Attributes | Values |
---|
rdf:type
| |
http://linked.open...gbank/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. (en)
|
http://linked.open...y/drugbank/dosage
| |
http://linked.open...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 (en)
|
http://linked.open...gy/drugbank/group
| |
http://linked.open...drugbank/halfLife
| - Immediate release form = 3.5 hours; Extended release form = 5.47 hours; (en)
|
http://linked.open...ugbank/indication
| - Dalfampridine is a neurofunctional modifier that helps improve walking speed in patients with multiple sclerosis (MS). (en)
|
sameAs
| |
Title
| |
adms:identifier
| |
http://linked.open...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. (en)
|
http://linked.open...outeOfElimination
| - 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%) (en)
|
http://linked.open.../drugbank/synonym
| - Fampridine (en)
- Dalfampridine (en)
- 4-Aminopyridine (en)
- 4-Pyridinamine (en)
- 4-AP (en)
- 4-Pyridylamine (en)
- Ampyra (en)
- Avitrol (en)
- EL-970 (en)
- Fampridina (en)
- Fampridine-SR (en)
- Fampridinum (en)
- N07XX07 (en)
- P-Aminopyridine (en)
- gamma-Aminopyridine (en)
|
http://linked.open...drugbank/toxicity
| - LD50, oral, mouse = 19 mg/kg LD50, oral, rat = 21 mg/kg (en)
|
http://linked.open...umeOfDistribution
| - 10 mg extended release = 2.6 L/kg (en)
|
http://linked.open.../drug/hasAHFSCode
| |
http://linked.open...k/foodInteraction
| - A high fat meal significantly increases Cmax but this effect is not clinically relevant. May take dalfampridine without regard to meals (en)
|
http://linked.open...nk/proteinBinding
| - 10 mg extended release = 1-3% protein bound (en)
|
http://linked.open...ynthesisReference
| - Fabio GARAVAGLIA, Alessandro BAROZZA, Jacopo ROLETTO, Paolo PAISSONI, "ONE-POT PROCESS FOR THE SYNTHESIS OF DALFAMPRIDINE." U.S. Patent US20110319628, issued December 29, 2011. (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...logy/drugbank/pKa
| |
http://linked.open...l/drug/hasATCCode
| |
http://linked.open...nd-Acceptor-Count
| |
http://linked.open...-Bond-Donor-Count
| |
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...ugbank/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% (en)
|
http://linked.open.../affectedOrganism
| - Humans and other mammals (en)
|
http://linked.open...casRegistryNumber
| |
http://linked.open...drugbank/category
| |
http://linked.open...k/Bioavailability
| |
http://linked.open...ank/Boiling-Point
| |
http://linked.open...bank/Ghose-Filter
| |
http://linked.open...nk/MDDR-Like-Rule
| |
http://linked.open...ank/Melting-Point
| |
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-
| |