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Last updated on November 22nd, 2021

Drug Approvals

(British Approved Name, rINN)

International Nonproprietary Names (INNs) in main languages (French, Latin, and Spanish): Amobarbitaali; Amobarbital; Amobarbitalis; Amobarbitalum; Amylobarbitone; Pentymalum. 5-Ethyl-5-isopentylbarbituric acid.

C11H18N2O3 = 226.3.

CAS 57-43-2.

ATC N05CA02.

Note. The following terms have been used as ’street names’ or slang names for various forms of amobarbital: Amys; Birds; Blue; Blue angels; Blue birds; Blue bullets; Blue clouds; Blue devils; Blue dolls; Blue heaven; Blue heavens; Blues.

Pharmacopoeias. In China, Europe, and Japan.

European Pharmacopoeia, 6th ed. (Amobarbital). A white or almost white, crystalline powder. Very slightly soluble in water freely soluble in alcohol soluble in dichloromethane. Forms water-soluble compounds with alkali hydroxides and carbonates and with ammonia.

Drug Approvals

(British Approved Name Modified, rINNM)

International Nonproprietary Names (INNs) in main languages (French, Latin, and Spanish): Amobarbitaalinatrium; Amobarbital sodico; Amobarbital sodique; Amobarbital sodna sul; Amobarbitalio natrio druska; Amobarbitalnatrium; Amobarbital-natrium; Amobarbitalum natricum; Amylobarbitone Sodium; Barbamylum; Natrii Amobarbitalum; Pentymalnatrium; Sodium Amobarbital; Soluble Amylobarbitone.

C11H17N2NaO3 = 248.3

CAS 64-43-7


Pharmacopoeias. In China, Europe, and US. Japan includes Amobarbital Sodium for Injection. European Pharmacopoeia, 6th ed. (Amobarbital Sodium). A white or almost white, hygroscopic, granular powder. Very soluble in carbon dioxide-free water (a small fraction may be insoluble) freely soluble in alcohol. A 10% solution in water has apHofnotmorethan 11.0. Store in airtight containers.

The United States Pharmacopeia 31, 2008 (Amobarbital Sodium). A white, odourless, hygroscopic, friable, granular powder. Very soluble in water soluble in alcohol practically insoluble in chloroform and in ether. Solutions decompose on standing decomposition is accelerated by heat. pH of a 10% solution in water is not more than 11.0. Store in airtight containers.


Amobarbital may be precipitated from preparations containing amobarbital sodium, depending on the concentration and pH. Amobarbital sodium has, therefore, been reported to be incompatible with many other drugs, particularly acids and acidic salts.


Dependence and Withdrawal of Barbiturates

The development of dependence is a high risk with amobarbital and other barbiturates and may occur after regular use even in therapeutic doses for short periods. Barbiturates should not therefore be stopped abruptly, but should be withdrawn by gradual reduction of the dose over a period of days or weeks. A long-acting barbiturate such as phenobarbital may be substituted for a short- or intermediate-acting one, followed by gradual reduction of the phenobarbital dose.

Withdrawal symptoms are similar to those of alcohol withdrawal and are characterised after several hours by apprehension and weakness, followed by anxiety, headache, dizziness, irritability, tremors, nausea and vomiting, abdominal cramps, insomnia, distortion in visual perception, muscle twitching, and tachycardia. Orthostatic hypotension and convulsions may develop after a day or two, sometimes leading to status epilepticus. Hallucinations and delirium tremens may develop after several days followed by coma before the symptoms disappear or death occurs.

Adverse Effects

Drowsiness, sedation, and ataxia are the most frequent adverse effects of amobarbital and other barbiturates and are a consequence of dose-related CNS depression. Other adverse effects include respiratory depression, headache, gastrointestinal disturbances, skin reactions, confusion, and memory defects. Paradoxical excitement and irritability may occur, particularly in children, the elderly, and patients in acute pain.

Hypersensitivity reactions occur rarely and include skin rashes (erythema multi-forme and exfoliative dermatitis, sometimes fatal, have been reported), hepatitis and cholestasis, and photo sensitivity. Blood disorders, including megaloblastic anaemia after chronic use of barbiturates, have also occurred occasionally. Neonatal intoxication, drug dependence, and symptoms resembling vitamin-K deficiency have been reported in infants born to mothers who received barbiturates during pregnancy. Congenital malformations have been reported in children of women who took barbiturates during pregnancy, but the causal role is a matter of some debate.

Nystagmus, miosis, slurred speech, and ataxia may occur with excessive doses of barbiturates. The toxic effects of overdosage result from profound central depression and include coma, respiratory and cardiovascular depression, with hypotension and shock leading to renal failure and death. Hypothermia may occur with subsequent pyrexia on recovery. Erythematous or haemor-rhagic blisters reportedly occur in about 6% of patients, but are not characteristic solely of barbiturate poisoning. Solutions of the sodium salts of barbiturates are extremely alkaline, and necrosis has followed subcutaneous injection. Intravenous injection may be hazardous hypotension, shock, laryngos-pasm, and apnoea have occurred particularly after rapid injection. Gangrene has resulted from intra-arterial injection into an extremity.


A detailed review of drug-induced stupor and coma, including that caused by barbiturates.

Treatment of Adverse Effects

After an overdose of a barbiturate, endotracheal intubation may be necessary if the patient is unconscious. Giving activated charcoal by mouth or nasogastric tube is recommended in patients who have ingested more than 10 mg/kg and present within 1 hour of ingestion repeat doses may be necessary. Patients should be managed with intensive supportive therapy, with particular attention being paid to the maintenance of cardiovascular, respiratory, and renal functions, and to the maintenance of the electrolyte balance. Charcoal haemoperfusion can be life-saving in the most severe cases and should be considered if there is no improvement after 24 hours of supportive care. The value of other measures aimed at the active removal of barbiturates is questionable.


Amobarbital and other barbiturates are best avoided in elderly and debilitated patients, in young adults, in children, and in those with depression.

Amobarbital is contra-indicated in patients with pulmonary insufficiency, sleep apnoea, pre-existing CNS depression or coma, and severe hepatic impairment, and should be given with caution to those with renal impairment. Barbiturates given to patients in pain may provoke a paradoxical excitatory reaction, unless an analgesic is also given. With continued use, tolerance develops to the sedative or hypnotic effects of the barbiturates to a greater extent than to their lethal effects. Barbiturates may cause drowsiness which may persist the next day affected patients should not drive or operate machinery.

See Adverse Effects, above, for the hazards of giving barbiturates during pregnancy and Breast Feeding, below, for cautions on their use in nursing mothers.

Dependence readily develops after use of barbiturates with a withdrawal syndrome if stopped abruptly (see Dependence and Withdrawal, above). Barbiturates are abused for their euphoriant effects.

Breast feeding.

Small amounts of barbiturates are distributed into breast milk, and most authorities, such as the BNF, consider that they should not be taken while breast feeding. The American Academy of Pediatrics notes that the long-acting antiepileptic barbiturate, phenobarbital, has been associated with significant effects on some nursing infants, although it suggests that some other barbiturates may be compatible with breast feeding.


Barbiturates including amobarbital have been associated with acute attacks of porphyria and are considered unsafe in porphyric patients.


Sedation or respiratory depression may be enhanced by drugs with CNS-depressant properties in particular alcohol should be avoided. Barbiturates generally induce liver enzymes, and thus increase the rate of metabolism (and decrease the activity) of many other drugs as well as endogenous substances. Continued use may result in induction of their own metabolism. MAO Is may prolong the CNS depressant effects of some barbiturates, probably by inhibition of their metabolism. However, MAO Is, like other antidepressants, also reduce the convulsive threshold and thereby antagonise the anticonvulsant action of barbiturates. For some further interactions involving barbiturates, see under Phenobarbital.


Amobarbital is readily absorbed from the gastrointestinal tract. It is about 60% bound to plasma proteins. It has a half-life of about 20 to 25 hours which is considerably extended in neonates. It crosses the placenta and small amounts are distributed into breast milk. Amobarbital is metabolised in the liver up to about 50% is excreted in the urine as 3′-hy droxy amy lobarbital and up to about 30% as AT-hydroxyamylobarbital, less than 1% appearing unchanged up to about 5% is excreted in the faeces.

Uses and Administration

Amobarbital is a barbiturate that has been used as a hypnotic and sedative. Its use can no longer be recommended because of its adverse effects and risk of dependence, although continued use may occasionally be considered necessary for severe intractable insomnia in patients already taking it. The usual oral dose was 100 to 200 mg of the base or 60 to 200 mg of the sodium salt, taken at bedtime. A more rapid onset of effect was obtained with the sodium salt.

Barbiturates with a longer action such as phenobarbital are still used in epilepsy and those with a shorter action such as methohexital orthiopental for anaesthesia.

Cerebrovascular disorders.

For reference to the use of barbiturate-induced coma in the management of patients with cerebral ischaemia.


Amobarbital is used for specialised procedures in expert epilepsy centres only. It is given by deep intramuscular or slow intravenous injection as the sodium salt.


The United States Pharmacopeia 31, 2008: Amobarbital Sodium for Injection Secobarbital Sodium and Amobarbital Sodium Capsules.

Proprietary Preparations

Australia: Amytal † Neur-Amyl †

Canada: Amytal †

Hungary: Dorlotyn †

United Kingdom: Amytal

USA: Amytal


Argentina: Cuait N

Hungary: Tardyl †

South Africa: Repasma

Thailand: Ama

United Kingdom: Tuinal

USA: Tuinal

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