A 65-year-old patient with an anterior STEMI receives tenecteplase. Unlike streptokinase, tenecteplase is preferred because it:
- A Does not require a cofactor and directly cleaves fibrin-bound plasminogen
- B Activates both plasminogen and directly dissolves thrombus through enzymatic digestion of fibrin
- C Inhibits plasminogen activator inhibitor-1 (PAI-1) indirectly increasing native plasminogen activator levels
- D Has greater fibrin specificity, longer half-life enabling single bolus dosing, and is non-antigenic ✓
Explanation
Tenecteplase is an engineered variant of tPA (tissue plasminogen activator) with three modifications: T103N (increased fibrin binding), N117Q (reduced clearance), and KHRR→AAAA (50-fold reduced sensitivity to PAI-1 inhibition). These modifications confer greater fibrin specificity (less systemic plasminogenolysis, reducing systemic bleeding), a longer half-life (~20 minutes, allowing single IV bolus instead of infusion), and it is non-antigenic unlike streptokinase (which is derived from Streptococcus and cannot be re-used).
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.