3111 Methsuximide Methsuximide is only found in individuals that have used or taken this drug. It is an anticonvulsant medication. It is sold by Pfizer under the name Petinutin. [Wikipedia] 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. 77-41-8 6476 C12H13NO2 203.094630 White powder. 52.5°C 121.5°C at 1.00E-01 mm Hg 2.13e+00 g/L Oral 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. Half Life: 1.4-2.6 hours for mesuximide and 28-38 hours for the active metabolite. No indication of carcinogenicity to humans (not listed by IARC). For the control of absence (petit mal) seizures that are refractory to other drugs. May cause a potentially dangerous rash that may develop into Stevens Johnson syndrome, an extremely rare but potentially fatal skin disease. Acute overdoses may produce nausea, vomiting, and CNS depression including coma with respiratory depression. Levels greater than 40 µg/mL have caused toxicity and coma has been seen at levels of 150 µg/mL. Treatment should include emesis (unless the patient is or could rapidly become obtunded, comatose, or convulsing) or gastric lavage, activated charcoal, cathartics, and general supportive measures. Charcoal hemoperfusion may be useful in removing the N-desmethyl metabolite of methsuximide. Forced diuresis and exchange transfusions are ineffective. (L1712) 2009-07-21T20:29:00Z 2014-12-24T20:25:56Z Methsuximide 131857 Methsuximide DB05246 true CN1C(=O)CC(C)(C1=O)C1=CC=CC=C1 C12H13NO2 InChI=1/C12H13NO2/c1-12(9-6-4-3-5-7-9)8-10(14)13(2)11(12)15/h3-7H,8H2,1-2H3 InChIKey=AJXPJJZHWIXJCJ-UHFFFAOYNA-N 203.2371 203.094628665 Exogenous Solid HMDB15611 CHEMBL697 6231