Butorphanol (CHEM002229)
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| Version | 1.0 | ||||||||
| Creation Date | 2009-07-21 20:27:15 UTC | ||||||||
| Update Date | 2026-05-14 16:44:01 UTC | ||||||||
| Accession Number | CHEM002229 | ||||||||
| Identification | |||||||||
| Common Name | Butorphanol | ||||||||
| Class | Small Molecule | ||||||||
| Description | Butorphanol is only found in individuals that have used or taken this drug. It is a synthetic morphinan analgesic with narcotic antagonist action. It is used in the management of severe pain. [PubChem]The exact mechanism of action is unknown, but is believed to interact with an opiate receptor site in the CNS (probably in or associated with the limbic system). The opiate antagonistic effect may result from competitive inhibition at the opiate receptor, but may also be a result of other mechanisms. Butorphanol is a mixed agonist-antagonist that exerts antagonistic or partially antagonistic effects at mu opiate receptor sites, but is thought to exert its agonistic effects principally at the kappa and sigma opiate receptors. | ||||||||
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| Chemical Structure |  | ||||||||
| Synonyms | Not Available | ||||||||
| Chemical Formula | C21H29NO2 | ||||||||
| Average Molecular Mass | 327.461 g/mol | ||||||||
| Monoisotopic Mass | 327.220 g/mol | ||||||||
| CAS Registry Number | 42408-82-2 | ||||||||
| IUPAC Name | (1S,9R,10S)-17-(cyclobutylmethyl)-17-azatetracyclo[7.5.3.0^{1,10}.0^{2,7}]heptadeca-2(7),3,5-triene-4,10-diol | ||||||||
| Traditional Name | Not Available | ||||||||
| SMILES | [H][C@@]12CC3=C(C=C(O)C=C3)[C@]3(CCCC[C@@]13O)CCN2CC1CCC1 | ||||||||
| InChI Identifier | InChI=1S/C21H29NO2/c23-17-7-6-16-12-19-21(24)9-2-1-8-20(21,18(16)13-17)10-11-22(19)14-15-4-3-5-15/h6-7,13,15,19,23-24H,1-5,8-12,14H2/t19-,20+,21-/m1/s1 | ||||||||
| InChI Key | IFKLAQQSCNILHL-QHAWAJNXSA-N | ||||||||
| Chemical Taxonomy | |||||||||
| Classification | Not classified | ||||||||
| Biological Properties | |||||||||
| Status | Detected and Not Quantified | ||||||||
| Origin | Exogenous | ||||||||
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| Biofluid Locations | Not Available | ||||||||
| Tissue Locations | Not Available | ||||||||
| Pathways | Not Available | ||||||||
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| Chemical Roles | Not Available | ||||||||
| Physical Properties | |||||||||
| State | Solid | ||||||||
| Appearance | White powder. | ||||||||
| Experimental Properties |
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| Predicted Properties | Not Available | ||||||||
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| Spectra |
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| Toxicity Profile | |||||||||
| Route of Exposure | Rapidly absorbed after intramuscular injection and peak plasma levels are reached in 20-40 minutes. The absolute bioavailability is 60-70% and is unchanged in patients with allergic rhinitis. In patients using a nasal vasoconstrictor (oxymetazoline) the fraction of the dose absorbed was unchanged, but the rate of absorption was slowed. Oral bioavailability is only 5-17% because of extensive first-pass metabolism. | ||||||||
| Mechanism of Toxicity | The exact mechanism of action is unknown, but is believed to interact with an opiate receptor site in the CNS (probably in or associated with the limbic system). The opiate antagonistic effect may result from competitive inhibition at the opiate receptor, but may also be a result of other mechanisms. Butorphanol is a mixed agonist-antagonist that exerts antagonistic or partially antagonistic effects at mu opiate receptor sites, but is thought to exert its agonistic effects principally at the kappa and sigma opiate receptors. Its interactions with these receptors in the central nervous system apparently mediate most of its pharmacologic effects, including analgesia. | ||||||||
| Metabolism | Extensively metabolized in the liver. The pharmacological activity of butorphanol metabolites has not been studied in humans; in animal studies, butorphanol metabolites have demonstrated some analgesic activity. Route of Elimination: Butorphanol is extensively metabolized in the liver. Elimination occurs by urine and fecal excretion. Half Life: The elimination half-life of butorphanol is about 18 hours. In renally impaired patients with creatinine clearances <30 mL/min the elimination half-life is approximately doubled. After intravenous administration to patients with hepatic impairment, the elimination half-life of butorphanol was approximately tripled. | ||||||||
| Toxicity Values | Not Available | ||||||||
| Lethal Dose | Not Available | ||||||||
| Carcinogenicity (IARC Classification) | No indication of carcinogenicity to humans (not listed by IARC). | ||||||||
| Uses/Sources | The most common indication for butorphanol is management of migraine using the intranasal spray formulation. It may also be used parenterally for management of moderate-to-severe pain, as a supplement for balanced general anesthesia, and management of pain during labor. Butorphanol is more effective in reducing pain in women than in men. In veterinary use, butorphanol ("Torbugesic") is widely used as a sedative and analgesic in dogs, cats and horses. [Wikipedia] | ||||||||
| Minimum Risk Level | Not Available | ||||||||
| Health Effects | Medical problems can include congested lungs, liver disease, tetanus, infection of the heart valves, skin abscesses, anemia and pneumonia. Death can occur from overdose. | ||||||||
| Symptoms | The clinical manifestations of butorphanol overdose are those of opioid drugs in general. The most serious symptoms are hypoventilation, cardiovascular insufficiency, coma, and death. Medical problems can include congested lungs, liver disease, tetanus, infection of the heart valves, skin abscesses, anemia and pneumonia. Death can occur from overdose. | ||||||||
| Treatment | The management of suspected butorphanol overdosage includes maintenance of adequate ventilation, peripheral perfusion, normal body temperature, and protection of the airway. Patients should be under continuous observation with adequate serial measures of mental state, responsiveness, and vital signs. Oxygen and ventilatory assistance should be available with continual monitoring by pulse oximetry if indicated. In the presence of coma, placement of an artificial airway may be required. An adequate intravenous portal should be maintained to facilitate treatment of hypotension associated with vasodilation. The use of a specific opioid antagonist such as naloxone should be considered. As the duration of butorphanol action usually exceeds the duration of action of naloxone, repeated dosing with naloxone may be required. (3) | ||||||||
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| Identifiers | Not Available | ||||||||
| References | |||||||||
| Synthesis Reference | Monkovic, I. and Conway, T.T.; U.S. Patent 3,775,414; November 27,1973; Monkovic, I.,Wong, H. and Lim, G.; U.S. Patent 3,980,641; September 14, 1976; Pachter, IJ., Belleau, B.R. and Monkovic, I.; U.S. Patent 3,819,635; June 25,1974; and Lim, G. and Hooper, J.W.; U.S. Patent 4,017,497; April 12,1977; all assigned to Bristol-Myers Company. | ||||||||
| MSDS | Link | ||||||||
| General References | Not Available | ||||||||
