Methyl-Calminal - General Information
A barbiturate that is metabolized to phenobarbital. It has been used for similar purposes, especially in epilepsy, but there is no evidence mephobarbital offers any advantage over phenobarbital. [PubChem]
Pharmacology of Methyl-Calminal
Methyl-Calminal, a barbiturate, is used in combination with acetaminophen or aspirin and caffeine for its sedative and relaxant effects in the treatment of tension headaches, migraines, and pain. Barbiturates act as nonselective depressants of the central nervous system (CNS), capable of producing all levels of CNS mood alteration from excitation to mild sedation, hypnosis, and deep coma. In sufficiently high therapeutic doses, barbiturates induce anesthesia.
Methyl-Calminal for patients
Most reports of clinically significant drug interactions occurring with the barbiturates have involved phenobarbital. However, the application of these data to other barbiturates appears valid and warrants serial blood level determinations of the relevant drugs when there are multiple therapies.
1. Anticoagulants: Phenobarbital lowers the plasma levels of dicumarol (name previously used: bishydroxycoumarin) and causes a decrease in anticoagulant activity as measured by the prothrombin time. Barbiturates can induce hepatic microsomal enzymes resulting in increased metabolism and decreased anticoagulant response of oral anticoagulants (eg, warfarin, acenocoumarol, dicumarol, and phenprocoumon). Patients stabilized on anticoagulant therapy may require dosage adjustments if barbiturates are added to or withdrawn from their dosage regimen.
2. Corticosteroids: Barbiturates appear to enhance the metabolism of exogenous corticosteroids probably through the induction of hepatic microsomal enzymes. Patients stabilized on corticosteroid therapy may require dosage adjustments if barbiturates are added to or withdrawn from their dosage regimen.
3. Griseofulvin: Phenobarbital appears to interfere with the absorption of orally administered griseofulvin, thus decreasing its blood level. The effect of the resultant decreased blood levels of griseofulvin on therapeutic response has not been established. However, it would be preferable to avoid concomitant administration of these drugs.
4. Doxycycline: Phenobarbital has been shown to shorten the half-life of doxycycline for as long as 2 weeks after barbiturate therapy is discontinued. This mechanism is probably through the induction of hepatic microsomal enzymes that metabolize the antibiotic. If phenobarbital and doxycycline are administered concurrently, the clinical response to doxycycline should be monitored closely.
5. Phenytoin, Sodium Valproate, Valproic Acid: The effect of barbiturates on the metabolism of phenytoin appears to be variable. Some investigators report an accelerating effect, while others report no effect. Because the effect of barbiturates on the metabolism of phenytoin is not predictable, phenytoin and barbiturate blood levels should be monitored more frequently if these drugs are given concurrently. Sodium valproate and valproic acid appear to decrease barbiturate metabolism; therefore, barbiturate blood levels should be monitored and appropriate dosage adjustments made as indicated.
6. Central Nervous System Depressants: The concomitant use of other central nervous system depressants, including other sedatives or hypnotics, antihistamines, tranquilizers, or alcohol, may produce additive depressant effects.
7. Monoamine Oxidase Inhibitors (MAOI): MAOI prolong the effects of barbiturates probably because metabolism of the barbiturate is inhibited.
8. Estradiol, Estrone, Progesterone, and other Steroidal Hormones. Pretreatment with or concurrent administration of phenobarbital may decrease the effect of estradiol by increasing its metabolism. There have been reports of patients treated with antiepileptic drugs (e.g. phenobarbital) who become pregnant while taking oral contraceptives. An alternant contraceptive method might be suggested to women taking phenobarbital.
Hypersensitivity to any barbiturate. Manifest or latent porphyria.
Additional information about Methyl-Calminal
Methyl-Calminal Indication: For the relief of anxiety, tension, and apprehension, also used as an anticonvulsant for the treatment of epilepsy.
Mechanism Of Action: Methyl-Calminal binds at a distinct binding site associated with a Cl- ionopore at the GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.
Drug Interactions: Not Available
Food Interactions: Not Available
Generic Name: Methylphenobarbital
Synonyms: Mephobarbital; Mephobarbitone; Methyl Phenobarbitone; Methylphenobarbitalum [Inn-Latin]; Methylphenobarbitonum; Methylphenolbarbital; Methylphenylbarbituric acid; Metilfenobarbital [Inn-Spanish]; Metilfenobarbitale [Dcit]; N-Ethylmethylphenylbarbituric acid; N-Methylethylphenylbarbituric acid; N-Methylphenobarbital; N-Methylphenolbarbitol
Drug Category: Hypnotics and Sedatives; Anticonvulsants
Drug Type: Small Molecule; Approved
Absorption: Approximately 50% of an oral dose of mephobarbital is absorbed from the gastrointestinal tract.
Toxicity (Overdose): Not Available
Protein Binding: 70-76%
Biotransformation: Hepatic, primarily by the hepatic microsomal enzyme system. About 75% of a single oral dose of mephobarbital is metabolized to phenobarbital in 24 hours.
Half Life: 34 (range 11-67) hours
Dosage Forms of Methyl-Calminal: Tablet Oral
Chemical IUPAC Name: 5-ethyl-1-methyl-5-phenyl-1,3-diazinane-2,4,6-trione
Chemical Formula: C13H14N2O3
Methylphenobarbital on Wikipedia: https://en.wikipedia.org/wiki/Mephobarbital
Organisms Affected: Humans and other mammals