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Namespace Prefixes

PrefixIRI
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dctermshttp://purl.org/dc/terms/
n21http://linked.opendata.cz/resource/AHFS/
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n14http://linked.opendata.cz/resource/drugbank/drug/DB08907/identifier/kegg-drug/
n13http://linked.opendata.cz/resource/drugbank/drug/DB08907/identifier/drugbank/
n5http://linked.opendata.cz/resource/drugbank/dosage/
n8http://www.drugs.com/
n9http://www.rxlist.com/
n19http://bio2rdf.org/drugbank:
n16http://linked.opendata.cz/resource/drugbank/drug/DB08907/identifier/national-drug-code-directory/
admshttp://www.w3.org/ns/adms#
n6http://linked.opendata.cz/resource/drugbank/patent/
n15http://linked.opendata.cz/resource/drugbank/drug/DB08907/identifier/chebi/
rdfhttp://www.w3.org/1999/02/22-rdf-syntax-ns#
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n4http://linked.opendata.cz/resource/drugbank/property/
n17http://linked.opendata.cz/resource/drugbank/drug/DB08907/identifier/wikipedia/
xsdhhttp://www.w3.org/2001/XMLSchema#
n11http://linked.opendata.cz/resource/atc/
n10http://linked.opendata.cz/ontology/sukl/drug/

Statements

Subject Item
n2:DB08907
rdf:type
n3:Drug
n3:description
Canagliflozin belongs to a new class of anti-diabetic drugs that works by inhibiting the sodium-glucose transport protein (SGLT2). This transport protein is found in the kidney and is responsible for reabsorbing glucose that has been filtered. FDA approved on March 29, 2013.
n3:dosage
n5:271B5C20-363D-11E5-9242-09173F13E4C5 n5:271B5C1E-363D-11E5-9242-09173F13E4C5 n5:271B5C1F-363D-11E5-9242-09173F13E4C5 n5:271B5C1D-363D-11E5-9242-09173F13E4C5
n3:generalReferences
# Lamos EM, Younk LM, Davis SN: Canagliflozin , an inhibitor of sodium-glucose cotransporter 2, for the treatment of type 2 diabetes mellitus. Expert Opin Drug Metab Toxicol. 2013 Jun;9(6):763-75. doi: 10.1517/17425255.2013.791282. Epub 2013 Apr 17. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/23590413
n3:group
approved
n3:halfLife
The apparent terminal half-life (t1/2) was 10.6 hours and 13.1 hours for the 100 mg and 300 mg doses, respectively.
n3:indication
Canagliflozin is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. Use in type 1 diabetes mellitus patients or in treatment of diabetic ketoacidosis is not recommended.
owl:sameAs
n19:DB08907
dcterms:title
Canagliflozin
adms:identifier
n13:DB08907 n14:D09592 n15:73274 n16:50458-141-30 n17:Canagliflozin
n3:mechanismOfAction
Sodium-glucose co-transporter 2 (SGLT2), expressed in the proximal renal tubules, is responsible for the majority of the reabsorption of filtered glucose from the tubular lumen. Canagliflozin is an inhibitor of SGLT2. By inhibiting SGLT2, canagliflozin reduces reabsorption of filtered glucose and lowers the renal threshold for glucose (RTG), and thereby increases urinary glucose excretion.
n3:patent
n6:8222219 n6:7943582 n6:7943788
n3:routeOfElimination
Enterohepatic circulation of canagliflozin was negligible. When a single oral dose is administered to a healthy subject, canagliflozin is eliminated via the following: Feces (41.5%, 7.0%, 3.2% as canagliflozin, a hydroxylated metabolite, and an O-glucuronide metabolite, respectively). Urine (33%; 30.5% as O-glucuronide metabolite, <1% as unchanged drug).
n3:synonym
1-(Glucopyranosyl)-4-methyl-3-(5-(4-fluorophenyl)-2-thienylmethyl)benzene Canagliflozin hydrate
n3:toxicity
Most common adverse reactions associated with canagliflozin (5% or greater incidence): female genital mycotic infections, urinary tract infection, and increased urination.
n3:volumeOfDistribution
Steady state, single IV infusion, healthy subject = 119 L. This high value suggests that cangliflozin is extensively distributed to tissue.
n10:hasAHFSCode
n21:68-20-18
n3:proteinBinding
>99% protein bound, mainly to albumin. It also binds to alpha-acid glycoprotein. Protein binding is independent of canagliflozin plasma concentrations. Plasma protein binding is not meaningfully altered in patients with renal or hepatic impairment.
foaf:page
n8:invokana.html n9:invokana-drug.htm
n3:IUPAC-Name
n4:271B5C25-363D-11E5-9242-09173F13E4C5
n3:InChI
n4:271B5C2B-363D-11E5-9242-09173F13E4C5
n3:Molecular-Formula
n4:271B5C2A-363D-11E5-9242-09173F13E4C5
n3:Molecular-Weight
n4:271B5C27-363D-11E5-9242-09173F13E4C5
n3:Monoisotopic-Weight
n4:271B5C28-363D-11E5-9242-09173F13E4C5
n3:SMILES
n4:271B5C29-363D-11E5-9242-09173F13E4C5
n3:Water-Solubility
n4:271B5C23-363D-11E5-9242-09173F13E4C5
n3:logP
n4:271B5C21-363D-11E5-9242-09173F13E4C5 n4:271B5C24-363D-11E5-9242-09173F13E4C5
n3:logS
n4:271B5C22-363D-11E5-9242-09173F13E4C5
n10:hasATCCode
n11:A10BX11
n3:H-Bond-Acceptor-Count
n4:271B5C31-363D-11E5-9242-09173F13E4C5
n3:H-Bond-Donor-Count
n4:271B5C32-363D-11E5-9242-09173F13E4C5
n3:InChIKey
n4:271B5C2C-363D-11E5-9242-09173F13E4C5
n3:Polar-Surface-Area--PSA-
n4:271B5C2D-363D-11E5-9242-09173F13E4C5
n3:Polarizability
n4:271B5C2F-363D-11E5-9242-09173F13E4C5
n3:Refractivity
n4:271B5C2E-363D-11E5-9242-09173F13E4C5
n3:Rotatable-Bond-Count
n4:271B5C30-363D-11E5-9242-09173F13E4C5
n3:absorption
The pharmacokinetics of canagliflozin is similar in healthy subjects and patients with type 2 diabetes. Plasma Cmax and AUC of canagliflozin increased in a dose-proportional manner from 50 mg to 300 mg. Accumulation in plasma has been observed following multiple doses of 100 - 300 mg. Food does not affect the absorption of canagliflozin. Tmax = 1- 2 hours; Cmax = 1059 - 3148 ng/mL; Time to steady state, once daily dose, 100 - 300 mg = 4-5 days; Absolute oral bioavailability = 65%.
n3:affectedOrganism
Humans and other mammals
n3:casRegistryNumber
842133-18-0
n3:category
n3:clearance
Mean systemic clearance, healthy subjects, IV administration = 192 mL/min. Renal clearance of canagliflozin 100 mg and 300 mg doses ranged from 1.30 to 1.55 mL/min.
n3:Bioavailability
n4:271B5C37-363D-11E5-9242-09173F13E4C5
n3:Ghose-Filter
n4:271B5C39-363D-11E5-9242-09173F13E4C5
n3:MDDR-Like-Rule
n4:271B5C3A-363D-11E5-9242-09173F13E4C5
n3:Number-of-Rings
n4:271B5C36-363D-11E5-9242-09173F13E4C5
n3:Physiological-Charge
n4:271B5C35-363D-11E5-9242-09173F13E4C5
n3:Rule-of-Five
n4:271B5C38-363D-11E5-9242-09173F13E4C5
n3:Traditional-IUPAC-Name
n4:271B5C26-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-acidic-
n4:271B5C33-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-basic-
n4:271B5C34-363D-11E5-9242-09173F13E4C5