This HTML5 document contains 189 embedded RDF statements represented using HTML+Microdata notation.

The embedded RDF content will be recognized by any processor of HTML5 Microdata.

Namespace Prefixes

PrefixIRI
n2http://linked.opendata.cz/resource/drugbank/drug/
dctermshttp://purl.org/dc/terms/
n29http://linked.opendata.cz/resource/drugbank/drug/DB00178/identifier/chebi/
n25http://linked.opendata.cz/resource/AHFS/
foafhttp://xmlns.com/foaf/0.1/
n15http://linked.opendata.cz/resource/mesh/concept/
n4http://linked.opendata.cz/resource/drugbank/company/
n23http://linked.opendata.cz/resource/drugbank/dosage/
n24http://linked.opendata.cz/resource/drugbank/mixture/
n12http://linked.opendata.cz/resource/drugbank/drug/DB00178/identifier/wikipedia/
n31http://linked.opendata.cz/resource/drugbank/drug/DB00178/identifier/pharmgkb/
n13http://www.drugs.com/
n20http://bio2rdf.org/drugbank:
n7http://linked.opendata.cz/resource/drugbank/drug/DB00178/identifier/pubchem-compound/
n22http://www.pdrhealth.com/drugs/rx/
admshttp://www.w3.org/ns/adms#
n10http://www.rxlist.com/cgi/generic/
n8http://linked.opendata.cz/resource/drugbank/drug/DB00178/identifier/pubchem-substance/
n18http://linked.opendata.cz/resource/drugbank/patent/
n32http://linked.opendata.cz/resource/drugbank/drug/DB00178/identifier/kegg-drug/
n27http://wifo5-03.informatik.uni-mannheim.de/drugbank/resource/drugs/
n28http://linked.opendata.cz/resource/drugbank/drug/DB00178/identifier/drugbank/
rdfhttp://www.w3.org/1999/02/22-rdf-syntax-ns#
n11http://linked.opendata.cz/resource/drugbank/medicinal-product/
n14http://linked.opendata.cz/ontology/mesh/
owlhttp://www.w3.org/2002/07/owl#
n3http://linked.opendata.cz/ontology/drugbank/
n30http://linked.opendata.cz/resource/drugbank/drug/DB00178/identifier/national-drug-code-directory/
n5http://linked.opendata.cz/resource/drugbank/property/
xsdhhttp://www.w3.org/2001/XMLSchema#
n17http://linked.opendata.cz/resource/atc/
n26http://linked.opendata.cz/resource/drugbank/drug/DB00178/identifier/chemspider/
n16http://linked.opendata.cz/ontology/sukl/drug/

Statements

Subject Item
n2:DB00178
rdf:type
n3:Drug
n3:description
Ramipril is a prodrug belonging to the angiotensin-converting enzyme (ACE) inhibitor class of medications. It is metabolized to ramiprilat in the liver and, to a lesser extent, kidneys. Ramiprilat is a potent, competitive inhibitor of ACE, the enzyme responsible for the conversion of angiotensin I (ATI) to angiotensin II (ATII). ATII regulates blood pressure and is a key component of the renin-angiotensin-aldosterone system (RAAS). Ramipril may be used in the treatment of hypertension, congestive heart failure, nephropathy, and to reduce the rate of death, myocardial infarction and stroke in individuals at high risk of cardiovascular events.
n3:dosage
n23:271B5280-363D-11E5-9242-09173F13E4C5 n23:271B5281-363D-11E5-9242-09173F13E4C5 n23:271B5282-363D-11E5-9242-09173F13E4C5 n23:271B5283-363D-11E5-9242-09173F13E4C5 n23:271B527F-363D-11E5-9242-09173F13E4C5 n23:271B5284-363D-11E5-9242-09173F13E4C5 n23:271B5285-363D-11E5-9242-09173F13E4C5
n3:generalReferences
# Cacciapuoti F, Capasso A, Mirra G, De Nicola A, Minicucci F, Gentile S: Prevention of left ventricular hypertrophy by ACE-inhibitor, ramipril in comparison with calcium-channel antagonist, felodipine. Int J Cardiol. 1998 Jan 31;63(2):175-8. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/9510492 # Kleinert S: HOPE for cardiovascular disease prevention with ACE-inhibitor ramipril. Heart Outcomes Prevention Evaluation. Lancet. 1999 Sep 4;354(9181):841. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/10485736
n3:group
approved
n3:halfLife
Plasma concentrations of ramiprilat decline in a triphasic manner. Initial rapid decline represents distribution into tissues and has a half life of 2-4 hours. The half life of the apparent elimination phase is 9-18 hours and that of the terminal elimination phase is > 50 hours. Two elimination phases occur as a result of ramiprilat's potent binding to ACE and slow dissociation from the enzyme. The half life of ramiprilat after multiple daily doses (MDDs) is dose-dependent, ranging from 13-17 hours with 5-10 mg MDDs to 27-36 hours for 2.5 mg MDDs.
n3:indication
For the management of mild to severe hypertension. May be used to reduce cardiovascular mortality following myocardial infarction in hemodynamically stable individuals who develop clinical signs of congestive heart failure within a few days following myocardial infarction. To reduce the rate of death, myocardial infarction and stroke in individuals at high risk of cardiovascular events. May be used to slow the progression of renal disease in individuals with hypertension, diabetes mellitus and microalubinuria or overt nephropathy.
n3:manufacturer
n4:271B5245-363D-11E5-9242-09173F13E4C5 n4:271B5246-363D-11E5-9242-09173F13E4C5 n4:271B5243-363D-11E5-9242-09173F13E4C5 n4:271B5244-363D-11E5-9242-09173F13E4C5 n4:271B5247-363D-11E5-9242-09173F13E4C5 n4:271B523A-363D-11E5-9242-09173F13E4C5 n4:271B523D-363D-11E5-9242-09173F13E4C5 n4:271B523E-363D-11E5-9242-09173F13E4C5 n4:271B523B-363D-11E5-9242-09173F13E4C5 n4:271B523C-363D-11E5-9242-09173F13E4C5 n4:271B5241-363D-11E5-9242-09173F13E4C5 n4:271B5242-363D-11E5-9242-09173F13E4C5 n4:271B523F-363D-11E5-9242-09173F13E4C5 n4:271B5240-363D-11E5-9242-09173F13E4C5
owl:sameAs
n20:DB00178 n27:DB00178
dcterms:title
Ramipril
adms:identifier
n7:5362129 n8:46506390 n12:Ramipril n26:4514937 n28:DB00178 n29:8774 n30:54868-5896-0 n31:PA451223 n32:D00421
n3:mechanismOfAction
There are two isoforms of ACE: the somatic isoform, which exists as a glycoprotein comprised of a single polypeptide chain of 1277; and the testicular isoform, which has a lower molecular mass and is thought to play a role in sperm maturation and binding of sperm to the oviduct epithelium. Somatic ACE has two functionally active domains, N and C, which arise from tandem gene duplication. Although the two domains have high sequence similarity, they play distinct physiological roles. The C-domain is predominantly involved in blood pressure regulation while the N-domain plays a role in hematopoietic stem cell differentiation and proliferation. ACE inhibitors bind to and inhibit the activity of both domains, but have much greater affinity for and inhibitory activity against the C-domain. Ramiprilat, the principle active metabolite of ramipril, competes with ATI for binding to ACE and inhibits and enzymatic proteolysis of ATI to ATII. Decreasing ATII levels in the body decreases blood pressure by inhibiting the pressor effects of ATII as described in the Pharmacology section above. Ramipril also causes an increase in plasma renin activity likely due to a loss of feedback inhibition mediated by ATII on the release of renin and/or stimulation of reflex mechanisms via baroreceptors.
n3:packager
n4:271B5234-363D-11E5-9242-09173F13E4C5 n4:271B5221-363D-11E5-9242-09173F13E4C5 n4:271B5222-363D-11E5-9242-09173F13E4C5 n4:271B521F-363D-11E5-9242-09173F13E4C5 n4:271B5220-363D-11E5-9242-09173F13E4C5 n4:271B521D-363D-11E5-9242-09173F13E4C5 n4:271B521E-363D-11E5-9242-09173F13E4C5 n4:271B521B-363D-11E5-9242-09173F13E4C5 n4:271B521C-363D-11E5-9242-09173F13E4C5 n4:271B5219-363D-11E5-9242-09173F13E4C5 n4:271B521A-363D-11E5-9242-09173F13E4C5 n4:271B5217-363D-11E5-9242-09173F13E4C5 n4:271B5218-363D-11E5-9242-09173F13E4C5 n4:271B5215-363D-11E5-9242-09173F13E4C5 n4:271B5216-363D-11E5-9242-09173F13E4C5 n4:271B5231-363D-11E5-9242-09173F13E4C5 n4:271B5232-363D-11E5-9242-09173F13E4C5 n4:271B522F-363D-11E5-9242-09173F13E4C5 n4:271B5230-363D-11E5-9242-09173F13E4C5 n4:271B522D-363D-11E5-9242-09173F13E4C5 n4:271B522E-363D-11E5-9242-09173F13E4C5 n4:271B522B-363D-11E5-9242-09173F13E4C5 n4:271B522C-363D-11E5-9242-09173F13E4C5 n4:271B5229-363D-11E5-9242-09173F13E4C5 n4:271B522A-363D-11E5-9242-09173F13E4C5 n4:271B5227-363D-11E5-9242-09173F13E4C5 n4:271B5228-363D-11E5-9242-09173F13E4C5 n4:271B5225-363D-11E5-9242-09173F13E4C5 n4:271B5226-363D-11E5-9242-09173F13E4C5 n4:271B5223-363D-11E5-9242-09173F13E4C5 n4:271B5224-363D-11E5-9242-09173F13E4C5 n4:271B5239-363D-11E5-9242-09173F13E4C5 n4:271B5237-363D-11E5-9242-09173F13E4C5 n4:271B5238-363D-11E5-9242-09173F13E4C5 n4:271B5235-363D-11E5-9242-09173F13E4C5 n4:271B5236-363D-11E5-9242-09173F13E4C5 n4:271B5233-363D-11E5-9242-09173F13E4C5
n3:patent
n18:1338344 n18:7368469 n18:2382387 n18:5403856
n3:synonym
Tritace (2S-(1(R*(r*)),2alpha,3abeta,6abeta))-1-(2-((1-(ethoxycarbonyl)-3-phenylpropyl)amino)-1-oxopropyl)octahydrocyclopenta(b)pyrrole-2-carboxylic acid Altace (tn) Ramiprilum Ramipril
n3:toxicity
Symptoms of overdose may include excessive peripheral vasodilation (with marked hypotension and shock), bradycardia, electrolyte disturbances, and renal failure. The most likely adverse reactions are symptoms attributable to its blood-pressure lowing effect. May cause headache, dizziness, asthenia, chest pain, nausea, peripheral edema, somnolence, impotence, rash, arthritis, and dyspnea. LD<sub>50</sub> = 10933 mg/kg (orally in mice).
n16:hasAHFSCode
n25:24-32-04
n3:foodInteraction
Alcohol may increase the vasodilatory effects of ramipril. Herbs that may attenuate the antihypertensive effect of ramipril include: bayberry, blue cohash, cayenne, ephedra, ginger, ginseng (American), kola and licorice. Ramipril decreases the excretion of potassium. Salt substitutes containing potassium increase the risk of hyperkalemia. Take without regard to meals. High salt intake may attenuate the antihypertensive effect of ramipril.
n3:mixture
n24:271B5214-363D-11E5-9242-09173F13E4C5
n3:proteinBinding
Protein binding of ramipril is about 73% and that of ramiprilat about 56%.
n3:synthesisReference
Edward Wilson, Martin Beasley, "Stabilized ramipril compositions and methods of making." U.S. Patent US20060134213, issued June 22, 2006.
n14:hasConcept
n15:M0026184
foaf:page
n10:ramipril.htm n13:ramipril.html n22:rx-mono.aspx?contentFileName=alt1014.html&contentName=Altace&contentId=44
n3:IUPAC-Name
n5:271B528A-363D-11E5-9242-09173F13E4C5
n3:InChI
n5:271B5290-363D-11E5-9242-09173F13E4C5
n3:Molecular-Formula
n5:271B528F-363D-11E5-9242-09173F13E4C5
n3:Molecular-Weight
n5:271B528C-363D-11E5-9242-09173F13E4C5
n3:Monoisotopic-Weight
n5:271B528D-363D-11E5-9242-09173F13E4C5
n3:SMILES
n5:271B528E-363D-11E5-9242-09173F13E4C5
n3:Water-Solubility
n5:271B5288-363D-11E5-9242-09173F13E4C5 n5:271B52A0-363D-11E5-9242-09173F13E4C5
n3:logP
n5:271B5289-363D-11E5-9242-09173F13E4C5 n5:271B5286-363D-11E5-9242-09173F13E4C5 n5:271B52A2-363D-11E5-9242-09173F13E4C5
n3:logS
n5:271B5287-363D-11E5-9242-09173F13E4C5
n16:hasATCCode
n17:C09AA05
n3:H-Bond-Acceptor-Count
n5:271B5296-363D-11E5-9242-09173F13E4C5
n3:H-Bond-Donor-Count
n5:271B5297-363D-11E5-9242-09173F13E4C5
n3:InChIKey
n5:271B5291-363D-11E5-9242-09173F13E4C5
n3:Polar-Surface-Area--PSA-
n5:271B5292-363D-11E5-9242-09173F13E4C5
n3:Polarizability
n5:271B5294-363D-11E5-9242-09173F13E4C5
n3:Refractivity
n5:271B5293-363D-11E5-9242-09173F13E4C5
n3:Rotatable-Bond-Count
n5:271B5295-363D-11E5-9242-09173F13E4C5
n3:absorption
The extent of absorption is at least 50-60%. Food decreases the rate of absorption from the GI tract without affecting the extent of absorption. The absolute bioavailabilities of ramipril and ramiprilat were 28% and 44%, respectively, when oral administration was compared to intravenous administration.
n3:affectedOrganism
Humans and other mammals
n3:casRegistryNumber
87333-19-5
n3:category
n3:containedIn
n11:271B5270-363D-11E5-9242-09173F13E4C5 n11:271B5271-363D-11E5-9242-09173F13E4C5 n11:271B526E-363D-11E5-9242-09173F13E4C5 n11:271B526F-363D-11E5-9242-09173F13E4C5 n11:271B526C-363D-11E5-9242-09173F13E4C5 n11:271B526D-363D-11E5-9242-09173F13E4C5 n11:271B526A-363D-11E5-9242-09173F13E4C5 n11:271B526B-363D-11E5-9242-09173F13E4C5 n11:271B5268-363D-11E5-9242-09173F13E4C5 n11:271B5269-363D-11E5-9242-09173F13E4C5 n11:271B5266-363D-11E5-9242-09173F13E4C5 n11:271B5267-363D-11E5-9242-09173F13E4C5 n11:271B5264-363D-11E5-9242-09173F13E4C5 n11:271B5265-363D-11E5-9242-09173F13E4C5 n11:271B5262-363D-11E5-9242-09173F13E4C5 n11:271B5263-363D-11E5-9242-09173F13E4C5 n11:271B527E-363D-11E5-9242-09173F13E4C5 n11:271B527C-363D-11E5-9242-09173F13E4C5 n11:271B527D-363D-11E5-9242-09173F13E4C5 n11:271B527A-363D-11E5-9242-09173F13E4C5 n11:271B527B-363D-11E5-9242-09173F13E4C5 n11:271B5278-363D-11E5-9242-09173F13E4C5 n11:271B5279-363D-11E5-9242-09173F13E4C5 n11:271B5276-363D-11E5-9242-09173F13E4C5 n11:271B5277-363D-11E5-9242-09173F13E4C5 n11:271B5274-363D-11E5-9242-09173F13E4C5 n11:271B5275-363D-11E5-9242-09173F13E4C5 n11:271B5272-363D-11E5-9242-09173F13E4C5 n11:271B5273-363D-11E5-9242-09173F13E4C5 n11:271B5250-363D-11E5-9242-09173F13E4C5 n11:271B5251-363D-11E5-9242-09173F13E4C5 n11:271B524E-363D-11E5-9242-09173F13E4C5 n11:271B524F-363D-11E5-9242-09173F13E4C5 n11:271B524C-363D-11E5-9242-09173F13E4C5 n11:271B524D-363D-11E5-9242-09173F13E4C5 n11:271B524A-363D-11E5-9242-09173F13E4C5 n11:271B524B-363D-11E5-9242-09173F13E4C5 n11:271B5248-363D-11E5-9242-09173F13E4C5 n11:271B5249-363D-11E5-9242-09173F13E4C5 n11:271B5260-363D-11E5-9242-09173F13E4C5 n11:271B5261-363D-11E5-9242-09173F13E4C5 n11:271B525E-363D-11E5-9242-09173F13E4C5 n11:271B525F-363D-11E5-9242-09173F13E4C5 n11:271B525C-363D-11E5-9242-09173F13E4C5 n11:271B525D-363D-11E5-9242-09173F13E4C5 n11:271B525A-363D-11E5-9242-09173F13E4C5 n11:271B525B-363D-11E5-9242-09173F13E4C5 n11:271B5258-363D-11E5-9242-09173F13E4C5 n11:271B5259-363D-11E5-9242-09173F13E4C5 n11:271B5256-363D-11E5-9242-09173F13E4C5 n11:271B5257-363D-11E5-9242-09173F13E4C5 n11:271B5254-363D-11E5-9242-09173F13E4C5 n11:271B5255-363D-11E5-9242-09173F13E4C5 n11:271B5252-363D-11E5-9242-09173F13E4C5 n11:271B5253-363D-11E5-9242-09173F13E4C5
n3:Bioavailability
n5:271B529C-363D-11E5-9242-09173F13E4C5
n3:Ghose-Filter
n5:271B529E-363D-11E5-9242-09173F13E4C5
n3:MDDR-Like-Rule
n5:271B529F-363D-11E5-9242-09173F13E4C5
n3:Melting-Point
n5:271B52A1-363D-11E5-9242-09173F13E4C5
n3:Number-of-Rings
n5:271B529B-363D-11E5-9242-09173F13E4C5
n3:Physiological-Charge
n5:271B529A-363D-11E5-9242-09173F13E4C5
n3:Rule-of-Five
n5:271B529D-363D-11E5-9242-09173F13E4C5
n3:Traditional-IUPAC-Name
n5:271B528B-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-acidic-
n5:271B5298-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-basic-
n5:271B5299-363D-11E5-9242-09173F13E4C5