Abstract
The direct effect of ancrod is defibrinogenation. This results in several secondary effects that differentiate ancrod from typical thrombolytics such as rt-PA. The combined actions of indirect fibrinolysis, reduced fibrin deposition, and decreased blood viscosity represent a constellation of actions that should be beneficial in a variety of thrombotic conditions. The clinical condition explored most thoroughly in recent years with ancrod has been its acute application to ischemic stroke. Two clinical studies (one of them with a 6 h time-to-treatment window) have demonstrated significant benefit in increasing the proportion of patients alive and disability-free at 3 months, but higher doses of the drug appear to increase the risk of symptomatic intracranial hemorrhage and reduce efficacy. Although the evidence is not conclusive, it suggests that, with modified dosing, ancrod could yield a favorable risk–benefit ratio in stroke by limiting the risk of symptomatic intracranial hemorrhage.
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