iTTP is characterized by uncontrolled blood clotting in small blood vessels resulting from an autoimmune attack on the ADAMTS13 enzyme. Conventional treatment involves plasma exchange, which can only partially restore ADAMTS13 activity. The new drug, a genetically modified version of the missing enzyme called rADAMTS13, offers significant advances by potentially providing higher levels of ADAMTS13.
Despite initial doubts about the drug’s effectiveness due to the presence of inhibitory autoantibodies in patients with iTTP, rADAMTS13 rapidly reversed the disease process in a critically ill patient, noted the study’s lead author, Pavan K. Bendapudi. This patient, a young mother, did not respond to standard plasma exchange therapy.
Bendapudi emphasized that rADAMTS13 could replace existing treatments and advocated for larger studies to further evaluate its effectiveness.
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Source: Ferra
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