About: Epoprostenol     Goto   Sponge   NotDistinct   Permalink

An Entity of Type : http://linked.opendata.cz/ontology/drugbank/Drug, within Data Space : linked.opendata.cz associated with source document(s)

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rdf:type
http://linked.open...gbank/description
  • A prostaglandin that is a powerful vasodilator and inhibits platelet aggregation. It is biosynthesized enzymatically from prostaglandin endoperoxides in human vascular tissue. The sodium salt has been also used to treat primary pulmonary hypertension. (en)
http://linked.open...y/drugbank/dosage
http://linked.open...gy/drugbank/group
  • approved (en)
http://linked.open...drugbank/halfLife
  • The in vitro half-life of epoprostenol in human blood at 37°C and pH 7.4 is approximately 6 minutes; the in vivo half-life of epoprostenol in humans is therefore expected to be no greater than 6 minutes. (en)
http://linked.open...ugbank/indication
  • For the long-term intravenous treatment of primary pulmonary hypertension and pulmonary hypertension associated with the scleroderma spectrum of disease in NYHA Class III and Class IV patients who do not respond adequately to conventional therapy. (en)
sameAs
Title
  • Epoprostenol (en)
adms:identifier
http://linked.open...mechanismOfAction
  • Prostaglandins are present in most body tissues and fluids and mediate many biological functions. Epoprostenol (PGI2) is a member of the family of prostaglandins that is derived from arachidonic acid. The major pharmacological actions of epoprostenol is ultimately inhibition of platelet aggregation. Prostacyclin (PGI2) is released by healthy endothelial cells and performs its function through a paracrine signaling cascade that involves G protein-coupled receptors on nearby platelets and endothelial cells. The platelet Gs protein-coupled receptor (prostacyclin receptor) is activated when it binds to PGI2. This activation, in turn, signals adenylyl cyclase to produce cAMP. cAMP goes on to inhibit any undue platelet activation (in order to promote circulation) and also counteracts any increase in cytosolic calcium levels which would result from thromboxane A2 (TXA2) binding (leading to platelet activation and subsequent coagulation). PGI2 also binds to endothelial prostacyclin receptors and in the same manner raise cAMP levels in the cytosol. This cAMP then goes on to activate protein kinase A (PKA). PKA then continues the cascade by phosphorylating and inhibiting myosin light-chain kinase which leads to smooth muscle relaxation and vasodilation. Notably, PGI2 and TXA2 work as physiological antagonists. (en)
http://linked.open...drugbank/packager
http://linked.open...outeOfElimination
  • Epoprostenol is metabolized to 2 primary metabolites: 6-keto-PGF1α (formed by spontaneous degradation) and 6,15-diketo-13,14-dihydro-PGF1α (enzymatically formed), both of which have pharmacological activity orders of magnitude less than epoprostenol in animal test systems. Fourteen additional minor metabolites have been isolated from urine, indicating that epoprostenol is extensively metabolized in humans. (en)
http://linked.open.../drugbank/synonym
  • Epoprostenol (en)
  • Flolan (en)
  • PGI2 (en)
  • Prostacyclin (en)
  • Prostaglandin I2 (en)
  • PGX (en)
  • (5Z,13e)-(15S)-6,9alpha-Epoxy-11alpha,15-dihydroxyprosta-5,13-dienoate (en)
  • (5Z,9alpha,11alpha,13e,15S)-6,9-Epoxy-11,15-dihydroxyprosta-5,13-dien-1-oic acid (en)
  • Prostaglandin x (en)
  • Vasocyclin (en)
http://linked.open...drugbank/toxicity
  • Symptoms of overdose are extensions of its dose-limiting pharmacologic effects and include flushing, headache, hypotension, nausea, vomiting, and diarrhea. Most events were self-limiting and resolved with reduction or withholding of epoprostenol. Single intravenous doses at 10 and 50 mg/kg (2703 and 27,027 times the recommended acute phase human dose based on body surface area) were lethal to mice and rats, respectively. Symptoms of acute toxicity were hypoactivity, ataxia, loss of righting reflex, deep slow breathing, and hypothermia. (en)
http://linked.open...umeOfDistribution
  • * 357 mL/kg (en)
http://linked.open.../drug/hasAHFSCode
http://linked.open...ynthesisReference
  • Nagesh R. Palepu, "NOVEL EPOPROSTENOL FORMULATION AND METHOD OF MAKING THEREOF." U.S. Patent US20090088468, issued April 02, 2009. (en)
foaf:page
http://linked.open...ugbank/IUPAC-Name
http://linked.open...gy/drugbank/InChI
http://linked.open...Molecular-Formula
http://linked.open.../Molecular-Weight
http://linked.open...noisotopic-Weight
http://linked.open...y/drugbank/SMILES
http://linked.open.../Water-Solubility
http://linked.open...ogy/drugbank/logP
http://linked.open...ogy/drugbank/logS
http://linked.open...l/drug/hasATCCode
http://linked.open...nd-Acceptor-Count
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http://linked.open...drugbank/InChIKey
http://linked.open...urface-Area--PSA-
http://linked.open...nk/Polarizability
http://linked.open...bank/Refractivity
http://linked.open...atable-Bond-Count
http://linked.open.../affectedOrganism
  • Humans and other mammals (en)
http://linked.open...casRegistryNumber
  • 35121-78-9 (en)
http://linked.open...drugbank/category
  • (en)
http://linked.open...gbank/containedIn
http://linked.open...k/Bioavailability
http://linked.open...bank/Ghose-Filter
http://linked.open...nk/MDDR-Like-Rule
http://linked.open...k/Number-of-Rings
http://linked.open...siological-Charge
http://linked.open...bank/Rule-of-Five
http://linked.open...tional-IUPAC-Name
http://linked.open...strongest-acidic-
http://linked.open...-strongest-basic-
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