Pulmonary embolism (PE)

Pulmonary embolism (PE) is a clinical condition and a major cause of cardiovascular morbidity and mortality, characterized by the obstruction of the pulmonary arteries by material (most commonly a thrombus) that has traveled from elsewhere in the body [1][2]. It is not a molecular target, receptor, or enzyme, but rather a disease state resulting from a breakdown in the balance of the hemostatic system [2]. PE is typically the result of deep vein thrombosis (DVT) where a blood clot dislodges and lodges in the pulmonary vasculature, leading to impaired gas exchange and potential right-sided heart failure [1][3]. Pharmacological intervention for PE focuses on targets within the coagulation cascade—such as Factor Xa, Factor IIa (thrombin), and Vitamin K epoxide reductase—to prevent further clot formation and allow for endogenous fibrinolysis [2][4]. Thrombolytic agents like alteplase are used in high-risk cases to actively dissolve the obstruction by targeting plasminogen [2]. Because it describes a macro-scale pathological event rather than a specific protein or signaling molecule, 'Pulmonary embolism' is considered an indication rather than a therapeutic target in the context of drug discovery. Sources: [1] NIH NHLBI; [2] StatPearls (Pulmonary Embolism); [3] Mayo Clinic; [4] ESC Guidelines 2019.

Other names

Venous thromboembolismPulmonary thromboembolismPELung blood clot

Inhibition of the coagulation cascade (specifically targeting Factor Xa, Thrombin/Factor IIa, or Vitamin K epoxide reductase) or induction of fibrinolysis via the activation of plasminogen.