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Namespace Prefixes

PrefixIRI
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Statements

Subject Item
n2:DB06637
rdf:type
n3:Drug
n3:description
Dalfampridine is a potassium channel blocker used to help multiple sclerosis patients walk. This is the first drug that was specifically approved to help with mobility in these patients. FDA approved on January 22, 2010.
n3:dosage
n11:271B4DA2-363D-11E5-9242-09173F13E4C5 n11:271B4DA3-363D-11E5-9242-09173F13E4C5
n3:generalReferences
# Panitch H, Applebee A: Treatment of walking impairment in multiple sclerosis: an unmet need for a disease-specific disability. Expert Opin Pharmacother. 2011 Jul;12(10):1511-21. doi: 10.1517/14656566.2011.586338. Epub 2011 Jun 2. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/21635193 # Pikoulas TE, Fuller MA: Dalfampridine: a medication to improve walking in patients with multiple sclerosis. Ann Pharmacother. 2012 Jul-Aug;46(7-8):1010-5. doi: 10.1345/aph.1Q714. Epub 2012 Jul 3. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/22764324 # Cornblath DR, Bienen EJ, Blight AR: The safety profile of dalfampridine extended release in multiple sclerosis clinical trials. Clin Ther. 2012 May;34(5):1056-69. doi: 10.1016/j.clinthera.2012.03.007. Epub 2012 Apr 11. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/22497693 # McDonald S, Clements JN: Dalfampridine: a new agent for symptomatic management of multiple sclerosis. Am J Health Syst Pharm. 2011 Dec 15;68(24):2335-40. doi: 10.2146/ajhp110134. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/22135060 # Judge SI, Bever CT Jr: Potassium channel blockers in multiple sclerosis: neuronal Kv channels and effects of symptomatic treatment. Pharmacol Ther. 2006 Jul;111(1):224-59. Epub 2006 Feb 9. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/16472864
n3:group
approved
n3:halfLife
Immediate release form = 3.5 hours; Extended release form = 5.47 hours;
n3:indication
Dalfampridine is a neurofunctional modifier that helps improve walking speed in patients with multiple sclerosis (MS).
owl:sameAs
n21:DB06637
dcterms:title
Dalfampridine
adms:identifier
n6:D04127 n7:10144-427-60 n8:DB06637 n10:C13728 n12:4-Aminopyridine n13:34385
n3:mechanismOfAction
In MS, axons are progressively demyelinated which exposes potassium channels. As a result, there is a leak of potassium ions which results in the repolarization of cells and a decrease in neuronal excitability. The overall impact is the impairment of neuromuscular transmission as it is harder to trigger an action potential. Dalfampridine inhibits voltage-gated potassium channels in the CNS to maintain the transmembrane potential and prolong action potential. In other words, dalfampridine works to make sure that the current available is high enough to stimulate conduction in demyelinated axons that are exposed in MS patients. Furthermore, it facilitates neuromuscular and synaptic transmission by relieving conduction blocks in demyelinated axons.
n3:routeOfElimination
Almost all of the dose and its metabolites are completely eliminated by the kidneys after 24 hours. Urine (96%; 90% of total dose as unchanged drug); Feces (0.5%)
n3:synonym
N07XX07 Fampridine EL-970 Fampridine-SR P-Aminopyridine Fampridinum 4-Aminopyridine Fampridina Ampyra 4-AP 4-Pyridylamine gamma-Aminopyridine 4-Pyridinamine Dalfampridine Avitrol
n3:toxicity
LD50, oral, mouse = 19 mg/kg LD50, oral, rat = 21 mg/kg
n3:volumeOfDistribution
10 mg extended release = 2.6 L/kg
n17:hasAHFSCode
n18:92-92
n3:foodInteraction
A high fat meal significantly increases Cmax but this effect is not clinically relevant. May take dalfampridine without regard to meals
n3:proteinBinding
10 mg extended release = 1-3% protein bound
n3:synthesisReference
Fabio GARAVAGLIA, Alessandro BAROZZA, Jacopo ROLETTO, Paolo PAISSONI, "ONE-POT PROCESS FOR THE SYNTHESIS OF DALFAMPRIDINE." U.S. Patent US20110319628, issued December 29, 2011.
foaf:page
n15:ampyra-drug.htm n16:ampyra.html
n3:IUPAC-Name
n4:271B4DA8-363D-11E5-9242-09173F13E4C5
n3:InChI
n4:271B4DAE-363D-11E5-9242-09173F13E4C5
n3:Molecular-Formula
n4:271B4DAD-363D-11E5-9242-09173F13E4C5
n3:Molecular-Weight
n4:271B4DAA-363D-11E5-9242-09173F13E4C5
n3:Monoisotopic-Weight
n4:271B4DAB-363D-11E5-9242-09173F13E4C5
n3:SMILES
n4:271B4DAC-363D-11E5-9242-09173F13E4C5
n3:Water-Solubility
n4:271B4DA6-363D-11E5-9242-09173F13E4C5 n4:271B4DBE-363D-11E5-9242-09173F13E4C5
n3:logP
n4:271B4DA7-363D-11E5-9242-09173F13E4C5 n4:271B4DA4-363D-11E5-9242-09173F13E4C5
n3:logS
n4:271B4DA5-363D-11E5-9242-09173F13E4C5
n3:pKa
n4:271B4DC1-363D-11E5-9242-09173F13E4C5
n17:hasATCCode
n19:N07XX07
n3:H-Bond-Acceptor-Count
n4:271B4DB4-363D-11E5-9242-09173F13E4C5
n3:H-Bond-Donor-Count
n4:271B4DB5-363D-11E5-9242-09173F13E4C5
n3:InChIKey
n4:271B4DAF-363D-11E5-9242-09173F13E4C5
n3:Polar-Surface-Area--PSA-
n4:271B4DB0-363D-11E5-9242-09173F13E4C5
n3:Polarizability
n4:271B4DB2-363D-11E5-9242-09173F13E4C5
n3:Refractivity
n4:271B4DB1-363D-11E5-9242-09173F13E4C5
n3:Rotatable-Bond-Count
n4:271B4DB3-363D-11E5-9242-09173F13E4C5
n3:absorption
Orally-administered dalfampridine is rapidly and completely absorbed from the gastrointestinal tract. Tmax, immediate release form = 1 hour; Tmax, extended release form = 3.5 hours; Cmax, 10 mg extended release = 17.3 - 21.6 ng/mL; Relative bioavailability of 10 mg extended-release tablets compared to aqueous oral solution = 96%
n3:affectedOrganism
Humans and other mammals
n3:casRegistryNumber
504-24-5
n3:category
n3:Bioavailability
n4:271B4DBA-363D-11E5-9242-09173F13E4C5
n3:Boiling-Point
n4:271B4DC0-363D-11E5-9242-09173F13E4C5
n3:Ghose-Filter
n4:271B4DBC-363D-11E5-9242-09173F13E4C5
n3:MDDR-Like-Rule
n4:271B4DBD-363D-11E5-9242-09173F13E4C5
n3:Melting-Point
n4:271B4DBF-363D-11E5-9242-09173F13E4C5
n3:Number-of-Rings
n4:271B4DB9-363D-11E5-9242-09173F13E4C5
n3:Physiological-Charge
n4:271B4DB8-363D-11E5-9242-09173F13E4C5
n3:Rule-of-Five
n4:271B4DBB-363D-11E5-9242-09173F13E4C5
n3:Traditional-IUPAC-Name
n4:271B4DA9-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-acidic-
n4:271B4DB6-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-basic-
n4:271B4DB7-363D-11E5-9242-09173F13E4C5