caused clear-cut, dose-dependent, reversible inhibition of epinephrine- and collagen-induced platelet aggregation. Platelet factor 3 availability and platelet factor 4 release were not affected by the lower dose but were markedly reduced by the 300-mg dose. Bleeding time was slightly influenced by 100 mg, and 300 mg had a more pronounced effect. Indobufen 300 mg was also intravenously injected to five subjects. When washed platelets obtained before indobufen were resuspended in plasma obtained after indobufen, aggregation was inhibited. This was not the case when washed platelets obtained after indobufen were resuspended in plasma obtained before indobufen. These experiments indicate tha indobufen causes reversible inhibition of platelet functions unlike the effect of acetylsalicylic acid.

MeSH terms

  • Aged
  • Bleeding Time
  • Blood Coagulation / drug effects
  • Collagen / pharmacology
  • Drug Interactions
  • Epinephrine / pharmacology
  • Female
  • Humans
  • Indoles / adverse effects
  • Indoles / pharmacology*
  • Isoindoles
  • Male
  • Middle Aged
  • Phenylbutyrates / adverse effects
  • Phenylbutyrates / pharmacology*
  • Platelet Aggregation / drug effects*
  • Platelet Factor 3 / metabolism
  • Platelet Factor 4 / metabolism
  • Viper Venoms / pharmacology

Substances

  • Indoles
  • Isoindoles
  • Phenylbutyrates
  • Viper Venoms
  • Platelet Factor 3
  • Platelet Factor 4
  • indobufen
  • Collagen
  • Epinephrine