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1. Celontin
2. Mesuximid
3. Mesuximide
4. Methsuximide, (+)-isomer
5. Methsuximide, (+-)-isomer
6. Methsuximide, (-)-isomer
7. N,2-dimethyl-2-phenylsuccinimide
8. Petinutin
1. Mesuximide
2. 77-41-8
3. Celontin
4. 1,3-dimethyl-3-phenylpyrrolidine-2,5-dione
5. Methsuximid
6. Petinutin
7. Metsuccimide
8. Mesuximidum
9. 1,3-dimethyl-3-phenylsuccinimide
10. Alpha-methylphensuximide
11. N,2-dimethyl-2-phenylsuccinimide
12. Metosuccimmide [dcit]
13. Mesuximidum [inn-latin]
14. 1,3-dimethyl-3-phenyl-2,5-pyrrolidinedione
15. Mesuximida [inn-spanish]
16. 1,3-dimethyl-3-phenyl-2,5-dioxopyrrolidine
17. 1,3-dimethyl-3-phenyl-pyrrolidin-2,5-dione
18. 2,5-pyrrolidinedione, 1,3-dimethyl-3-phenyl-
19. Pm 396
20. N-methyl-alpha-methyl-alpha-phenylsuccinimide
21. Alpha-methyl-alpha-phenyl N-methyl Succinimide
22. (rs)-1,3-dimethyl-3-phenyl-2,5-pyrrolidindion
23. Succinimide, N,2-dimethyl-2-phenyl-
24. Mesuximide (inn)
25. Mesuximide [inn]
26. Methsuximide (usp)
27. Methsuximide [usp]
28. Mesuximid
29. Nsc-760075
30. 0g76k8x6c0
31. Mfcd00072132
32. Ncgc00189077-01
33. Metosuccimmide
34. Mesuximida
35. Celontin (tn)
36. (+/-)-mesuximide
37. Hsdb 3124
38. Einecs 201-026-7
39. Brn 0168315
40. (+-)-n,2-dimethyl-2-phenylsuccinimide
41. Unii-0g76k8x6c0
42. Methsuximide [mi]
43. .alpha.-methylphensuximide
44. Dsstox_cid_3293
45. Chembl697
46. 2,5-pyrrolidinedione,1,3-dimethyl-3-phenyl-
47. Methsuximide [hsdb]
48. Mesuximide [mart.]
49. Dsstox_rid_76960
50. Mesuximide [who-dd]
51. Methsuximide [vandf]
52. Dsstox_gsid_23293
53. Schembl34852
54. 5-21-11-00209 (beilstein Handbook Reference)
55. Methsuximide [usp-rs]
56. Chebi:6846
57. Gtpl7228
58. 2,5-pyrrolidinedione,1,3-dimethyl-3-phenyl-, (+-)-
59. Dtxsid5023293
60. Hms3264p21
61. Methsuximide [orange Book]
62. Pharmakon1600-01505443
63. Hy-b1376
64. Methsuximide [usp Monograph]
65. Tox21_113613
66. Ac9293
67. Nsc760075
68. Akos015962173
69. Ccg-213444
70. Db05246
71. Nsc 760075
72. Cas-77-41-8
73. Ac-15963
74. Sy251111
75. Cs-0013113
76. Ft-0671397
77. Ft-0671398
78. 1,3-dimethyl-3-phenyl-2,5-pyrrolidinedione #
79. D00404
80. (+/-)-n,2-dimethyl-2-phenylsuccinimide
81. Ab01563316_01
82. N-methyl-.alpha.,.alpha.-methylphenylsuccinimide
83. 077m418
84. N-methyl-.alpha.-methyl-.alpha.-phenylsuccinimide
85. Q906414
86. Sr-01000942246
87. .alpha.-methyl-.alpha.-phenyl N-methyl Succinimide
88. Sr-01000942246-1
89. 2,5-pyrrolidinedione,1,3-dimethyl-3-phenyl-, (+/-)-
| Molecular Weight | 203.24 g/mol |
|---|---|
| Molecular Formula | C12H13NO2 |
| XLogP3 | 1.2 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 2 |
| Rotatable Bond Count | 1 |
| Exact Mass | 203.094628657 g/mol |
| Monoisotopic Mass | 203.094628657 g/mol |
| Topological Polar Surface Area | 37.4 Ų |
| Heavy Atom Count | 15 |
| Formal Charge | 0 |
| Complexity | 294 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 1 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
| 1 of 2 | |
|---|---|
| Drug Name | Celontin |
| PubMed Health | Methsuximide (By mouth) |
| Drug Classes | Anticonvulsant |
| Drug Label | Celontin (methsuximide) is an anticonvulsant succinimide, chemically designated as N,2-Dimethyl-2-phenylsuccinimide, with the following structural formula:Each Celontin capsule contains 300 mg methsuximide, USP. Also contains starch, NF. The capsule... |
| Active Ingredient | Methsuximide |
| Dosage Form | Capsule |
| Route | Oral |
| Strength | 300mg; 150mg |
| Market Status | Prescription |
| Company | Parke Davis |
| 2 of 2 | |
|---|---|
| Drug Name | Celontin |
| PubMed Health | Methsuximide (By mouth) |
| Drug Classes | Anticonvulsant |
| Drug Label | Celontin (methsuximide) is an anticonvulsant succinimide, chemically designated as N,2-Dimethyl-2-phenylsuccinimide, with the following structural formula:Each Celontin capsule contains 300 mg methsuximide, USP. Also contains starch, NF. The capsule... |
| Active Ingredient | Methsuximide |
| Dosage Form | Capsule |
| Route | Oral |
| Strength | 300mg; 150mg |
| Market Status | Prescription |
| Company | Parke Davis |
Anticonvulsants
National Library of Medicine's Medical Subject Headings online file (MeSH, 1999)
Methsuximide is indicated for the management of absence seizures refractory to other medication. /Included in US product label/
Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 271
Methsuximide may be used in the treatment of complex partial seizures (epilepsy). /Not included in US product label/
Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 271
The use of methsuximide to control seizures in 25 children (mean age, 10.2 yr) with intractable epilepsy who were given methsuximide at a mean dose of 20.4 mg/kg/day in addition to their regular antiepileptic drug /therapy was examined/. Results showed that in 15 patients the drug was well tolerated and resulted in a 50% or greater reduction in seizure frequency. No serious or irreversible adverse effects were seen. Methsuximide is frequently overlooked and may be an effective adjunctive antiepileptic for children with intractable seizures.
PMID:1987529 Tennison MB, et al; Pediatrics 87 (2): 186-9 (1991)
Methsuximide was administered for 8 weeks to 26 patients with complex partial seizures (CPS) refractory to phenytoin and carbamazepine and phenobarbital or primidone. A 50% or greater reduction in CPS frequency was obtained in eight patients. MSM therapy was continued chronically in these eight patients, and five continued to have a 50% or greater reduction in CPS frequency after 3 to 34 months of follow-up. ...
PMID:6403891 Browne T et al; Neurology 33 (4): 414-8 (1983)
The blood dyscrasia-causing effects of succinimide anticonvulsants may result in an increased incidence of microbial infection, delayed healing, and gingival bleeding. If leukopenia or thrombocytopenia occurs, dental work should be deferred until blood counts have returned to normal. Patients should be instructed in proper oral hygiene during treatment, including caution in use of regular toothbrushes, dental floss, and toothpicks. /Succinimide anticonvulsants/
Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 272
Adverse GI effects occur frequently during methsuximide therapy and include nausea or vomiting, weight loss, anorexia, epigastric or abdominal pain, diarrhea, and constipation.
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 2219
Adverse nervous system effects of methsuximide include drowsiness, ataxia, dizziness, irritability and nervousness, headache, photophobia, blurred vision, hiccups, and insomnia. The most common adverse nervous system effects are drowsiness, ataxia, and dizziness. Adverse psychologic effects have included instability, hypochondriacal behavior, aggressiveness, and mental confusion, depression, and slowness. Rarely, psychosis, suicidal behavior, and auditory hallucinations have been reported.
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 2219
Adverse hematologic effects associated with methsuximide include eosinophilia, leukopenia, monocytosis, and pancytopenia. Adverse dermatologic effects may include urticaria, pruritic erythematous rash, and Steven-Johnson syndrome. Adverse genitourinary effects associated with methsuximide include proteinuria and microscopic hematuria. Periorbital edema and hyperemia have also occurred. Systemic lupus erythematosus has been associated with succinimide use.
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 2219
For more Drug Warnings (Complete) data for METHSUXIMIDE (9 total), please visit the HSDB record page.
For the control of absence (petit mal) seizures that are refractory to other drugs.
Used in the treatment of epilepsy. Methsuximide suppresses the paroxysmal three cycle per second spike and wave activity associated with lapses of consciousness which is common in absence (petit mal) seizures. The frequency of epileptiform attacks is reduced, apparently by depression of the motor cortex and elevation of the threshold of the central nervous system to convulsive stimuli.
Anticonvulsants
Drugs used to prevent SEIZURES or reduce their severity. (See all compounds classified as Anticonvulsants.)
N - Nervous system
N03 - Antiepileptics
N03A - Antiepileptics
N03AD - Succinimide derivatives
N03AD03 - Mesuximide
Methsuximide is absorbed from the GI tract and peak plasma concentrations are achieved in 1-3 hours. In one study, mean peak serum concentrations were 3 ug/mL following a single 600-mg dose and 6-7 ug/mL following a single 1.2-g dose of methsuximide.
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 2219
Methsuximide is rapidly absorbed & metabolized. It is not bound significantly to plasma proteins.
Goodman, L.S., and A. Gilman. (eds.) The Pharmacological Basis of Therapeutics. 5th ed. New York: Macmillan Publishing Co., Inc., 1975., p. 213
Methsuximide is rapidly distributed throughout body after.../oral/ doses to rats, &.../it/ freely crosses blood-brain barrier.
The Chemical Society. Foreign Compound Metabolism in Mammals Volume 3. London: The Chemical Society, 1975., p. 126
Succinimide anticonvulsants are freely distributed to all body tissues, except fat.
Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 271
For more Absorption, Distribution and Excretion (Complete) data for METHSUXIMIDE (7 total), please visit the HSDB record page.
Limited studies in patients who have taken extremely high doses of methsuximide and one study involving a small number of patients receiving methsuximide for the management of epilepsy indicate that the drug is metabolized via N-demethylation to N-demethylmethsuximide (NDM). Profound CNS depression following methsuximide overdosage has been attributed to this metabolite, and it is probable that the anticonvulsant effects of the drug result from NDM. Overdosage of methsuccimide may follow a biphasic course; patients have awakened and relapsed into coma within 24 hours. In one study in patients receiving methsuximide chronically, the plasma concentration of NDM was 700 times greater than the simultaneous plasma concentration of methsuximide. On the basis of this one study, a tentative therapeutic plasma NDM concentration of 10-40 ug/mL has been proposed; plasma NDM concentrations exceeding 40 ug/mL have been associated with toxicity and coma has been reported at plasma NDM concentrations of 150 ug/mL.
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 2219
The pharmacokinetics of methsuximide and its major metabolite 2-methyl-2-phenylsuccinimide were studied in dogs after single intravenous doses. Plasma methsuximide levels were described by a two-compartment open model, and those of the metabolite were described by a one-compartment open model. An expression was derived that describes both methsuximide and metabolite plasma levels after methsuximide administration. Excellent fits were obtained between observed data and those predicted from the model. The metabolite, 2-methyl-2-phenylsuccinimide accounted for 40% of the overall elimination of methsuximide, and the half-life of the metabolite (15 hr) was much greater than that of the parent drug (1-3.5 hr). The results suggest that pharmacological effects after methsuximide administration may be due primarily to the metabolite, which may accumulate in the body during repeated doses.
PMID:577506 Dobrinska M et al; J Pharm Sci 66 (5): 688-92 (1977)
Metabolism by hepatic microsomal enzymes in dog yields n-demethyl & parahydroxyphenyl derivatives & their glucuronides. ...
Goodman, L.S., and A. Gilman. (eds.) The Pharmacological Basis of Therapeutics. 5th ed. New York: Macmillan Publishing Co., Inc., 1975., p. 213
Following oral admin of 1-2 g methsuximide to dogs, alpha-(p-hydroxyphenyl)-alpha-methylsuccinimide & n-methyl-alpha-(p-hydroxyphenyl)-alpha-methylsuccinimide isolated from 48 hr urine as major metab & alpha-methyl-alpha-phenylsuccinimide as minor. No parent drug found.
PMID:4150991 DUDLEY KH ET AL; DRUG METAB DISPOS 2: 113 (1974)
Metab, n-desmethylmethsuximide level higher in phensuximide than methsuximide treated patients. Plasma elimination was 32 & 1-2 hr.
TUPFERBERG HJ ET AL; ANTIEPILEPTIC DRUG MONIT, (PROC INT WORKSHOP DETERMINATION ANTIEPILEPTIC DRUGS BODY FLUIDS), 3RD, 173-80 (1977)
1.4-2.6 hours for mesuximide and 28-38 hours for the active metabolite.
The plasma half-life of methsuximide is slightly less than 3 hours.
McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2007., p. 2219
The clinical efficacy of ... methsuximide was studied in relation to plasma concentrations of this compound and its desmethyl metabolite. Single- and chronic-dose studies of /methsuximide/ were carried out in five patients with intractable seizures. Patients were evaluated before and during treatment by 6-hour simultaneous video and telemetered electroencephalographic recordings to characterize the seizure type and by daily determinations of plasma antiepileptic drug concentrations. ... Methsuximide had a short half-life, averaging 1.4 hours, but its desmethyl metabolite had a mean half-life of 38 hours and therefore accumulated to levels in excess of 40 micrograms per milliliter. ...
PMID:116142 Porter R et al; Neurology 29 (11): 1509-13 (1979)
Methsuximide ... was administered for 8 wk to 26 patients with complex partial seizures refractory to phenytoin and carbamazepine and phenobarbital or primidone. A 50% or greater reduction of complex partial seizure frequency was obtained in 8 patients. ... N-desmethylmethsuximide was the principle /metabolite/ detected in plasma and had the following pharmacokinetic values: accumulation half life, 49.7 hr; time to steady state, 10.4 days; elimination half life, 72.2 hr. ...
PMID:6403891 Browne TR, et al; Neurology 33 (4): 414-8 (1983)
Binds to T-type voltage sensitive calcium channels. Voltage-sensitive calcium channels (VSCC) mediate the entry of calcium ions into excitable cells and are also involved in a variety of calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division and cell death. The isoform alpha-1G gives rise to T-type calcium currents. T-type calcium channels belong to the "low-voltage activated (LVA)" group and are strongly blocked by mibefradil. A particularity of this type of channels is an opening at quite negative potentials and a voltage-dependent inactivation. T-type channels serve pacemaking functions in both central neurons and cardiac nodal cells and support calcium signaling in secretory cells and vascular smooth muscle. They may also be involved in the modulation of firing patterns of neurons which is important for information processing as well as in cell growth processes.
Succinimide anticonvulsants are thought to increase the seizure threshold and suppress the paroxysmal three-cycle-per-second spike-and-wave pattern seen with absence (petit mal) seizures. The frequency of attacks is reduced by depression of nerve transmission in the motor cortex. These effects may be due to direct modification of membrane function in excitable cells and/or alteration of chemically mediated neurotransmission. The specific effect of ethosuximide against absence seizures appears to be due to its ability to block T-type calcium channels at concentrations that do not affect other ion channels. /Succinimide anticonvulsants/
Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2007., p. 271
Inhibition of T-type Ca(2+) channels has been proposed to play a role in the therapeutic action of succinimide antiepileptic drugs. Despite the widespread acceptance of this hypothesis, recent studies using rat and cat neurons have failed to confirm inhibition of T-type currents at therapeutically relevant concentrations. The present study re-examines this issue using the three cloned human channels that constitute the T-type family: alpha 1G, alpha 1H, and alpha 1I. The cloned cDNAs were stably transfected and expressed into mammalian cells, leading to the appearance of typical T-type currents. The results demonstrate that both ethosuximide and the active metabolite of methsuximide, alpha-methyl-alpha-phenylsuccinimide (MPS), block human T-type channels in a state-dependent manner, with higher affinity for inactivated channels. In contrast, succinimide analogs that are not anticonvulsive were relatively poor blockers. The apparent affinity of MPS for inactivated states of the three channels was estimated using two independent measures: K(I) for alpha 1G and alpha 1I was 0.3 to 0.5 mM and for alpha 1H was 0.6 to 1.2 mM. T-type channels display current at the end of long pulses (persistent current), and this current was especially sensitive to block (ethosuximide IC(50) = 0.6 mM). These drugs also reduced both the size of the T-type window current region and the currents elicited by a mock low threshold spike. /The authors/ conclude that succinimide antiepileptic drugs are capable of blocking human T-type channels at therapeutically relevant concentrations.
PMID:11641441 Gomora J et al; Mol Pharmacol 60 (5): 1121-32 (2001)
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