Pathways

Antrafenine is a piperazine derivative drug that acts as an analgesic and anti-inflammatory drug used for the relief of mild to moderate pain. It targets the prostaglandin G/H synthase-1 (COX-1) and prostaglandin G/H synthase-2 (COX-2) in the cyclooxygenase pathway. The cyclooxygenase pathway begins in the cytosol with phospholipids being converted into arachidonic acid by the action of phospholipase A2. The rest of the pathway occurs on the endoplasmic reticulum membrane, where prostaglandin G/H synthase 1 & 2 converts arachidonic acid into prostaglandin H2. Prostaglandin H2 can either be converted into thromboxane A2 via thromboxane A synthase, prostacyclin/prostaglandin I2 via prostacyclin synthase or prostaglandin E2 via prostaglandin E synthase. COX-2 is an inducible enzyme, and during inflammation, it is responsible for prostaglandin synthesis. It leads to the formation of prostaglandin E2 which is responsible for contributing to the inflammatory response by activating immune cells and for increasing pain sensation by acting on pain fibers. Antrafenine inhibits the action of COX-1 and COX-2 on the endoplasmic reticulum membrane. This reduces the formation of prostaglandin H2 and therefore, prostaglandin E2 (PGE2). The low concentration of prostaglandin E2 attenuates the effect it has on stimulating immune cells and pain fibers, consequently reducing inflammation and pain. Fever is triggered by inflammatory and infectious diseases. Cytokines are produced in the central nervous system (CNS) during an inflammatory response. These cytokines induce COX-2 production that increases the synthesis of prostaglandin, specifically prostaglandin E2 which adjusts hypothalamic temperature control by increasing heat production. Because antrafenine decrease PGE2 in the CNS, it has an antipyretic effect.

Antrafenine (also named Stakane) acts as an anti-inflammatory and analgesic drug. It is not widely used as it has largely been replaced by newer drugs. Antrafenine can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of antrafenine.

Metabolites of Antipyrine are predicted with biotransformer.

Antipyrine is an NSAID used for the symptomatic treatment of acute otitis media, most commonly in combination with benzocaine. Antipyrine possesses anti-inflammatory, analgesic and antipyretic activity. It targets the prostaglandin G/H synthase-1 (COX-1) and prostaglandin G/H synthase-2 (COX-2) in the cyclooxygenase pathway. The cyclooxygenase pathway begins in the cytosol with phospholipids being converted into arachidonic acid by the action of phospholipase A2. The rest of the pathway occurs on the endoplasmic reticulum membrane, where prostaglandin G/H synthase 1 & 2 converts arachidonic acid into prostaglandin H2. Prostaglandin H2 can either be converted into thromboxane A2 via thromboxane A synthase, prostacyclin/prostaglandin I2 via prostacyclin synthase or prostaglandin E2 via prostaglandin E synthase. COX-2 is an inducible enzyme, and during inflammation, it is responsible for prostaglandin synthesis. It leads to the formation of prostaglandin E2 which is responsible for contributing to the inflammatory response by activating immune cells and for increasing pain sensation by acting on pain fibers. Antipyrine inhibits the action of COX-1 and COX-2 on the endoplasmic reticulum membrane. This reduces the formation of prostaglandin H2 and therefore, prostaglandin E2 (PGE2). The low concentration of prostaglandin E2 attenuates the effect it has on stimulating immune cells and pain fibers, consequently reducing inflammation and pain. Fever is triggered by inflammatory and infectious diseases. Cytokines are produced in the central nervous system (CNS) during an inflammatory response. These cytokines induce COX-2 production that increases the synthesis of prostaglandin, specifically prostaglandin E2 which adjusts hypothalamic temperature control by increasing heat production. Because antipyrine decreases PGE2 in the CNS, it has an antipyretic effect. Antipyretic effects results in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation.

Antipyrine (also named Fenazone or Phenazone) is often used for testing the effect of other drugs on drug-metabolizing enzymes in the liver. Antipyrine can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of antipyrine.

Antihemophilic factor, human recombinant of the coagulation Factor VIII, also known as Advate, Adynovate, Helixate, Kogenate, Kovaltry, Novoeight, Recombinate, to treat hemophilia A, von Willebrand disease and Factor XIII deficiency. Antihemophilic factor, human recombinant is administered intravenously and acts to correct coagulation defects, by activating coagulation factor X and IX.

Antihemophilic factor human, also known as Hemofil, Koate, and Wilate is used as factor VIII replacement therapy to treat hemophilia A. It is a non-recombinant concentrate of the endogenous coagulation factor VIII, produced by reducing von Willebrand Factor antigen and purified by affinity chromatography. Hemophilia A is caused by mutations in the coagulation factor VIII gene that leads to functional deficiency and or complete loss of the coagulation factor. These mutations lead to bleeding and being able to bruise easily, exogenous replacement of coagulation factor VIII in order to counteract the deficiencies. Administered intravenously the antihemophilic factor human replaces the abnormal coagulation factor VIII, acting as a cofactor to activate coagulation factor IX and X.