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1. 3,4 Diaminopyridine
2. Amifampridine
3. Amifampridine Phosphate
4. Firdapse
5. Ruzurgi
1. 54-96-6
2. Pyridine-3,4-diamine
3. Amifampridine
4. 3,4-pyridinediamine
5. 3,4-dap
6. 4,5-diaminopyridine
7. Diamino-3,4 Pyridine
8. Amifampridin
9. Ruzurgi
10. Pyridine, 3,4-diamino-
11. 3,4 Diaminopyridine
12. Dynamine
13. 3-amino-4-pyridinylamine
14. Nsc-521760
15. Ru4s6e2g0j
16. 54-96-6 (free Base)
17. Chembl354077
18. Ncgc00167560-01
19. Dsstox_cid_26715
20. Dsstox_rid_81847
21. Dsstox_gsid_46715
22. Cas-54-96-6
23. Smr000752913
24. Amifampridine [inn]
25. Einecs 200-220-9
26. Unii-ru4s6e2g0j
27. Nsc 521760
28. Brn 0110232
29. Amifampridine [usan:inn:ban]
30. Ruzurgi (tn)
31. Mfcd00006401
32. Pyridine,4-diamino-
33. 3,4-diamino Pyridine
34. 3,4-diamino-pyridine
35. 3,4-diammoniopyridinium
36. Amifampridine [mi]
37. Wln: T6nj Cz Dz
38. Amifampridine (usan/inn)
39. 4-dap
40. Amifampridine [usan]
41. Schembl21273
42. 5-22-11-00266 (beilstein Handbook Reference)
43. Mls001304911
44. Mls001333181
45. Mls001333182
46. Amifampridine [mart.]
47. Amifampridine [who-dd]
48. Gtpl8032
49. 3,4-diamino[3,4-b]pyridine
50. Amifampridine [ema Epar]
51. Dtxsid6046715
52. Ampd00217
53. Chebi:135948
54. Hms2233k06
55. Zinc164000
56. Amifampridine [orange Book]
57. Act01546
58. Albb-005969
59. Bcp22343
60. Amifampridin (3,4-diaminopyridine)
61. Tox21_112555
62. 3,4 Diaminopyridine [vandf]
63. Bbl013269
64. Bdbm50416493
65. Cl0116
66. Nsc521760
67. Nsc790505
68. S4622
69. Stk503647
70. Akos000672436
71. Tox21_112555_1
72. Ccg-304141
73. Db11640
74. Nsc-790505
75. Pb48915
76. Ps-9273
77. Ncgc00167560-02
78. Bp-12781
79. Hy-14946
80. Db-011105
81. Am20070030
82. D1149
83. Ft-0614203
84. D10228
85. 006d401
86. Ac-907/34116043
87. Q411707
88. J-610017
89. W-105592
90. F0001-1409
91. L89
| Molecular Weight | 109.13 g/mol |
|---|---|
| Molecular Formula | C5H7N3 |
| XLogP3 | -0.5 |
| Hydrogen Bond Donor Count | 2 |
| Hydrogen Bond Acceptor Count | 3 |
| Rotatable Bond Count | 0 |
| Exact Mass | 109.063997236 g/mol |
| Monoisotopic Mass | 109.063997236 g/mol |
| Topological Polar Surface Area | 64.9 Ų |
| Heavy Atom Count | 8 |
| Formal Charge | 0 |
| Complexity | 74.1 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
Amifampridine is indicated for the symptomatic treatment of Lambert-Eaton myasthenic syndrome (LEMS) in adults and in patients aged 6 to less than 17 years of age. Nevertheless, it is important to note that at the current time only the Firdapse brand of amifampridine is indicated for the treatment of LEMS in adults and the Ruzurgi brand of amifampridine is indicated for the treatment of LEMS in patients aged 6 to less than 17 years.
FDA Label
Symptomatic treatment of Lambert-Eaton myasthenic syndrome (LEMS) in adults.
Administration of amifampridine to patients with LES in clinical trials resulted in improvement of the compound muscle action potential (CMAP), muscle function, and quantitative myasthenia gravis (QMG) score. One case of a slight prolongation of the QTc interval in male patient with LEMS and euthyroid Hashimotos disease treated with 90 mg of amifampridine in combination with 100 mg azathioprine was reported. I_n vitro_, amifampridine was shown to modulate cardiac conduction and induce phasic contractions in different arteries from several species. In addition, it stimulated potassium-evoked dopamine and noradrenaline release in rat hippocampal slices and upregulate acetylcholine release in the brain. It may also potentiate adrenergic and cholinergic neuromuscular transmission in the gatrointestinal tract. In a single pharmacokinetic study, no effect was observed of amifampridine phosphate on cardiac repolarization as assessed using the QTc interval. There were no changes in heart rate, atrioventricular conduction or cardiac depolarization as measured by the heart rate, PR and QRS interval durations.
Neuromuscular Agents
Drugs used for their actions on skeletal muscle. Included are agents that act directly on skeletal muscle, those that alter neuromuscular transmission (NEUROMUSCULAR BLOCKING AGENTS), and drugs that act centrally as skeletal muscle relaxants (MUSCLE RELAXANTS, CENTRAL). Drugs used in the treatment of movement disorders are ANTI-DYSKINESIA AGENTS. (See all compounds classified as Neuromuscular Agents.)
Potassium Channel Blockers
A class of drugs that act by inhibition of potassium efflux through cell membranes. Blockade of potassium channels prolongs the duration of ACTION POTENTIALS. They are used as ANTI-ARRHYTHMIA AGENTS and VASODILATOR AGENTS. (See all compounds classified as Potassium Channel Blockers.)
N07XX05
N - Nervous system
N07 - Other nervous system drugs
N07X - Other nervous system drugs
N07XX - Other nervous system drugs
N07XX05 - Amifampridine
Absorption
Orally-administered amifampridine is rapidly absorbed in humans to reach the peak plasma concentrations within by 0.6 to 1.3 hours. A single oral dose of 20 mg amifampridine in fasted individuals resulted in mean peak plasma concentrations (Cmax) ranging from 16 to 137 ng/mL. Bioavailability is approximately 93-100% based on recoveries of unmetabolised amifampridine and a major 3-N-acetylated amifampridine metabolite in urine. Food consumption decreases amifampridine absorption and exposure with a decrease in the time to reach maximum concentrations (Tmax). It is approximated that food consumption lowers the Cmax on average by ~44% and lowers AUC by ~20%. based on geometric mean ratios. Systemic exposure to amifampridine is affected by the overall metabolic acetylation activity of NAT enzymes and NAT2 genotype. The NAT enzymes are highly polymorphic that results in variable slow acetylator (SA) and rapid acetylator (RA) phenotypes. Slow acetylators are more prone to increased systemic exposure to amifampridine, and may require higher doses for therapeutic efficacy.
Route of Elimination
Following oral administration, more than 93% of total amifampridine is renally eliminated within 24 hours. About 19% of the total renally-excreted dose is in the parent drug form, and about 74-81.7% of the dose is in its metabolite form.
Volume of Distribution
In rats, orally-administered amifampridine was extensively absorbed in the gastrointestinal tract and widely distributed. Drug concentrations were highest in organs of excretion, including liver, kidney and the gastrointestinal tract, and some tissues of glandular function, such as lacrimal, salivary, mucous, pituitary and thyroid glands. Concentrations in tissues are generally similar to or greater than concentrations in plasma.
Clearance
Overall clearance of amifampridine is both metabolic and renal; it is mostly cleared from the plasma via metabolism by N-acetylation.
3-N-acetylated amifampridine is the major metabolite based on _in vivo_ and _in vitro_ human studies.
The plasma elimination half-life is approximately 2.5 hours for amifampridine and 4 hours for 3-N-acetylamifampridine.
Amifampridine is a symptomatic treatment that increases acetylcholine concentrations at the neuromuscular junction. It selectively blocks presynaptic fast voltage-gated potassium channels, thereby prolonging cell membrane depolarization and action potential, and augmenting calcium transport into the nerve endings. Increased intracellular calcium enhances the exocytosis of acetylcholine-containing vesicles and enhances impulse transmission at central, autonomic, and neuromuscular synapses. Amifampridine improves muscle strength and resting compound muscle action potential (CMAP) amplitudes with an overall weighted mean difference of 1.69 mV.
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