Butorphanol Stats & Data

Depressant Opioid

Stadol Dolorex Torbutrol Torbugesic

NPS DataHub

MW327.47

FormulaC21H29NO2

CAS42408-82-2

IUPAC(1~{S},9~{R},10~{S})-17-(cyclobutylmethyl)-17-azatetracyclo[7.5.3.0^{1,10}.0^{2,7}]heptadeca-2(7),3,5-triene-4,10-diol

SMILESOc1ccc2CC3N(CC4CCC4)CCC4(CCCCC34O)c2c1

InChIKeyIFKLAQQSCNILHL-QHAWAJNXSA-N

Chemical Class Opioid

Psychoactive Class Depressant

Half-Life Highly variable; DrugBank lists ~18 h elimination half-life and reports further prolongation with renal (≈2×) or hepatic impairment (≈3×). Apparent effect duration is shorter (typically 2–6 h).

Pharmacology

DrugBank

Protein binding Serum protein binding is approximately 80%. State Solid Vd * 305 to 901 L

Description

A synthetic morphinan analgesic with narcotic antagonist action. It is used in the management of severe pain.

Mechanism of Action

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.

Pharmacodynamics

Butorphanol is a synthetic opioid agonist-antagonist analgesic with a pharmacological and therapeutic profile that has been well established since its launch as a parenteral formulation in 1978. The introduction of a transnasal formulation of butorphanol represents a new and noninvasive presentation of an analgesic for moderate to severe pain. This route of administration bypasses the gastrointestinal tract, and this is an advantage for a drug such as butorphanol that undergoes significant first-pass metabolism after oral administration. The onset of action and systemic bioavailability of butorphanol following transnasal delivery are similar to those after parenteral administration. Butorphanol blocks pain impulses at specific sites in the brain and spinal cord.

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.

Absorption

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.

Toxicity

The clinical manifestations of butorphanol overdose are those of opioid drugs in general. The most serious symptoms are hypoventilation, cardiovascular insufficiency, coma, and death.

Indication

For the relief of moderate to severe pain.

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.

Elimination

Butorphanol is extensively metabolized in the liver. Elimination occurs by urine and fecal excretion.

Clearance

* 99 +/- 23 L/h Young with IV 2 mg * 82 +/- 21 Eldery with IV 2 mg

Effect Profile

Curated + 12 Reports

Opioid 6.3

Strong euphoria with moderate itching/nausea, mild pain relief, low sedation

Euphoria / Warmth×3

Analgesia×2

Sedation / Relaxation×1

Itching / Nausea×1

Based on reports from:

Erowid Experience Reports PsychonautWiki Butorphanol

Tolerance & Pharmacokinetics

drugs.wiki

Half-Life

Highly variable; DrugBank lists ~18 h elimination half-life and reports further prolongation with renal (≈2×) or hepatic impairment (≈3×). Apparent effect duration is shorter (typically 2–6 h).

Addiction Potential

Low-to-moderate. Mixed agonist–antagonist profile (κ-agonism, partial μ-activity) tends to limit classic opioid euphoria at higher doses and can blunt effects of full μ-agonists. Physical dependence can occur with repeated use; withdrawal possible on cessation and can be precipitated in μ-agonist–dependent individuals.

Tolerance Decay

Full tolerance 3d Half tolerance 7d Baseline ~14d

Patterns are extrapolated from general opioid tolerance behavior and limited user reports. κ‑agonist dysphoria can reduce compulsive redosing for some, but physiological tolerance and dependence can still develop after several consecutive days. Data quality is low; individual variation is high.

Cross-Tolerances

Other opioids (μ‑agonists)

50% ●○○

Experience Report Analysis

Erowid

12 Reports

2001–2017 Date Range

4 With Age Data

8 Effects Detected

Demographics

Gender Distribution

Age Distribution

Reports Over Time

Effect Analysis

Erowid

Effects aggregated from 12 experience reports (12 Erowid)

12 Reports

8 Effects Detected

5 Positive

2 Adverse

1 Neutral

Effect Sentiment Distribution

Confidence Distribution

Positive Effects 5

Sedation 41.7% 70%

Euphoria 33.3% 70%

Anxiety Suppression 33.3% 70%

Stimulation 25.0% 70%

Empathy 25.0% 70%

Adverse Effects 2

Nausea 41.7% 70%

Confusion 33.3% 70%

Real-World Dose Distribution

62K Doses

From 13 individual dose entries

Oral (n=5)

Median: 5.0mg 25th: 5.0mg 75th: 5.0mg 90th: 5.0mg

mg/kg median: 0.064 mg/kg 75th: 0.064

Form / Preparation

Most common forms and preparations reported

Redose Patterns

Redosing behavior across 10 reports

50.0% Redosed

1.7 Avg Doses

60m Median Interval

Opioid Equivalence (MME)

NIH HEAL 2024 & CDC 2022

⚠ Citation & Disclaimer: Conversion factors sourced from the NIH HEAL Initiative MME Calculator (Adams et al., PAIN 2025), the CDC 2022 Clinical Practice Guideline for Prescribing Opioids for Pain, and the MDCalc MME Calculator. These are approximate equianalgesic ratios for educational reference only. Individual responses vary significantly based on genetics, tolerance, cross-tolerance, and route of administration. This is not medical advice. Do not use these conversions to adjust opioid dosing without professional medical guidance.

1.42 mg Butorphanol ≈ 10 mg Morphine (oral)

MME factor 7.0×

Butorphanol 1.42 mg oral ≈ 10 mg Morphine oral

ⓘ Mixed agonist-antagonist. Evidence level: High (A).

Read full reports on Erowid →

Harm Reduction

drugs.wiki

- Butorphanol is a mixed agonist–antagonist opioid: κ-opioid receptor agonism with partial μ-agonist/antagonist effects. This profile can antagonize effects of full μ-agonists (morphine, oxycodone, methadone), which may precipitate acute withdrawal in physically dependent people; avoid using butorphanol to 'boost' or on top of maintenance/full agonists. Carry naloxone if opioids are used in any context.

- Intranasal bioavailability is high relative to oral (approx. 70% vs ~17%), so intranasal dosing is more potent than the same oral milligram amount. Start with the lowest effective dose and wait at least a full peak window (≥90 minutes) before redosing to avoid stacking.

- Combining with other CNS depressants (alcohol, benzodiazepines, barbiturates, gabapentinoids, Z‑drugs) markedly increases risk of respiratory depression, accidental injury, and fatal overdose. If any sedatives are on board, reduce dose substantially, avoid redosing, and do not use alone.

- κ‑agonism commonly produces dysphoria, anxiety, and ‘spacey’ or unpleasant headspace in some users; this can limit compulsive redosing but also increases risk of panic, confusion, and dangerous behavior in unfamiliar settings. Avoid operating vehicles or hazardous equipment during and after effects until fully alert.

- Effect duration is short relative to elimination; sedation and impaired coordination can outlast perceived analgesia. Plan for residual impairment (2–6 h) and avoid rapid redose cycles.

- Oral use is inefficient and unpredictable because of extensive first‑pass metabolism. If oral dosing is attempted, expect weaker, delayed effects and higher interindividual variability.

- Injection carries infection risks (skin/soft‑tissue infection, bacteremia, endocarditis). Use new sterile equipment each time, rotate sites, and avoid non‑sterile/veterinary preparations for human injection.

- Hepatic or renal impairment significantly prolongs elimination and increases exposure; use smaller doses with longer intervals or avoid non‑medical use altogether in these conditions. Older adults also clear butorphanol more slowly; start low and go slow.

- Because butorphanol can block or blunt full μ‑agonists, it may reduce the effectiveness of opioids given for emergency pain control for several hours; disclose recent use to clinicians.

- Intranasal solutions are often 10 mg/mL; product-specific sprays can deliver different mg per actuation. Verify the exact per‑spray amount before use to prevent unintended high doses.

References

Drugs.wiki References

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