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Namespace Prefixes

PrefixIRI
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n7http://linked.opendata.cz/resource/drugbank/drug/DB00375/identifier/wikipedia/
n22http://linked.opendata.cz/resource/drugbank/drug/DB00375/identifier/pharmgkb/
n24http://linked.opendata.cz/resource/drugbank/drug/DB00375/identifier/kegg-compound/
n14http://bio2rdf.org/drugbank:
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n28http://www.drugs.com/cdi/
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Statements

Subject Item
n2:DB00375
rdf:type
n3:Drug
n3:description
Highly crosslinked and insoluble basic anion exchange resin used as anticholesteremic. It may also may reduce triglyceride levels. [PubChem]
n3:dosage
n17:271B63A8-363D-11E5-9242-09173F13E4C5 n17:271B63A9-363D-11E5-9242-09173F13E4C5 n17:271B63A6-363D-11E5-9242-09173F13E4C5 n17:271B63A7-363D-11E5-9242-09173F13E4C5
n3:group
approved
n3:indication
For use, as adjunctive therapy to diet, for the reduction of elevated serum total and LDL-C in patients with primary hypercholesterolemia (elevated LDL-C) who do not respond adequately to diet.
n3:manufacturer
n5:271B6399-363D-11E5-9242-09173F13E4C5 n5:271B639A-363D-11E5-9242-09173F13E4C5
owl:sameAs
n14:DB00375 n20:DB00375
dcterms:title
Colestipol
adms:identifier
n7:Colestipol n18:DB00375 n21:56550 n22:PA449096 n23:62816 n24:C06925 n25:59762-0260-1 n26:46505777
n3:mechanismOfAction
Colestipol is a non-absorbed, lipid-lowering polymer that binds bile acids in the intestine, impeding their reabsorption. As the bile acid pool becomes depleted, the hepatic enzyme, cholesterol 7-(alpha)-hydroxylase, is upregulated, which increases the conversion of cholesterol to bile acids. This causes an increased demand for cholesterol in the liver cells, resulting in the dual effect of increasing transcription and activity of the cholesterol biosynthetic enzyme, hydroxymethyl-glutaryl-coenzyme A (HMG-CoA) reductase, and increasing the number of hepatic low-density lipoprotein (LDL) receptors. These compensatory effects result in increased clearance of LDL cholesterol (LDL-C) from the blood, resulting in decreased serum LDL-C levels. Serum triglyceride levels may increase or remain unchanged. The end result is increased clearance of LDL-cholesterol from the blood with decreased serum LDL-cholesterol.
n3:packager
n5:271B6397-363D-11E5-9242-09173F13E4C5 n5:271B6398-363D-11E5-9242-09173F13E4C5 n5:271B6395-363D-11E5-9242-09173F13E4C5 n5:271B6396-363D-11E5-9242-09173F13E4C5 n5:271B6393-363D-11E5-9242-09173F13E4C5 n5:271B6394-363D-11E5-9242-09173F13E4C5 n5:271B6391-363D-11E5-9242-09173F13E4C5 n5:271B6392-363D-11E5-9242-09173F13E4C5 n5:271B638F-363D-11E5-9242-09173F13E4C5 n5:271B6390-363D-11E5-9242-09173F13E4C5
n3:patent
n8:5490987
n3:routeOfElimination
Colestipol hydrochloride binds bile acids in the intestine forming a complex that is excreted in the feces. In humans, less than 0.17% of a single 14C-labeled colestipol hydrochloride dose is excreted in the urine when given following 60 days of chronic dosing of 20 grams of colestipol hydrochloride per day. The increased fecal loss of bile acids due to colestipol hydrochloride administration leads to an increased oxidation of cholesterol to bile acids.
n3:synonym
Copolymer of bis(2-aminoethyl)amine and 2-(chloromethyl)oxirane Epichlorohydrin-tetraethylenepentamine polymer Colestipolum
n3:toxicity
Oral LD<sub>50</sub> in rats is > 1000 mg/kg. Symptoms of overdose may include eye irritation, constipation, abdominal cramps, nausea, vomiting, diarrhea, and hypersensitivity. However, as colestipol is not absorbed, the risk of systemic toxicity is low.
n15:hasAHFSCode
n16:24-06-04
n3:foodInteraction
Take with food.
n3:proteinBinding
Not applicable (not hydrolyzed by digestive enzymes and not absorbed).
n3:salt
n3:synthesisReference
Lednicer, D. and Peery,C.Y.; US. Patent 3,803,237; April 9, 1974; assigned to The Upjohn Co.
n11:hasConcept
n12:M0004739
foaf:page
n10:colestipol.htm n28:colestipol.html n30:col1094.shtml
n3:IUPAC-Name
n4:271B63AB-363D-11E5-9242-09173F13E4C5
n3:InChI
n4:271B63B1-363D-11E5-9242-09173F13E4C5
n3:Molecular-Formula
n4:271B63B0-363D-11E5-9242-09173F13E4C5
n3:Molecular-Weight
n4:271B63AD-363D-11E5-9242-09173F13E4C5
n3:Monoisotopic-Weight
n4:271B63AE-363D-11E5-9242-09173F13E4C5
n3:SMILES
n4:271B63AF-363D-11E5-9242-09173F13E4C5
n3:Water-Solubility
n4:271B63C0-363D-11E5-9242-09173F13E4C5
n3:logP
n4:271B63AA-363D-11E5-9242-09173F13E4C5 n4:271B63C1-363D-11E5-9242-09173F13E4C5
n15:hasATCCode
n29:C10AC02
n3:H-Bond-Acceptor-Count
n4:271B63B7-363D-11E5-9242-09173F13E4C5
n3:H-Bond-Donor-Count
n4:271B63B8-363D-11E5-9242-09173F13E4C5
n3:InChIKey
n4:271B63B2-363D-11E5-9242-09173F13E4C5
n3:Polar-Surface-Area--PSA-
n4:271B63B3-363D-11E5-9242-09173F13E4C5
n3:Polarizability
n4:271B63B5-363D-11E5-9242-09173F13E4C5
n3:Refractivity
n4:271B63B4-363D-11E5-9242-09173F13E4C5
n3:Rotatable-Bond-Count
n4:271B63B6-363D-11E5-9242-09173F13E4C5
n3:absorption
Not absorbed from the gastrointestinal tract.
n3:affectedOrganism
Humans and other mammals
n3:casRegistryNumber
50925-79-6
n3:category
n3:containedIn
n27:271B63A4-363D-11E5-9242-09173F13E4C5 n27:271B63A5-363D-11E5-9242-09173F13E4C5 n27:271B63A2-363D-11E5-9242-09173F13E4C5 n27:271B63A3-363D-11E5-9242-09173F13E4C5 n27:271B63A0-363D-11E5-9242-09173F13E4C5 n27:271B63A1-363D-11E5-9242-09173F13E4C5 n27:271B639E-363D-11E5-9242-09173F13E4C5 n27:271B639F-363D-11E5-9242-09173F13E4C5 n27:271B639C-363D-11E5-9242-09173F13E4C5 n27:271B639D-363D-11E5-9242-09173F13E4C5 n27:271B639B-363D-11E5-9242-09173F13E4C5
n3:Bioavailability
n4:271B63BC-363D-11E5-9242-09173F13E4C5
n3:Ghose-Filter
n4:271B63BE-363D-11E5-9242-09173F13E4C5
n3:MDDR-Like-Rule
n4:271B63BF-363D-11E5-9242-09173F13E4C5
n3:Number-of-Rings
n4:271B63BB-363D-11E5-9242-09173F13E4C5
n3:Physiological-Charge
n4:271B63BA-363D-11E5-9242-09173F13E4C5
n3:Rule-of-Five
n4:271B63BD-363D-11E5-9242-09173F13E4C5
n3:Traditional-IUPAC-Name
n4:271B63AC-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-basic-
n4:271B63B9-363D-11E5-9242-09173F13E4C5