2. Membrane Transporter/Ion Channel
  3. Potassium Channel
  4. Amifampridine phosphate

Amifampridine phosphate  (Synonyms: 3,4-Diaminopyridine phosphate)

Cat. No.: HY-14946A
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Amifampridine (3,4-Diaminopyridine) phosphate is an orally active, potent and cell permeable voltage-gated potassium (Kv) channel blocker (PCB). Amifampridine phosphate is efficacy in the reversal of BoNT/A (HY-P79153) intoxication. Amifampridine phosphate increases transmitter release from neuromuscular junctions (NMJs). Amifampridine phosphate can be used for Lambert-Eaton myasthenic syndrome (LEMS) research.

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Amifampridine phosphate Chemical Structure

Amifampridine phosphate Chemical Structure

CAS No. : 446254-47-3

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Description

Amifampridine (3,4-Diaminopyridine) phosphate is an orally active, potent and cell permeable voltage-gated potassium (Kv) channel blocker (PCB). Amifampridine phosphate is efficacy in the reversal of BoNT/A (HY-P79153) intoxication. Amifampridine phosphate increases transmitter release from neuromuscular junctions (NMJs). Amifampridine phosphate can be used for Lambert-Eaton myasthenic syndrome (LEMS) research[1][2][3].

In Vitro

Amifampridine phosphate (1.5 μM) significantly reduces Kv3.3 and Kv3.4 currents by about 10% in HEK293T cells, has no effect on Cav2.1 or Cav1.2 current[3].
Amifampridine phosphate (0-100 μM) increases the duration of the presynaptic AP (action potential) waveform at mammalian and frog NMJs in a dose-dependent manner[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Amifampridine phosphate Related Antibodies
In Vivo

Amifampridine phosphate (Oral gavage; 10 mg/kg; once) can antagonize muscle paralysis following BoNT/A intoxication[2].
Amifampridine phosphate (2.5 mg/kg (IV); 10 mg/kg (PO); once) shows 1 hour plasma half-life and about 57% bioavailability (F) in mice[2].
Amifampridine phosphate has a short plasma half-life and can induce seizures when present at high concentrations, following penetration of the blood-brain barrier[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: CD-1 mouse (female,25 g, 6 weeks old)[2]
Dosage: 10 mg/kg
Administration: Oral gavage, once, after BoNT/A administration (IP)
Result: Revealed that neither LEMs alone (182 ± 43 min) nor the maximum safe orally deliverable dose of 3,4-DAP alone (225 ± 24 min) could significantly increase the time to death following toxin administration (216 ± 29 min). However, when the 10/50/40 3,4-DAP/LEM/shellac formulation was administered at 25 mg/kg the time to death was 302 ± 26 min - a 40% increase as compared to toxin alone.
Animal Model: CD-1 mouse (30-35 g, 8 weeks old)[2]
Dosage: 2.5 mg/kg (IV); 10 mg/kg (PO)
Administration: IV, orally, once (Pharmacokinetic Analysis)
Result: Pharmacokinetic Parameters of Amifampridine in CD-1 mouse[1].
IV (2.5 mg/kg) PO (10 mg/kg)
t1/2 (h) 1.04 1.28
AUC0-24 (μM·h) 4.29 9.72
F (%) 100 56.7
Clinical Trial
Molecular Weight

207.12

Formula

C5H10N3O4P
CAS No.
SMILES

NC1=C(N)C=CN=C1.O=P(O)(O)O
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Room temperature in continental US; may vary elsewhere.
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Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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Amifampridine phosphate Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Amifampridine446254-47-33,4-DiaminopyridinePotassium ChannelKcsAneuromuscular junctionvoltage-gated potassiumKvneurological diseaseLEMSmyasthenic syndromeOralInhibitorinhibitorinhibit

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