Generic Name:
desflurane

Trade Name:
Suprane® [Baxter]

IUPAC Name:
2-(difluoromethoxy)-1,1,1,2-tetrafluoro-
ethane

Dosage Forms/Routes:
volatile liquid/inhalation

Major Metabolite:
trifluoroacetic acid

Database Search Links:
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[Search PubMed for
Randomized Controlled Trials]
[PubChem]
[PDSP K_i database]

Initial Approval:
09/18/1992

Manufacturers:
[FDA Search]

Prescribing
Information:
[Link]

RxList:
[Link]

Empirical Formula:
C₃H₂F₆O

Molecular Mass:
168.038 g/mol

Possible Mechanisms of Action:
Desflurane is a noncompetitive antagonist of NMDA receptor channels (1). In addition, desflurane increases the effect of GABA at GABA-A receptor channels (2). The drug may also activate the human tandem pore domain potassium channel, TRESK (3). Desflurane may affect other types of potassium channels as well, but more research is necessary to provide a more comprehensive profile of the drug's effects on ion channels. Compared with halothane, desflurane is a relatively weak inducer of Ca²⁺ release from sarcoplasmic reticulum Ca²⁺ release channels in muscle cells (4). Nevertheless, the drug should definitely be avoided in all patients susceptible to malignant hyperthermia (5) .

Because the other fluorinated volatile anesthetics enhance the effect of glycine at glycine receptors, desflurane is likely to share this mechanism of action. However, further experimentation is needed in order to clarify the matter. In addition, desflurane is likely to share another key property with other fluorinated anesthetics: the ability to inhibit the exchange of GTPγS for GDP bound to the nucleotide binding site of a subset of Gα proteins that may include Gα_q (6).

Indications:
Desflurane is indicated as an inhalation agent for induction and/or maintenance of anesthesia for inpatient and outpatient surgery in adults (see PRECAUTIONS in the prescribing information).

Desflurane is not recommended for induction of anesthesia in pediatric patients because of a high incidence of moderate to severe upper airway adverse events (see WARNINGS in the prescribing information). After induction of anesthesia with agents other than desflurane, and tracheal intubation, desflurane is indicated for maintenance of anesthesia in infants and children.

Chemical Class:
haloether

PubChem 2D Structure:

"3D" Structure (Requires Chime):
[Link] 

Generic Name:
enflurane

Trade Name:
Ethrane ® [Baxter]

IUPAC Name:
2-chloro-1-(difluoromethoxy)-1,1,2-trifluoro-
ethane

Dosage Forms/Routes:
volatile liquid/inhalation

Major Metabolite:
trifluoroacetic acid

Database Search Links:
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[Search PubMed for
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Initial Approval:
08/28/1972

Manufacturers:
[FDA Search]

Prescribing
Information:
[Link]

Empirical Formula:
C₃H₂ClF₅O

Molecular Mass:
184.492 g/mol

Possible Mechanisms of Action:
Enflurane is a noncompetitive inhibitor of NMDA and AMPA glutamate receptor channels (7, 8). Enflurane enhances the effect of glutamate at GluR6 kainate receptor channels (9, 10). In addition, the drug enhances the effect of glycine at glycine receptor channels and the effect of GABA at GABA-A receptor channels (11). Furthermore, enflurane may inhibit voltage-gated Na⁺ channels (12). Enflurane may also inhibit certain types of potassium channels, such as the human intermediate conductance Ca²⁺ activated K⁺ channel hIK1 (13). The drug may also have a small inhibitory effect at Kv1.1 voltage-gated K⁺ channels (14).

At sub-anesthetic doses, enflurane inhibits the exchange of GTPγS for GDP bound to the nucleotide binding site of a subset of Gα (G alpha) proteins; these include Gα_i2 > Gα_i1 > Gα_i3 > Gα_s (15).

Enflurane inhibits plasma membrane Ca²⁺-ATPase and sarcoplasmic reticulum Ca²⁺-ATPase (16). The drug may also increase the release of Ca²⁺ from sarcoplasmic reticulum Ca²⁺ release channels in muscle cells (17). Depending on the cell type considered, enflurane might inhibit T-type and L-type voltage-gated Ca²⁺ channels (18). The drug may inhibit the effect of GABA at rho₁ GABA-C receptors as well (19). Finally, enflurane may enhance the effect of serotonin at 5-HT3 receptor channels (20).

Indications:
Enflurane may be used for induction and maintenance of general anesthesia. Enflurane may be used to provide analgesia for vaginal delivery. Low concentrations of enflurane (see DOSAGE AND ADMINISTRATION in the prescribing information) may also be used to supplement other general anesthetic agents during delivery by Cesarean section. Higher concentrations of enflurane may produce uterine relaxation and an increase in uterine bleeding.

Chemical Class:
haloether

PubChem 2D Structure:

"3D" Structure (Requires Chime):
[Link] 

Generic Name:
etomidate

Trade Name:
Amidate® [Hospira]

IUPAC Name:
ethyl 3-(1-phenylethyl)imidazole-4-carboxylate

Dosage Forms/Routes:
injectable/injection

Major Metabolite:
R-(+)-1-(1- phenylethyl)-1H-imidazole-
5-carboxylic acid

Database Search Links:
[PubMed]
[Search PubMed for
Randomized Controlled Trials]
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[PDSP K_i database]

Initial Approval:
09/07/1982

Manufacturers:
[FDA Search]

Prescribing
Information:
[Link] (for generic)

Empirical Formula:
C₁₄H₁₆N₂O₂

Molecular Mass:
244.289 g/mol

Possible Mechanisms of Action:
Etomidate potentiates the effect of GABA at GABA-A receptor channels (21). At T-type voltage-gated calcium channels, etomidate may have an inhibitory effect (22, 23). Etomidate is also an inhibitor of adrenocortical 11 beta-hydroxylase (24).

Indications:
Etomidate injection is indicated by intravenous injection for the induction of general anesthesia. When considering use of etomidate, the usefulness of its hemodynamic properties (see CLINICAL PHARMACOLOGY in the prescribing information) should be weighed against the high frequency of transient skeletal muscle movements (see ADVERSE REACTIONS in the prescribing information). Intravenous etomidate is also indicated for the supplementation of subpotent anesthetic agents, such as nitrous oxide in oxygen, during maintenance of anesthesia for short operative procedures such as dilation and curettage or cervical conization.

Chemical Class:
carboxylated imidazole

PubChem 2D Structure:

"3D" Structure (Requires Chime):
[Link] 

Generic Name:
halothane

IUPAC Name:
2-bromo-2-chloro-1,1,1-trifluoro-ethane

Dosage Forms/Routes:
volatile liquid/inhalation

Major Metabolite:
trifluoroacetic acid

Database Search Links:
[PubMed]
[Search PubMed for
Randomized Controlled Trials]
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[PDSP K_i database]

Initial Approval:
03/12/1958

Manufacturers:
[FDA Search]

RxList:
[Link]

Empirical Formula:
C₂HBrClF₃

Molecular Mass:
197.381 g/mol

Possible Mechanisms of Action:
Halothane is a noncompetitive antagonist of NMDA receptor channels (25). In addition, halothane potentiates the effect of GABA at GABA-A receptor channels (26). The drug also potentiates the effect of glycine at glycine receptor channels (27). Halothane may act as an antagonist at glutamate AMPA receptors expressing subunits such as GluR1, GluR3, and GluR2+3, but the drug enhances the effect of glutamate at GluR6 kainate receptor channels (9). Halothane may also potentiate the effect of serotonin at 5-HT3 receptors (28, 29). In addition, the drug is an antagonist at some neuronal nicotinic acetylcholine receptor subtypes such as the alpha7 (29) and alpha4beta2 (30) subtypes.Enflurane might also inhibit the effect of GABA at rho₁ GABA-C receptors (19).

Halothane activates human tandem pore domain potassium channels such as TRESK (3), TREK-1 (31), TREK-2 (32), TASK-1 (31, 33), and TASK-3 (33). In addition, halothane may inhibit voltage-gated Na⁺ channels (12). The drug may also inhibit L-type voltage-gated calcium channels (34). Furthermore, halothane might weakly inhibit T-type voltage-gated calcium channels (35). Halothane also inhibits plasma membrane Ca²⁺-ATPase and sarcoplasmic reticulum Ca²⁺-ATPase (16). In skeletal muscle, the drug induces the release of Ca²⁺ from the sarcoplasmic reticulum Ca²⁺ release channel, also known as the ryanodine receptor (36).

At sub-anesthetic doses, halothane inhibits the exchange of GTPγS for GDP bound to the nucleotide binding site of a subset of Gα (G alpha) proteins; these include Gα_i2 > Gα_i1 > Gα_i3 > Gα_s (15).

Indications:
Halothane is indicated for the induction and maintenance of general anesthesia.

Chemical Class:
haloalkane

PubChem 2D Structure:

"3D" Structure (Requires Chime):
[Link] 

Generic Name:
isoflurane

Trade Name:
Forane® [Baxter]

IUPAC Name:
2-chloro-2-(difluoromethoxy)-1,1,1-trifluoro-
ethane

Dosage Forms/Routes:
volatile liquid/inhalation

Major Metabolite:
trifluoroacetic acid

Database Search Links:
[PubMed]
[Search PubMed for
Randomized Controlled Trials]
[PubChem]
[PDSP K_i database]

Initial Approval:
12/18/1979

Manufacturers:
[FDA Search]

Prescribing
Information:
[Link]

RxList:
[Link]

Empirical Formula:
C₃H₂ClF₅O

Molecular Mass:
184.492 g/mol

Possible Mechanisms of Action:
Isoflurane is a noncompetitive antagonist of NMDA receptor channels (1). In addition, isoflurane potentiates the effect of GABA at GABA-A receptor channels (26). Glycine's effect at glycine receptor channels is also potentiated by isoflurane (37). Isoflurane may weakly inhibit glutamate AMPA receptors expressing subunits such as GluR1, GluR3, and GluR2+3, but the drug enhances the effect of glutamate at GluR6 kainate receptor channels (9). Isoflurane may also potentiate the effect of serotonin at 5-HT3 receptors (28, 29). In addition, the drug is an antagonist at some neuronal nicotinic acetylcholine receptor subtypes such as the alpha7 (29) and alpha4beta2 (30) subtypes. Isoflurane might also inhibit the effect of GABA at rho₁ GABA-C receptors (19).

Isoflurane may inhibit voltage-gated Na⁺ channels (12). The drug may also inhibit L-type voltage-gated calcium channels (34). Isoflurane might also weakly inhibit T-type voltage-gated calcium channels (22, 38). Isoflurane is likely to activate human tandem pore domain potassium channels such as TRESK (3), TREK-1 (31), TREK-2 (32), TASK-1 (31), and TASK-3 (39). Isoflurane also inhibits plasma membrane Ca²⁺-ATPase and sarcoplasmic reticulum Ca²⁺-ATPase (16). The drug may also increase the release of Ca²⁺ from sarcoplasmic reticulum Ca²⁺ release channels in muscle cells (17).

At sub-anesthetic doses, isoflurane inhibits the exchange of GTPγS for GDP bound to the nucleotide binding site of a subset of Gα (G alpha) proteins; these include Gα_i2 > Gα_i1 > Gα_i3 > Gα_s (15).

Indications:
Isoflurane may be used for the induction and maintenance of general anesthesia. Adequate data have not been developed to establish its application in obstetrical anesthesia.

Chemical Class:
haloether

PubChem 2D Structure:

"3D" Structure (Requires Chime):
[Link] 

Generic Name:
ketamine hydrochloride

Trade Name:
Ketalar® [Parkedale]

IUPAC Name:
2-(2-chlorophenyl)-2-methylamino-
cyclohexan-1-one hydrochloride

Dosage Forms/Routes:
injectable/injection

Major Metabolites:
norketamine;
hydroxynorketamine

Database Search Links:
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[Search PubMed for
Randomized Controlled Trials]
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[PDSP K_i database]

Initial Approval:
02/19/1970

Manufacturers:
[FDA Search]

Prescribing
Information:
[Link]

RxList:
[Link]

Empirical Formula:
C₁₃H₁₇Cl₂NO

Molecular Mass:
274.186 g/mol

Possible Mechanisms of Action:
Ketamine is a noncompetitive antagonist of NMDA receptor channels (1). The drug also inhibits some subtypes of neuronal nicotinic acetylcholine receptors in a noncompetitive and voltage-dependent manner (40). In addition, ketamine may be an antagonist at muscarinic M1 receptors (41). Further research is needed to clarify whether ketamine affects additional receptors at clinical concentrations.

Indications:
Ketamine hydrochloride injection is indicated as the sole anesthetic agent for diagnostic and surgical procedures that do not require skeletal muscle relaxation. Ketamine hydrochloride injection is best suited for short procedures but it can be used, with additional doses, for longer procedures.

Ketamine hydrochloride injection is indicated for the induction of anesthesia prior to the administration of other general anesthetic agents.

Ketamine hydrochloride injection is indicated to supplement low-potency agents, such as nitrous oxide.

Specific areas of application are described in the CLINICAL PHARMACOLOGY section of the prescribing information.

Chemical Class:
arylcyclohexylamine

PubChem 2D Structure:

"3D" Structure (Requires Chime):
[Link] 

Generic Name:
methohexital

Trade Name:
Brevital® Sodium [King]

IUPAC Name:
1-methyl-5-(1-methylpent-2-ynyl)-5-prop-
2-enyl-hexahydropyrimidine-2,4,6-trione

Dosage Forms/Routes:
injectable/injection

Major Metabolite:
4'-hydroxymethohexital

Database Search Links:
[PubMed]
[Search PubMed for
Randomized Controlled Trials]
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[PDSP K_i database]

Initial Approval:
06/27/1960

Manufacturers:
[FDA Search]

Prescribing
Information:
[Link]

RxList:
[Link]

Empirical Formula:
C₁₄H₁₇N₂NaO₃

Molecular Mass:
284.286 g/mol

Possible Mechanisms of Action:
Methohexital potentiates the effect of GABA at GABA-A receptor channels and directly causes the channels to open at higher concentrations (42). Methohexital may also act as an antagonist at kainate glutamate receptors (43, 44). Methohexital is likely to bind to glycine receptors without activating them or blocking glycine's effects; however, the drug may block the effects of thiopental and pentobarbital at glycine receptors (45).

Indications:
Brevital Sodium can be used in adults as follows:

1. For intravenous induction of anesthesia prior to the use of other general anesthetic agents.
2. For intravenous induction of anesthesia and as an adjunct to subpotent inhalational anesthetic agents (such as nitrous oxide in oxygen) for short surgical procedures; Brevital Sodium may be given by infusion or intermittent injection.
3. For use along with other parenteral agents, usually narcotic analgesics, to supplement subpotent inhalational anesthetic agents (such as nitrous oxide in oxygen) for longer surgical procedures.
4. As intravenous anesthesia for short surgical, diagnostic, or therapeutic procedures associated with minimal painful stimuli (see WARNINGS in the prescribing information). 5. As an agent for inducing a hypnotic state.

Brevital Sodium can be used in pediatric patients older than 1 month as follows:

1. For rectal or intramuscular induction of anesthesia prior to the use of other general anesthetic agents.
2. For rectal or intramuscular induction of anesthesia and as an adjunct to subpotent inhalational anesthetic agents for short surgical procedures.
3. As rectal or intramuscular anesthesia for short surgical, diagnostic, or therapeutic procedures associated with minimal painful stimuli.
   

Chemical Class:
barbiturate

PubChem 2D Structure:

"3D" Structure (Requires Chime):
[Link] 

Generic Name:
midazolam hydrochloride

IUPAC Name:
8-chloro-6-(2-fluorophenyl)-1-methyl-4H-
Imidazo(1,5-a)(1,4)benzodiazepine

Dosage Forms/Routes:
injectable/injection;
syrup/oral

Major Metabolites:
1-hydroxymidazolam;
4-hydroxymidazolam

Database Search Links:
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[Search PubMed for
Randomized Controlled Trials]
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[PDSP K_i database]

Initial Approval:
12/20/1985

Manufacturers:
[FDA Search]

Prescribing
Information:
[Link] (injectable)
[Link] (syrup)

RxList:
[Link]

Empirical Formula:
C₁₈H₁₄Cl₂FN₃

Molecular Mass:
362.228 g/mol

Possible Mechanism of Action:
Midazolam is a water soluble benzodiazepine agonist (46).

Indications:
Midazolam hydrochloride is indicated:

• intramuscularly or intravenously for preoperative sedation/ anxiolysis/amnesia;
• intravenously as an agent for sedation/anxiolysis/amnesia prior to or during diagnostic, therapeutic or endoscopic procedures, such as bronchoscopy, gastroscopy, cystoscopy, coronary angiography, cardiac catheterization, oncology procedures, radiologic procedures, suture of lacerations and other procedures either alone or in combination with other CNS depressants;
• intravenously for induction of general anesthesia, before administration of other anesthetic agents. With the use of narcotic premedication, induction of anesthesia can be attained within a relatively narrow dose range and in a short period of time. Intravenous midazolam can also be used as a component of intravenous supplementation of nitrous oxide and oxygen (balanced anesthesia);
• continuous intravenous infusion for sedation of intubated and mechanically ventilated patients as a component of anesthesia or during treatment in a critical care setting.
  

Chemical Class:
1,4-imidazole benzodiazepine

PubChem 2D Structure:

"3D" Structure (Requires Chime):
[Link] 

Generic Name:
nitrous oxide

IUPAC Name:
dinitrogen oxide

Dosage Forms/Routes:
gas/inhalation

Metabolism:
Nitrous oxide is not metabolized in the body.

Database Search Links:
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[PDSP K_i database]

Empirical Formula:
N₂O

Molecular Mass:
44.0129 g/mol

Possible Mechanisms of Action:
The key effect of nitrous oxide is its noncompetitive antagonism of NMDA receptor complexes (47). Nitrous oxide also slightly inhibits glutamate AMPA and kainate receptors (47). The drug is a noncompetitive antagonist at some subtypes of neuronal nicotinic acetylcholine receptors such as the alpha4beta2 subtype (47). Nitrous oxide weakly potentiates the effect of GABA at GABA-A receptor channels, but this effect may not be relevant at clinical concentrations (47). In addition, the drug might inhibit the effect of GABA at rho₁ GABA-C receptors (47). Glycine's effects at glycine receptor channels may be slightly potentiated by nitrous oxide (47). Nitrous oxide may slightly inhibit serotonin 5-HT3 receptors in a competitive manner (28, 47). The drug might also inhibit T-type voltage-gated calcium channels as well (48). Finally, nitrous oxide activates TREK-1, a two pore-domain potassium channel (49).

Nitrous oxide increases the production of nitric oxide (NO) via the neuronal isoform of nitric oxide synthase (nNOS) (50). Nitrous oxide- induced NO production may lead to the neuronal release of endogenous opioid peptides (50).

Indications:
Nitrous oxide is indicated for the induction and maintenance of sedation. In addition, it is approved for the induction and maintenance of general anesthesia. However, nitrous oxide is rarely used alone; other medications are frequently administered to induce or supplement anesthesia. Because of its weak anesthetic potency and muscle relaxant properties, nitrous oxide must be supplemented with another anesthetic or anesthesia adjunct (such as a barbiturate, benzodiazepine, opioid analgesic, or another inhalation anesthetic) and/or a neuromuscular blocking agent. Also, nitrous oxide is often administered concurrently with one of the other inhalation anesthetics to decrease the requirement for the more potent anesthetic.

Chemical Class:
inorganic nitrogen compound

PubChem 2D Structure:

"3D" Structure (Requires Chime):
[Link] 

Generic Name:
propofol

Trade Name:
Diprivan® [Abraxis]

IUPAC Name:
2,6-dipropan-2-ylphenol

Dosage Forms/Routes:
injectable/injection

Major Metabolites:
propofol-glucuronide;
4-(2,6-diisopropyl-1,4-quinol)-sulphate;
1-(2,6-diisopropyl-1,4-quinol)-glucuronide;
4-(2,6-diisopropyl-1,4-quinol)-glucuronide

Database Search Links:
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[Search PubMed for
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[PDSP K_i database]

Initial Approval:
10/02/1989

Manufacturers:
[FDA Search]

Prescribing
Information:
[Link]

RxList:
[Link]

Empirical Formula:
C₁₂H₁₈O

Molecular Mass:
178.271 g/mol

Possible Mechanisms of Action:
Propofol potentiates the effects of GABA at GABA-A receptors and glycine at glycine receptors (51). At higher concentrations, propofol directly causes both GABA-A and glycine receptor channels to open (51). Propofol may also inhibit and slow the activation of hyperpolarization-activated, cyclic nucleotide-gated channels such as HCN1, HCN2, and HCN4 (52).

In addition, propofol may have a small but significant inhibitory effect on voltage-dependent Na⁺ channels (12). Propofol may also inhibit T-type voltage-gated calcium channels (22, 23). Finally, propofol is an inhibitor of fatty acid amide hydrolase (53).

Indications:
Propofol is an IV sedative-hypnotic agent that can be used for both induction and/or maintenance of anesthesia as proof of a balanced anesthetic technique for inpatient and outpatient surgery in adults and in children 3 years of age or older.

Propofol, when administered intravenously as directed, can be used to initiate and maintain monitored anesthesia care (MAC) sedation during diagnostic procedures in adults. Propofol may also be used for MAC sedation in conjunction with local/regional anesthesia in patients undergoing surgical procedures. (See PRECAUTIONS in the prescribing information).

Propofol should only be administered to intubated, mechanically ventilated adult patients in the Intensive Care Unit (ICU) to provide continuous sedation and control of stress responses. In this setting, propofol should be administered only by persons skilled in the medical management of critically ill patients and trained in cardiovascular resuscitation and airway management.

Chemical Class:
phenol derivative

PubChem 2D Structure:

"3D" Structure (Requires Chime):
[Link] 

Generic Name:
sevoflurane

Trade Name:
Ultane ® [Abbott]

IUPAC Name:
1,1,1,3,3,3-hexafluoro-2-
(fluoromethoxy)propane

Dosage Forms/Routes:
volatile liquid/inhalation

Major Metabolite:
hexafluoroisopropanol

Database Search Links:
[PubMed]
[Search PubMed for
Randomized Controlled Trials]
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[PDSP K_i database]

Initial Approval:
06/07/1995

Manufacturers:
[FDA Search]

Prescribing
Information:
[Link]

RxList:
[Link]

Empirical Formula:
C₄H₃F₇O

Molecular Mass:
200.055 g/mol

Possible Mechanisms of Action:
Sevoflurane is a noncompetitive antagonist of NMDA receptor channels (1). In addition, sevoflurane enhances the effect of GABA at GABA-A receptor channels (2). Glycine's effect at glycine receptor channels is also potentiated by sevoflurane (37). Sevoflurane may weakly inhibit glutamate AMPA receptors, and more research is necessary to better characterize its effects at these receptors (54). Sevoflurane is also a noncompetitive antagonist at serotonin 5-HT3 receptors (28). In addition, the drug is likely to be an antagonist at some neuronal nicotinic acetylcholine receptor subtypes such as the alpha4beta2 (30) subtype.

Sevoflurane may inhibit voltage-gated Na⁺ channels (55). The drug may also inhibit L-type voltage-gated calcium channels (56). Sevoflurane might inhibit T-type voltage-gated calcium channels as well (57). In skeletal muscle, sevoflurane induces the release of Ca²⁺ from the sarcoplasmic reticulum Ca²⁺ release channel, also known as the ryanodine receptor (36). Furthermore, sevoflurane is a potent activator of the human tandem pore domain potassium channel, TRESK (3). The drug is also likely to activate the human tandem pore domain potassium channel TASK-1 (58).

At sub-anesthetic doses, sevoflurane inhibits the exchange of GTPγS for GDP bound to the nucleotide binding site of a subset of Gα (G alpha) proteins; these include Gα_i2 > Gα_i1 > Gα_i3 > Gα_s (15).

Indications:
Sevoflurane is indicated for induction and maintenance of general anesthesia in adult and pediatric patients for inpatient and outpatient surgery.

Sevoflurane should be administered only by persons trained in the administration of general anesthesia. Facilities for maintenance of a patent airway, artificial ventilation, oxygen enrichment, and circulatory resuscitation must be immediately available. Since level of anesthesia may be altered rapidly, only vaporizers producing predictable concentrations of sevoflurane should be used.

Chemical Class:
haloether

PubChem 2D Structure:

"3D" Structure (Requires Chime):
[Link] 

Generic Name:
thiopental sodium

Trade Name:
Pentothal ® [Hospira]

IUPAC Name:
sodium 5-ethyl-6-oxo-5-pentan-2-
yl-2-sulfanylidene-pyrimidin-4-olate

Dosage Forms/Routes:
injectable/injection [the drug is prepared as a sterile powder and after reconstitution with an appropriate diluent is administered by the intravenous route]

Major Metabolite:
pentobarbital

Database Search Links:
[PubMed]
[Search PubMed for
Randomized Controlled Trials]
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[PDSP K_i database]

Initial Approval:
1959

Manufacturers:
[FDA Search]

Prescribing
Information:
[Link]

RxList:
[Link]

Empirical Formula:
C₁₁H₁₇N₂NaO₂S

Molecular Mass:
264.321 g/mol

Possible Mechanisms of Action:
Thiopental potentiates the effect of GABA at GABA-A receptor channels (59). The drug also potentiates the effect of glycine at glycine receptor channels (27). Furthermore, thiopental may potently inhibit voltage-gated calcium channels and weakly inhibit NMDA glutamate receptor channels (60). Thiopental may also inhibit neuronal nicotinic acetylcholine receptors (61).

Indications:
Pentothal (Thiopental Sodium for Injection, USP) is indicated (1) as the sole anesthetic agent for brief (15 minute) procedures, (2) for induction of anesthesia prior to administration of other anesthetic agents, (3) to supplement regional anesthesia, (4) to provide hypnosis during balanced anesthesia with other agents for analgesia or muscle relaxation, (5) for the control of convulsive states during or following inhalation anesthesia, local anesthesia, or other causes, (6) in neurosurgical patients with increased intracranial pressure, if adequate ventilation is provided, and (7) for narcoanalysis and narcosynthesis in psychiatric disorders.

Chemical Class:
thiobarbiturate

PubChem 2D Structure:

"3D" Structure (Requires Chime):
[Link]