Title:Colchicine Pharmacokinetics and Mechanism of Action
VOLUME: 24 ISSUE: 6
Author(s):Christos Angelidis*, Zoi Kotsialou, Charalampos Kossyvakis, Agathi-Rosa Vrettou, Achilleas Zacharoulis, Fotios Kolokathis, Vasilios Kekeris and Georgios Giannopoulos
Affiliation:2nd Department of Cardiology, Medical School, Attikon Hospital, National and Kapodistrian University of Athens, Athens, 2nd Department of Cardiology, Medical School, Attikon Hospital, National and Kapodistrian University of Athens, Athens, Department of Cardiology, "G. Gennimatas" General Hospital of Athens, Athens, 2nd Department of Cardiology, Medical School, Attikon Hospital, National and Kapodistrian University of Athens, Athens, 2nd Department of Cardiology, Medical School, Attikon Hospital, National and Kapodistrian University of Athens, Athens, 2nd Department of Cardiology, Medical School, Attikon Hospital, National and Kapodistrian University of Athens, Athens, Department of Cardiology, "G. Gennimatas" General Hospital of Athens, Athens, Department of Cardiology, "G. Gennimatas" General Hospital of Athens, Athens
Keywords:Colchicine, inflammation, mechanism of action, microtubules, pharmacokinetics, toxicity.
Abstract:Colchicine is a tricyclic, lipid-soluble alkaloid derived from the plant of the Lily family Colchicum
autumnale, sometimes called the “autumn crocus”. It is predominantly metabolized in the gastrointestinal tract.
Two proteins, P-glycoprotein (P-gp) and CYP3A4 seem to play a pivotal role, governing its pharmacokinetic. The
commonest side effects are gastrointestinal (nausea, vomiting and particularly dose-related-diarrhea) occurring in
5-10% of patients. Colchicine exerts its unique action mainly through inhibition of microtubule polymerization.
Microtubule polymerization affects a variety of cellular processes including maintenance of shape, signaling,
division, migration, and cellular transport. Colchicine interferes with several inflammatory pathways including
adhesion and recruitment of neutrophils, superoxide production, inflammasome activation, the RhoA/Rho effector
kinase (ROCK) pathway and the tumor necrosis factor alpha (TNF-α) -induced nuclear factor κΒ (NF-κΒ) pathway
attenuating the inflammatory response. This concise paper attempts to give a brief review of its pharmacokinetic
properties and its main mechanisms of action.
