The in vitro effects of Xancor, a synthetic astaxanthine derivative, on hemostatic biomarkers in aspirin-naïve and aspirin-treated subjects with multiple risk factors for vascular disease

Am J Ther. 2010 Mar-Apr;17(2):125-32. doi: 10.1097/MJT.0b013e31819cdbbd.

Abstract

Astaxanthine is a polar carotenoid metabolite derived from a proprietary prodrug, Xancor, which aligns parallel with the membrane phospholipids exhibiting potent antioxidant, anti-inflammatory, and cell protective properties, although the precise mechanism of action is unknown. This prodrug is currently under development for hepatic, neurologic, and vascular disease indications. Considering established links between heart disease and stroke with platelets, coagulation cascade, and fibrinolysis, the aim of the study was to assess the effect of asthaxantine on human biomarkers of hemostasis. The rationale was to test a hypothesis that the drug may diminish activation of hemostasis, making it a potentially attractive addition to treat patients with vascular disease. In vitro effects of whole blood preincubation with escalating concentrations of asthaxantine (0.3 microM, 1 microM, 3 microM, 10 microM, 30 microM, and 100 microM) were assessed from 12 aspirin-naïve and eight aspirin-treated volunteers with multiple risk factors for vascular disease. A total of 25 biomarkers were measured, of which 12 were related to platelet function, 10 to coagulation, and three to fibrinolysis. Platelet aggregation induced by ADP, collagen, and arachidonic acid and expression of CD31, CD41, GP IIb/IIIa, CD51/61, P-selectin, CD63, CD107a, CD151+CD14, and CD154 were not affected. Coagulation indices such as aPTT, prothrombin time, thrombin time, fibrinogen, antithrombin III (antigen and activity), Protein C, Protein S (free and activity), and von Willebrand factor remained unchanged after incubation with astaxanthine. Fibrinolytic activity biomarkers such as plasminogen, D-dimer, and FDP were also not affected after in vitro pretreatment of blood samples with astaxanthine. In the projected subclinical (less than 1 microM), therapeutic (3 microM to 30 microM), and supratherapeutic concentration (100 microM), astaxanthine in vitro does not affect platelet, coagulation, or fibrinolytic indices in either aspirin-naïve or aspirin-treated subjects. These results are important for the assessment of the safety profile, but remain to be confirmed preclinically, in vivo, and ultimately in the clinic.

Publication types

  • Controlled Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antioxidants / administration & dosage
  • Antioxidants / adverse effects
  • Antioxidants / pharmacology*
  • Aspirin / pharmacology*
  • Biomarkers / metabolism
  • Blood Coagulation / drug effects
  • Dose-Response Relationship, Drug
  • Drug Interactions
  • Female
  • Fibrinolysis / drug effects
  • Hemostasis / drug effects
  • Humans
  • Male
  • Middle Aged
  • Platelet Aggregation / drug effects
  • Platelet Aggregation Inhibitors / pharmacology
  • Prodrugs
  • Risk Factors
  • Single-Blind Method
  • Xanthophylls / administration & dosage
  • Xanthophylls / adverse effects
  • Xanthophylls / metabolism
  • Xanthophylls / pharmacology*

Substances

  • Antioxidants
  • Biomarkers
  • Platelet Aggregation Inhibitors
  • Prodrugs
  • Xancor
  • Xanthophylls
  • astaxanthine
  • Aspirin