Translational Sciences Inc.

Novel ?2-ANTIPLASMIN Inactivation for Lysis of Intravascular Thrombi (nail-it) Trial - Each Year Venous Thromboembolism Affects Up to 2 Million Americans and 24 Million People Worldwide. Patients With Venous Thromboembolism Have Blood Clots in the Legs (venous Thrombosis) That May Travel to the Lungs (pulmonary Embolism). Pulmonary Embolism (PE) Is a Leading Cause of Hospital Deaths. Pulmonary Emboli May Acutely Obstruct Blood Flow, Causing Right Heart Failure, Circulatory Collapse and Death Within Hours or Days. Over a Longer Period of Time, Persistent Pulmonary Emboli May Cause Serious, Disabling Complications Such as Chronic Thromboembolic Pulmonary Hypertension and Right Heart Failure for More Than 85 Years, Anticoagulation Has Been Standard Therapy for Pe. Anticoagulation Does Not Dissolve Thrombi and Is an Inadequate Treatment for Massive Pe. However, Treatment With a Thrombus- Dissolving Agent, Such as Recombinant Tissue Plasminogen Activator (r-tpa), Dissolves Pulmonary Emboli to Improve Heart Pressures, Reduce Clot Burden, Increase the Ability of the Lung Tissue to Oxygenate the Blood and Decrease Post-thrombotic Symptoms Better Than Standard Anticoagulation Therapy. Nevertheless, R-tpa-like Agents Cause Severe or Fatal Hemorrhage and the Benefit of R-tpa Therapy Exceeds the Risk of Bleeding Only in Patients That Face Imminent Death From Massive Pe. for the Vast Majority of Patients, R-tpa Therapy Is Not Safe, Even in Those Patients With Intermediate-risk Pe, Which May Have 30-DAY Death Rates as High as 10%.TO Save Lives, Reduce Recurrent Thrombosis and Decrease Long Term Complications in Patients With Pe, Translational Sciences (TSI) Seeks to Develop a Therapeutic A2AP-INACTIVATING Monoclonal Antibody (A2AP-I) as the First New Class of Safe, Thrombus-dissolving Agents Since Plasminogen Activator Therapy Was First Used in Humans > 60 Years Ago. This New Therapy Is Targeted to Neutralize A2AP, the Major Inhibitor of Thrombus Dissolution in Vivo. Extensive Research From Our Lab and Others Has Shown That A2AP Deficiency, or an A2AP-I Removes the Brakes on Thrombus Dissolution by Activating Endogenous Fibrinolysis, Causing Venous Thrombi and Pulmonary Emboli to Dissolve Spontaneously Without Causing Bleeding. Even in Experimental Stroke, Where the Ischemic Brain Is a Sensitive Test of Therapeutic Risk, A2AP-I Therapy Enhances Thrombus Dissolution, Reduces Brain Infarction, Decreases Brain Hemorrhage and Saves Lives by Comparison to R-tpa. an A2AP-I Has Extraordinary Potential for Improving the Treatment of Pe. on the Basis of Pre-clinical Data, We Project That by Comparison to Current Therapy, Treatment With TS23 Could Significantly Reduce Right Heart Failure, Improve Survival, Decrease Recurrent Thrombosis and Prevent Long-term Disability in Patients With Pulmonary Embolism. Tsi Currently Holds an Ind for Phase Ii Trial of TS23 in Pe and Now Brings Together Leading Investigators for an Efficient Trial to Assess the Safety and Efficacy of TS23 in Patients With Intermediate-risk Pulmonary Embolism.