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Barbituric acid, the basic structure of all barbiturates

Barbiturates are drugs that act as central nervous system depressants, and can therefore produce a wide spectrum of effects, from mild sedation to total anesthesia. They are also effective as anxiolytics, hypnotics, and anticonvulsants. Barbiturates also have analgesic effects; however, these effects are somewhat weak, preventing barbiturates from being used in surgery in the absence of other analgesics. They have addiction potential, both physical and psychological. Barbiturates have now largely been replaced by benzodiazepines in routine medical practice – for example, in the treatment of anxiety and insomnia – mainly because benzodiazepines are significantly less dangerous in overdose. However, barbiturates are still used in general anesthesia, for epilepsy, for the treatment of acute migraines and cluster headaches (in the compound drug fioricet), occasionally for the treatment of recurrent migraines and cluster headaches (under stringent protocols with mandatory physician monitoring for addiction and abuse), and (where legal) assisted suicide and euthanasia.[1] Barbiturates are derivatives of barbituric acid.[2]


Barbituric acid was first synthesized December 6, 1864, by German researcher Adolf von Baeyer. This was done by condensing urea (an animal waste product) with diethyl malonate (an ester derived from the acid of apples). There are several stories about how the substance got its name. The most likely story is that Baeyer and his colleagues went to celebrate their discovery in a tavern where the town's artillery garrison were also celebrating the feast of Saint Barbara—the patron saint of artillerymen. An artillery officer is said to have christened the new substance by amalgamating Barbara with urea.[3] Another story holds that Baeyer synthesized the substance from the collected urine of a Munich waitress named Barbara.[4] No substance of medical value was discovered, however, until 1903 when two German scientists working at Bayer, Emil Fischer and Joseph von Mering, discovered that barbital was very effective in putting dogs to sleep. Barbital was then marketed by Baeyer under the trade name Veronal. It is said that Mering proposed this name because the most peaceful place he knew was the Italian city of Verona.[3]

It was not until the 1950s that the behavioural disturbances and physical dependence potential of barbiturates became recognized.[5]

Barbituric acid itself does not have any direct effect on the central nervous system and chemists have derived over 2,500 compounds from it that possess pharmacologically active qualities. The broad class of barbiturates is further broken down and classified according to speed of onset and duration of action. Ultrashort-acting barbiturates are commonly used for anesthesia because their extremely short duration of action allows for greater control. These properties allow doctors to rapidly put a patient "under" in emergency surgery situations. Doctors can also bring a patient out of anesthesia just as quickly, should complications arise during surgery. The middle two classes of barbiturates are often combined under the title "short/intermediate-acting." These barbiturates are also employed for anesthetic purposes, and are also sometimes prescribed for anxiety or insomnia. This is not a common practice anymore, however, owing to the dangers of long-term use of barbiturates; they have been replaced by the benzodiazepines for these purposes. The final class of barbiturates are known as long-acting barbiturates (the most notable one being phenobarbital, which has a half-life of roughly 92 hours). This class of barbiturates is used almost exclusively as anticonvulsants, although on rare occasions they are prescribed for daytime sedation. Barbiturates in this class are not used for insomnia, because, owing to their extremely long half-life, patients would awake with a residual "hang-over" effect and feel groggy.

Barbiturates can in most cases be used either as the free acid or as salts of sodium, calcium, potassium, magnesium, lithium, etc. Codeine- and Dionine-based salts of barbituric acid have been developed. In 1912, Baeyer introduced another barbituric acid derivative, phenobarbital, under the trade name Luminal, as a sedative-hypnotic.[6]

Therapeutic uses

Barbiturates such as phenobarbital were long used as anxiolytics and hypnotics, but today have been largely replaced by benzodiazepines for these purposes because of less potential for lethal overdoses.[7][8][9] However, barbiturates are still used as anticonvulsants, as para-operative sedatives (ex. sodium thiopental), and analgesics for cluster headaches/ migraines (ex. fioricet).

Prescribing protocols

The high risk of addiction and abuse associated with barbiturates, their extreme toxicity relative to alternatives such as benzodiazepines, and their potentiation of other gabaminergic and sedative drugs (including alcohol) are all concerns with long term barbiturate use even when used on an as-needed basis. For this reason, many states have mandatory protocols for barbiturate prescription to assure patient compliance with usage instructions. Though protocols differ among jurisdictions, and not all states require all preventative measures, common requirements include:

  • Routine drug testing to ensure the patient is using the drug (not diverting it) and has not been using other prescription or street drugs the doctor is not aware of
  • Allowing only one pharmacy per patient to provide the drug
  • Reporting all other prescription drugs to the prescribing doctor (sometimes blocking the prescription if other sedatives or gabaminergics are used)
  • Requiring patients to accept pharmacist counseling
  • Increased scheduling of barbiturates (treating them as schedule 2 or 3 drugs, which may prevent doctors from adding automatic refills)
  • Treating barbiturates as second line agents (requiring alternative treatment attempts before prescribing them)
  • Specifying a maximum amount of pills or total dose of pills in each prescription.

Doctors often use these practices even when not legally required, as they are consistent with best-practice medical guidelines, and limit physician liability in the event of abuse or overdose.

Doctors are also told to re-evaluate the need for the prescription before each fill is written. It is not uncommon for prescribing doctors to require patients to enter a narcotics contract before receiving the drug. These contracts often include the above protocols as well as forbidding the patients to accept any barbiturate or opiate out-patient prescriptions from any other doctor (including emergency room doctors) for any purpose (including pre-medications for medical services such as anxiolytics prior to dental appointments) unless they have received prior permission from the doctor with whom the contract was entered (it is also considered a felony in most states to accept narcotics from multiple doctors); patients are generally but not always permitted to accept single doses of narcotics from emergency personnel when they are administered directly by that doctor (in the case of IV/IM administration) or the patient is directly observed when taking the drug (in the case of oral/rectal administration). In many cases, doctors also forbid patients from consuming alcohol while accepting treatment. The definition of narcotic varies among doctors, but always include opiates/opioids and barbiturates, with benzodiazepines and amphetamines often being included as well, and occasionally broad-term drug categories such as sedatives, muscle relaxers, and anxiolytics of any mechanism. Violation of narcotic contracts generally result in immediate and permanent dismissal of the patient from the practice and, when applicable (ex. diversion of the drug or collecting narcotics from multiple prescribers/practices), a report issued by the doctor to law enforcement. Occasionally, doctors accept patients who have been previously discharged for the use of street drugs if the patient has undergone (or is undergoing) treatment for their addiction, often with the additional requirement of much more frequent drug tests than would otherwise be required.

When another doctor (usually a specialist or an E.R. doctor) believes that the patient is in need of another narcotic (ex. for acute pain control after injury/surgery, treatment of epilepsy/anxiety/insomnia, pre-medication, etc.) it is common practice for them to contact the provider with whom the patient has signed a narcotics contract and have that doctor prescribe the medication according to the requesting doctors suggestion, although they may sometimes suggest a different drug or dosage due to concerns about drug interactions or known sensitivities to the suggested drug. In some cases the second doctor may be given permission to prescribe the drug themselves when the drug falls under the definition of a narcotic under the terms of the narcotics contract but not under the states legal definition as long as the second doctor informs the first whenever a prescription of that drug is issued (this is common with prescriptions of amphetamines, benzodiazepines, and z-drugs issued by a psychiatrist).

Other uses related to their physiological properties

Barbiturates in high doses are used for physician-assisted suicide (PAS), and in combination with a muscle relaxant for euthanasia and for capital punishment by lethal injection.[10][11]

Thiopental is an ultra-short acting barbiturate that is marketed under the name sodium pentothal. It is often mistaken for "truth serum" or sodium amytal, an intermediate-acting barbiturate that is used for sedation and to treat insomnia, but was also used in so-called sodium amytal "interviews" where the person being questioned would be much more likely to provide the truth whilst under the influence of this drug. When dissolved in water, sodium amytal can be swallowed, or it can be administered by intravenous injection. The drug does not itself force people to tell the truth, but is thought to decrease inhibitions, making subjects more likely to be caught off guard when questioned, and increasing the possibility of the subject revealing information through emotional outbursts.[12] The memory impairing effects and cognitive impairments induced by the drug are thought to reduce a subjects ability to invent and remember lies. This practice is no longer considered legally admissible in court due to findings that subjects undergoing such interrogations may form false memories, putting the reliability of all information obtained through such methods into question.[13]

Mechanism of action

The principal mechanism of action of barbiturates is believed to be positive allosteric modulation of GABAA receptors.[14] GABA is the principal inhibitory neurotransmitter in the mammalian central nervous system (CNS). Barbiturates bind to the GABAA receptor at multiple homologous transmembrane pockets located at subunit interfaces,[15] which are binding sites distinct from GABA itself and also distinct from the benzodiazepine binding site. Like benzodiazepines, barbiturates potentiate the effect of GABA at this receptor. In addition to this GABA-ergic effect, barbiturates also block the AMPA receptor, a subtype of glutamate receptor. Glutamate is the principal excitatory neurotransmitter in the mammalian CNS. Taken together, the findings that barbiturates potentiate inhibitory GABAA receptors and inhibit excitatory AMPA receptors can explain the CNS-depressant effects of these agents. At higher concentration, they inhibit the Ca2+-dependent release of neurotransmitters.[16] Barbiturates produce their pharmacological effects by increasing the duration of chloride ion channel opening at the GABAA receptor (pharmacodynamics: This increases the efficacy of GABA), whereas benzodiazepines increase the frequency of the chloride ion channel opening at the GABAA receptor (pharmacodynamics: This increases the potency of GABA). The direct gating or opening of the chloride ion channel is the reason for the increased toxicity of barbiturates compared to benzodiazepines in overdose.[17][18]

Further, barbiturates are relatively non-selective compounds that bind to an entire superfamily of ligand-gated ion channels, of which the GABAA receptor channel is only one of several representatives. This superfamily of ion channels includes the neuronal nAChR channel, the 5HT3R channel, the GlyR channel and others. However, while GABAA receptor currents are increased by barbiturates (and other general anaesthetics), ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nAChR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital.[19] Such findings implicate (non-GABA-ergic) ligand-gated ion channels, e.g. the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.[20] This is the mechanism responsible for the (mild to moderate) anesthetic effect of barbiturates in high doses when used in anesthetic concentration

Tolerance, dependence, overdose, and adverse reaction

There are special risks to consider for older adults, women who are pregnant, and babies. When a person ages, the body becomes less able to rid itself of barbiturates. As a result, people over the age of sixty-five are at higher risk of experiencing the harmful effects of barbiturates, including drug dependence and accidental overdose.[21] When barbiturates are taken during pregnancy, the drug passes through the mother's bloodstream to her fetus. After the baby is born, it may experience withdrawal symptoms and have trouble breathing. In addition, nursing mothers who take barbiturates may transmit the drug to their babies through breast milk.[22]

Tolerance and dependence

With regular use, tolerance to the effects of barbiturates develops.


Symptoms of an overdose typically include sluggishness, incoordination, difficulty in thinking, slowness of speech, faulty judgement, drowsiness, shallow breathing, staggering, and, in severe cases, coma or death. The lethal dosage of barbiturates varies greatly with tolerance and from one individual to another. A dose of 1 g orally can be highly poisonous, with dosages from 2 to 10 g generally being fatal depending on the person's tolerance level. Even in inpatient settings, however, the development of tolerance is still a problem, as dangerous and unpleasant withdrawal symptoms can result when the drug is stopped after dependence has developed. Tolerance to the anxiolytic and sedative effects of barbiturates tends to develop faster than tolerance to their effects on smooth muscle, respiration, and heart rate, making them generally unsuitable for long time psychiatric use. Tolerance to the anticonvulsant effects tends to correlate more with tolerance to physiological effects, however, meaning that they are still a viable option for long-term epilepsy treatment.

Barbiturates in overdose with other CNS (central nervous system) depressants (e.g. alcohol, opiates, benzodiazepines) are even more dangerous due to additive CNS and respiratory depressant effects. In the case of benzodiazepines, not only do they have additive effects, barbiturates also increase the binding affinity of the benzodiazepine binding site, leading to exaggerated benzodiazepine effects. (ex. If a benzodiazepine increases the frequency of channel opening by 300%, and a barbiturate increases the duration of their opening by 300%, then the combined effects of the drugs increase the channels overall function by 900%, not 600%).

Ingeborg Bachmann may have died of the consequences of barbiturate withdrawal.

Adverse reaction

A rare adverse reaction to barbiturates is Stevens-Johnson syndrome, which primarily affects the mucous membranes.

Recreational use

Recreational users report that a barbiturate high gives them feelings of relaxed contentment and euphoria. Physical and psychological dependence may also develop with repeated use.[23] Other effects of barbiturate intoxication include drowsiness, lateral and vertical nystagmus, slurred speech and ataxia, decreased anxiety, a loss of inhibitions. Barbiturates are also used to alleviate the adverse or withdrawal effects of illicit drug use, in a manner similar to long-acting benzodiazepines such as diazepam and clonazepam.[24][25]

Drug users tend to prefer short-acting and intermediate-acting barbiturates.[26] The most commonly abused are amobarbital (Amytal), pentobarbital (Nembutal), and secobarbital (Seconal). A combination of amobarbital and secobarbital (called Tuinal) is also highly abused. Short-acting and intermediate-acting barbiturates are usually prescribed as sedatives and sleeping pills. These pills begin acting fifteen to forty minutes after they are swallowed, and their effects last from five to six hours.

Slang terms for barbiturates include barbs, bluebirds, dolls, wallbangers, yellows, downers, goofballs, sleepers, 'reds & blues' and tooties.[27]

Legal status

In the 1940s, military personnel were given "Goofballs" during WWII in the South Pacific region to allow soldiers to tolerate the heat and humidity of daily working conditions. Goofballs were distributed to reduce the demand of the respiratory system, as well as maintain blood pressure to combat the extreme conditions. Many soldiers returned with addictions that required several months of rehabilitation before discharge. This led to addiction problems through the 1950s and 1960s.

In the 1950s and 1960s, increasing published reports of barbiturate overdoses and dependence problems appeared. This eventually led to scheduling barbiturates as controlled drugs.

In the United States, the Controlled Substances Act of 1970 classified several barbiturates as controlled substances—and they remain so classified as of December 2013. Barbital, methylphenobarbital also known as mephobarbital (brand name Mebaral), and phenobarbital are designated schedule IV drugs, and "Any substance which contains any quantity of a derivative of barbituric acid, or any salt of a derivative of barbituric acid"[28] (all other barbiturates) were designated as schedule III. No barbiturates are in schedule I, II, or V.[29]

In 1971, the Convention on Psychotropic Substances was signed in Vienna. Designed to regulate amphetamines, barbiturates, and other synthetics, the 34th version as of 25 January 2014 of the treaty regulates secobarbital as schedule II, amobarbital, butalbital, cyclobarbital, and pentobarbital as schedule III, and allobarbital, barbital, butobarbital, mephobarbital, phenobarbital, butabarbital, and vinylbital as schedule IV scheduled substances on its "Green List".[30] The butalbital compound medication Fioricet (butalbital, caffeine, paracetamol(acetaminophen)), however, is specifically exempted from controlled substance status, its sister compound Fiorinal (substitutes aspirin for paracetamol) remains a schedule IV drug.

Other uses in chemistry

In 1988, the synthesis and binding studies of an artificial receptor binding barbiturates by 6 complementary hydrogen bonds was published.[31] Since this first article, different kind of receptors were designed, as well as different barbiturates and cyanurates, not for their efficiencies as drugs but for applications in supramolecular chemistry, in the conception of materials and molecular devices.

Sodium barbital and barbital are the buffering components of the traditional Veronal buffer, which is widely used for serum electrophoresis in agarose gel.


Generic structure of a barbiturate, including numbering scheme
Short Name R1 R2 IUPAC Name
allobarbital CH2CHCH2 CH2CHCH2 5,5-diallylbarbiturate
amobarbital[32] CH2CH3 (CH2)2CH(CH3)2 5-ethyl-5-isopentyl-barbiturate
aprobarbital CH2CHCH2 CH(CH3)2 5-allyl-5-isopropyl-barbiturate
alphenal CH2CHCH2 C6H5 5-allyl-5-phenyl-barbiturate
barbital CH2CH3 CH2CH3 5,5-diethylbarbiturate
brallobarbital CH2CHCH2 CH2CBrCH2 5-allyl-5-(2-bromo-allyl)-barbiturate
pentobarbital[32] CH2CH3 CHCH3(CH2)2CH3 5-ethyl-5-(1-methylbutyl)-barbiturate
phenobarbital[32] CH2CH3 C6H5 5-ethyl-5-phenylbarbiturate
secobarbital[32] CH2CHCH2 CHCH3(CH2)2CH3 5-[(2R)-pentan-2-yl]-5-prop-2-enyl-barbiturate

See also


  1. ^ "DIGNITAS". Archived from the original on 21 July 2011. Retrieved 2011-06-14. 
  2. ^ Edward R. Garrett, Jacek T. Bojarski†, Gerald J. Yakatan (21 Sep 2006). "Kinetics of hydrolysis of barbituric acid derivatives". Journal of Pharmaceutical Sciences 60 (8): 1145–54.  
  3. ^ a b "Barbiturates". Archived from the original on 7 November 2007. Retrieved 2007-10-31. 
  4. ^ Medical Curiosities. Youngson, Robert M. London: Robinson Publishing, 1997. Page 276.
  5. ^ Galanter, Marc; Kleber, Herbert D. (1 July 2008). The American Psychiatric Publishing Textbook of Substance Abuse Treatment (4th ed.). United States of America: American Psychiatric Publishing Inc. p. 217.  
  6. ^ Sneader, Walter (2005-06-23). Drug Discovery. John Wiley and Sons. p. 369.  
  7. ^ Whitlock FA (June 14, 1975). "Suicide in Brisbane, 1956 to 1973: the drug-death epidemic". Med J Aust 1 (24): 737–43.  
  8. ^ Johns MW (1975). "Sleep and hypnotic drugs". Drugs 9 (6): 448–78.  
  9. ^ Jufe GS (Jul–August 2007). "[New hypnotics: perspectives from sleep physiology]". Vertex 18 (74): 294–9.  
  10. ^ "Administration and Compounding Of Euthanasic Agents". Archived from the original on 7 June 2008. Retrieved 15 July 2008. 
  11. ^ Daniel Engber. "Why do lethal injections have three drugs?". Slate Magazine. Archived from the original on 25 July 2008. Retrieved 15 July 2008. 
  12. ^ "Neuroscience for Kids - Barbiturates". Archived from the original on 16 June 2008. Retrieved 2008-06-02. 
  13. ^ Stocks, JT (1998). "Recovered memory therapy: a dubious practice technique". Social work 43 (5): 423–36.  
  14. ^ Löscher, W.; Rogawski, M. A. (2012). "How theories evolved concerning the mechanism of action of barbiturates". Epilepsia 53: 12–25.  
  15. ^ Chiara, D. C.; Jayakar, S. S.; Zhou, X.; Zhang, X.; Savechenkov, P. Y.; Bruzik, K. S.; Miller, K. W.; Cohen, J. B. (15 May 2013). "Specificity of Intersubunit General Anesthetic-binding Sites in the Transmembrane Domain of the Human α1β3γ2 γ-Aminobutyric Acid Type A (GABAA) Receptor". Journal of Biological Chemistry 288 (27): 19343–19357.  
  16. ^ Brunton, Laurence L.; Lazo, John S.; Parker, Keith L.; Goodman, Louis Sanford; Gilman, Alfred Goodman (2005). Goodman & Gilman's Pharmacological Basis of Therapeutics. McGraw-Hill.  
  17. ^ Neil Harrison; Wallace B Mendelson and Harriet de Wit (2000). "Barbiturates". Neuropsychopharmacology. Retrieved 15 July 2008. ...Barbiturates therefore promote entry of GABA-activated channels into a long-lived open state, whereas [benzodiazepines] increase only the frequency of channel opening into the initial open state. These mechanistic studies reveal interesting details of the changes in channel gating caused by barbiturates but as yet have yielded no insights into the molecular sites of action. An additional interesting effect of barbiturates is direct gating of the channels, i.e., the barbiturates may open the channel even in the absence of GABA. This usually occurs at significantly higher concentrations than those that potentiate the actions of GABA; these concentrations also are generally higher than those required for clinically effective anesthesia. 
  18. ^ Society for Neurochemistry, American; George J. Siegel M.D., Bernard W. Agranoff M.D., Stephen K. Fisher Ph.D., R. Wayne Albers Ph.D., Michael D. Uhler Ph.D. (1999) [1998]. "Part 2 Chapter 16". Basic Neurochemistry - Molecular, Cellular and Medical Aspects (Sixth ed.). Lippincott Williams and Wilkins.  
  19. ^ Weber, M; Motin, L; Gaul, S; Beker, F; Fink, RH; Adams, DJ (January 2005). "Intravenous anaesthetics inhibit nicotinic acetylcholine receptor-mediated currents and Ca2+ transients in rat intracardiac ganglion neurons".  
  20. ^ Franks, NP; Lieb, WR (23 November 1998). "Which molecular targets are most relevant to general anaesthesia?". Toxicology Letters. 100–101: 1–8.  
  21. ^ WebMD. "Toxicity, Barbiturate". eMedicine. Archived from the original on 20 July 2008. Retrieved 15 July 2008. 
  22. ^ Nau H; Kuhnz W; Egger HJ; Rating D; Helge H (Nov–December 1982). "Anticonvulsants during pregnancy and lactation. Transplacental, maternal and neonatal pharmacokinetics". Clin Pharmacokinet 7 (6): 508–43.  
  23. ^ Schlatter J; Sitbon N; Saulnier JL (February 17, 2001). "[Drugs and drug abusers]". Presse Med 30 (6): 282–7.  
  24. ^ Emedicine Health. "Barbiturate Abuse". p. 1. Archived from the original on 2 August 2008. Retrieved 15 July 2008. 
  25. ^ Faulkner TP; Hayden JH; Mehta CM; Olson DA; Comstock EG (1979). "Dose-response studies on tolerance to multiple doses of secobarbital and methaqualone in a polydrug abuse population". Clin Toxicol 15 (1): 23–37.  
  26. ^ Coupey SM (August 1997). "Barbiturates". Pediatr Rev 18 (8): 260–4.  
  27. ^ Hamid H.; El-Mallakh RS; Vandeveir K (March 2005). "Substance Abuse: Medical and Slang Terminology". South Med J (Medscape) 98 (3): 350–362.  
  28. ^ Pub. L. 91-513, October 27, 1970, Sec. 202(c) Sched. III(b)(1)
  29. ^ 21 U.S.C. § 812
  30. ^ "List of Psychotropic Substances under International Control ("Green List")" (PDF). International Narcotics Control Board. 25 January 2014. Retrieved 19 December 2013. 
  31. ^ Chang, Suk Kyu.; Hamilton, Andrew D. (1988). "Molecular recognition of biologically interesting substrates: Synthesis of an artificial receptor for barbiturates employing six hydrogen bonds". Journal of the American Chemical Society 110 (4): 1318–1319.  
  32. ^ a b c d Smith, Roger; Bogusz, Maciej J (September 22, 2011). Forensic Science (2 ed.). Elsevier. p. 245.  

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