Salvinorin A
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Salvinorin A (divinorin A) is a naturally-occurring dissociative of the neoclerodane diterpene class. It is the principal psychoactive compound in Salvia divinorum, distinguished as the most potent naturally occurring hallucinogen identified to date.[1] Salvinorin A is a selective kappa-opioid receptor agonist, producing its effects by activating opioid signaling pathways entirely independent of serotonin receptors.[2][3]
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Isolated from Salvia divinorum in 1982, salvinorin A remained pharmacologically uncharacterized for two decades until Bryan Roth identified it as a potent kappa-opioid receptor agonist in 2002.[2] That discovery overturned the longstanding assumption that plant hallucinogens must operate through serotonergic pathways, establishing salvinorin A as the first known non-nitrogenous psychoactive compound to act through opioid mechanisms. It remains unscheduled at the federal level in the United States, though approximately 27 states and numerous countries have enacted restrictions.
Subjective effects include intense dissociation, loss of body ownership, vivid internal imagery, ego dissolution, and amnesia. The experience is defined by its alien, dislocating quality — a rapid, involuntary departure from consensus reality that is more commonly described as bewildering and dysphoric than expansive, distinguishing it sharply from serotonergic psychedelics.[1] Confusion, profound dysphoria, and complete disconnection from external sensory input are characteristic unsought effects.[4]
Salvinorin A produces no physical dependence — its aversive effects and suppression of reward-circuit dopamine make compulsive use self-limiting.[5] The principal risks are psychological: near-instantaneous onset leaves no transitional period, and high doses produce complete incapacitation that creates acute physical danger from falls and uncontrolled movement.[6] Three controlled human studies and one fMRI investigation provide the current evidence base, but no clinical trials are active and no lethal dose has been established in any species.[5]
History[edit]
History
Discovery
In 1982, Alfredo Ortega, Anthony Blount, and Peter Manchand published the first isolation and structural characterization of the compound they named "salvinorin" from Salvia divinorum, confirming by X-ray crystallography that it was a neoclerodane diterpene — a terpenoid, not an alkaloid.[7] Two years later, Leander Valdés III independently isolated the same compound and named it "divinorin A".[8] The compound was subsequently renamed salvinorin A following Ortega's priority of publication.
Scientific significance
The compound's molecular target remained unknown for two decades until 2002, when Bryan Roth and colleagues identified the κ-opioid as salvinorin A's principal target — demonstrating potent, selective agonism with no activity at the 5-HT₂A serotonin receptor or 50 other molecular targets.[2] This made salvinorin A the first known naturally occurring non-nitrogenous opioid-receptor-selective agonist, fundamentally reframing it from an enigmatic hallucinogen into a pharmacological tool of exceptional specificity. Three controlled human studies followed between 2012 and 2016,[9][4][1] and in 2020 the first human fMRI study mapped its effects on brain network connectivity.[10]
Modern status
No active clinical trials are recruiting as of May 2026. Preclinical investigations into neuroprotective, anticonvulsant, and anti-inflammatory applications remain in early stages. In 2023, cryo-EM structures of active-state kappa-opioid receptor complexes with salvinorins were resolved, opening new avenues for drug design.[11]
The name salvinorin derives from the genus Salvia (Latin salvare, "to save" or "to heal"), while divinorin — Valdés's independent name — references Salvia divinorum ("sage of the diviners").[8] The Mazatec names ska María Pastora and hojas de la Pastora ("leaves of the Shepherdess") embed the plant in Catholic syncretic tradition, associating it with the Virgin Mary as spiritual intercessor.[3]
Salvia divinorum has been used by the Mazatec indigenous people of Oaxaca, Mexico, in spiritual healing and divination ceremonies for centuries.[3][13] José Luis Díaz, conducting ethnopharmacological field research between 1973 and 1983, documented the traditional water preparation as producing effects qualitatively milder than smoked extracts — light-headedness, proprioceptive distortion, and amplified imagery rather than the overwhelming dissociation of inhaled use.[13]
Chemistry[edit]
Chemistry
Structural class
Salvinorin A is a neoclerodane diterpene — a terpenoid natural product built from four isoprene units (C₂₀ skeleton) with a trans-fused decalin ring system.[7] It is pharmacologically unique among natural hallucinogens in containing no nitrogen atom; all previously identified plant psychedelics — tryptamines, phenethylamines, ergolines — are alkaloids.[2][3]
The molecule comprises a trans-fused decalin core bearing a furan ring, a lactone ring, a C-2 acetate ester, a methyl ester, and two ketone groups. Its eight oxygen atoms serve exclusively as hydrogen-bond acceptors with zero hydrogen-bond donors, contributing to poor aqueous solubility.[14]
| Molecular formula | C₂₃H₂₈O₈ |
| Molecular weight | 432.5 g/mol |
Structure-activity relationships
The C-2 acetate ester is critical for κ-opioid binding — its hydrolysis to the des-acetyl metabolite salvinorin B dramatically reduces receptor affinity.[15][16] This structural insight has driven medicinal chemistry efforts: Béguin and colleagues developed an N-methylacetamide structural analog with improved metabolic stability,[16] and Puls and colleagues used salvinorin A-based virtual screening to discover novel KOR agonists with refined signaling profiles.[17]
Stereochemistry and physical properties
Salvinorin A possesses seven stereocenters. The natural, pharmacologically active form is (–)-salvinorin A, confirmed by total synthesis.[18] Stereochemistry was originally established by X-ray crystallography.[7]
The compound presents as a white crystalline powder with a melting point of 238–244°C.[7][14] Aqueous solubility is poor — the absence of ionizable groups precludes salt formation.[14] It is soluble in ethanol and acetone, and exhibits photochemical instability below 220 nm.[14]
Natural occurrence
Salvinorin A is the principal psychoactive constituent of Salvia divinorum, concentrated in leaf glandular trichomes. The plant produces several related diterpenes (salvinorins B through I), but only salvinorin A possesses the intact C-2 acetate ester required for high-affinity receptor binding.[15] Salvinorin B, the primary metabolite, is not psychoactive at relevant concentrations.
Pharmacology[edit]
Pharmacology
Mechanism of action
Salvinorin A acts as a potent, selective, full agonist at the κ-opioid (KOR).[2] Its selectivity for KOR over the mu- and delta-opioid receptors exceeds 2,000-fold, and no significant activity has been detected across 50 additional receptor, transporter, and ion channel targets — including the 5-HT₂A serotonin receptor.[2]
Full agonist efficacy was confirmed by Chavkin and colleagues, who demonstrated activity equal to or exceeding that of dynorphin A — the brain's own KOR-activating peptide — across multiple functional assays.[15] The exclusive mediation of all psychoactive effects through KOR has been confirmed in humans: the opioid antagonist naltrexone completely blocks all subjective, cardiovascular, and neuroendocrine effects, while the 5-HT₂A antagonist ketanserin has no effect.[19]
Downstream of KOR activation, salvinorin A inhibits adenylyl cyclase, opens inward rectifier potassium channels, and closes voltage-gated calcium channels — producing widespread neuronal suppression.[15][5] It also suppresses dopamine release in the brain's reward circuitry, which underlies both its dysphoric quality and its lack of addictive potential.[5]
This pharmacological profile definitively separates salvinorin A from classical serotonergic psychedelics such as LSD and psilocybin, which produce their effects through 5-HT₂A agonism.[19]
Cannabinoid receptor involvement
Salvinorin A does not bind cannabinoid receptors in the brain.[2] CB1 and CB2 involvement has been documented only in the gastrointestinal tract, where salvinorin A reduces gut motility partly through cannabinoid-dependent mechanisms.[20][21][22] Walentiny and colleagues confirmed that salvinorin A's cannabinoid-like behavioral effects in rodents are mediated by KOR, not direct CB1 binding.[23]
Pharmacokinetics
When smoked or vaporized, salvinorin A reaches peak blood levels within approximately 2 minutes.[24] Brain imaging in primates showed peak brain uptake at 40 seconds, with highest concentrations in the cerebellum and visual cortex.[25] The brain half-life is approximately 8 minutes,[25] consistent with the clinically observed 5–20 minute duration of peak effects.
Johnson and colleagues confirmed that subjective effects track plasma levels directly — the temporal profile of the experience mirrors drug concentration in the blood rather than downstream receptor processes.[24] Plasma elimination half-life in nonhuman primates is 56.6 ± 24.8 minutes, with a notable sex difference: males 37.9 ± 5.6 minutes, females 80.0 ± 13.1 minutes.[26]
Sublingual administration is ineffective — doses up to 4 mg produced no significant effects in controlled studies, likely due to degradation by salivary esterases.[27] Oral administration is similarly inactive due to rapid enzymatic breakdown in the gut.[16]
The primary metabolic pathway is esterase-mediated hydrolysis of the C-2 acetate, producing the inactive metabolite salvinorin B.[16] Salvinorin A is actively pumped out of the brain by P-glycoprotein transport, further shortening its cerebral residence time.[14] Elimination occurs through both kidneys and bile.[25] No CYP enzyme interaction studies have been published, though the esterase-dominated metabolism reduces the expected likelihood of common drug-drug interactions.
Neuroscience[edit]
Neuroscience
Where it acts
The first human fMRI study of salvinorin A revealed decreased within-network connectivity and increased between-network connectivity during peak effects — a pattern of network boundary dissolution strikingly similar to serotonergic psychedelics despite operating through a completely different receptor system.[10] The default mode network showed prominent attenuation. Brain imaging in primates confirmed highest drug concentrations in the cerebellum and visual cortex,[25] consistent with the coordination impairment and visual disturbances observed clinically.
Comparative primate imaging showed that both salvinorin A and psilocybin disrupt the default mode network and cortico-claustro-cortical circuits, but thalamocortical effects diverge — thalamic gating disruption requires 5-HT₂A activation and is absent with κ-opioid agonism.[28] This establishes that default mode network dissolution can occur through at least two independent pharmacological mechanisms.
Why it matters
Salvinorin A's network-level effects align with the REBUS (relaxed beliefs under psychedelics) framework, which proposes that psychedelics relax high-level cognitive predictions and allow bottom-up sensory information to dominate. The progressive dose-dependent gating of external sensory input — from altered body sensation at lower doses to complete loss of external contact at the highest dose[1] — fits this model of disrupted predictive signaling.
KOR activation also opposes dopaminergic "wanting" signals in the reward circuitry, stripping environmental stimuli of motivational significance.[5] This may explain experiential reports of profound detachment from meaning and identity — mechanistically distinct from the ego dissolution of serotonergic psychedelics, which arises from cortical disruption rather than dopamine suppression.
Several fundamental questions remain unanswered. The kappa-opioid receptor is not traditionally associated with hallucinations — how KOR activation in the cerebellum, visual cortex, and claustrum generates elaborated internal imagery remains unknown. Whether KOR agonism produces any form of neuroplasticity (as serotonergic psychedelics do through distinct molecular pathways) has not been investigated.
Subjective Effects[edit]
The salvinorin A experience is a rapid, involuntary departure from ordinary reality — not the slow-building perceptual shift of serotonergic psychedelics but an abrupt dislocation into an interior space that users commonly describe as alien, bewildering, and difficult to integrate. At lower inhaled doses, interoception shifts and body boundaries soften; at higher doses, external sensory input ceases entirely and a fully autonomous internal landscape replaces consensus reality.[1] Set and setting profoundly shape whether the experience registers as terrifying or meaningful, and the presence of a sober sitter is widely recommended.
The closest phenomenological comparisons are to high-dose ketamine at the anesthetic boundary and to deliriant-class compounds, though neither analogy captures the combination of preserved internal imagery, complete external disconnection, and predominantly dysphoric tone that defines the salvinorin A experience. Unlike classical psychedelics, it is rarely described as connective or expansive — the dominant register is estrangement.
Effect Grid
Significant dissociation from the external environment. Internal imagery begins — vivid, often bizarre visual scenes that may feel more real than the surrounding room. Altered body ownership and body schema distortion are prominent. The ability to interact with surroundings is substantially reduced. Confusion, time alteration, and language suppression are typical. Cognitive dysphoria — an uncomfortable sense of wrongness or alienation — is frequently reported.
Motor control impairment is significant; users should be seated or lying down before administration. Laughter fits may occur. Spontaneous body sensations and vestibular distortion are common.
A sober sitter is essential. The experience is essentially all peak — there is no gradual come-up. Dysphoric tone predominates. Active effects resolve within 5–20 minutes, with aftereffects lasting 15–60 minutes.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Proprioceptive distortion · Color alteration · Vestibular distortion · Visual morphing · Geometry · Visual breathing · Brightness alteration · Visual drifting · Visual melting · Auditory suppression · Environmental patterning · Touch suppression · Tracers · Visual haze / noise · Visual magnification · After-images · Auditory distortion · Synesthesia · Internal hallucinations · External hallucinations · Object transformations · Object activation · Perspective hallucinations · Visual processing suppression · Auditory hallucinations · Visual flipping · Visual scenery slicing
Geometry · Visual breathing · Brightness alteration · Visual drifting · Visual melting · Auditory suppression · Environmental patterning · Touch suppression · Tracers · Visual haze / noise · Visual magnification · After-images · Auditory distortion · Synesthesia · Internal hallucinations · External hallucinations · Object transformations · Object activation · Perspective hallucinations · Visual processing suppression · Auditory hallucinations · Visual flipping · Visual scenery slicing
Laughter fits · Nausea · Body high · Physical fatigue · Sedation · Bodily heaviness · Bodily lightness · Bodily pressures · Breathing alteration · Heart rate perception changes · Muscle relaxation · Pupil constriction · Spontaneous body sensations · Tingling / electric sensations · Trembling · Vibrations / buzzing · Headache · Muscle tension · Nystagmus (eye wobbles) · Pain suppression · Sexual arousal suppression · Vomiting · Bodily dissociation · Tactile hallucination
Sedation · Bodily heaviness · Bodily lightness · Bodily pressures · Breathing alteration · Heart rate perception changes · Muscle relaxation · Pupil constriction · Spontaneous body sensations · Tingling / electric sensations · Trembling · Vibrations / buzzing · Headache · Muscle tension · Nystagmus (eye wobbles) · Pain suppression · Sexual arousal suppression · Vomiting · Bodily dissociation · Tactile hallucination
Focus suppression · Immersion enhancement · Information processing suppression · Language suppression · Memory suppression · Analysis suppression · Memory fragmentation · Novelty enhancement · Cognitive dysphoria · Thought loops · Humor enhancement · Cognitive fatigue · Conceptual thinking · Introspection enhancement · Memory replays · Multiple thought streams · Pattern recognition suppression · Thought deceleration · Cognitive euphoria · Delirium · Delusions
Language suppression · Memory suppression · Analysis suppression · Memory fragmentation · Novelty enhancement · Cognitive dysphoria · Thought loops · Humor enhancement · Cognitive fatigue · Conceptual thinking · Introspection enhancement · Memory replays · Multiple thought streams · Pattern recognition suppression · Thought deceleration · Cognitive euphoria · Delusions
Simultaneous emotions · Catharsis · Empathy suppression · Euphoria
Social disconnection · Sociability suppression · Automaticity · Disinhibition · Cognitive disconnection · Boundary dissolution · Ego dissolution · Identity alteration
Cognitive disconnection · Boundary dissolution · Ego dissolution · Identity alteration
Time cessation
Cessation · Death-rebirth sequence · Existential realization · Noetic insight · Non-dual awareness · Near-death experience
Non-dual awareness · Near-death experience
Timeline
Near-instantaneous transition from baseline. Effects emerge within seconds of exhalation — a sudden shift in awareness, often described as being 'pulled' out of ordinary reality. There is no gradual build; the onset IS the come-up.
Maximum intensity. At common doses and above: complete dissociation from external reality, vivid internal hallucinations, loss of body schema, motor incapacitation, and frequent amnesia. Dysphoric tone predominates.
Rapid return to baseline. Reorientation to the external environment occurs in stages — awareness of physical surroundings returns before full cognitive coherence. Residual confusion, difficulty articulating the experience, and mild disorientation are common.
Mild residual effects including reflective or confused mental state, physical fatigue, and subtle mood changes. Cognitive processing may feel slightly slowed. Some users report a contemplative or unsettled quality.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- —
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- dynorphin · U50488 · pentazocine
Toxicity
No lethal dose has been established for salvinorin A in any species, and no published reports of fatal overdose attributable solely to the compound exist.safety citation needed The toxic threshold in humans is uncharacterized.[5]
Cardiovascular effects
Controlled studies monitored heart rate and blood pressure during salvinorin A administration.[9][19] All cardiovascular effects were fully blocked by naltrexone, confirming they are κ-opioid-mediated.[19] No serious cardiovascular events occurred in any controlled human study.
Hormonal effects
Salvinorin A produces a transient rise in prolactin levels beginning approximately 5 minutes after inhalation and peaking at 15 minutes.[24] This is a characteristic consequence of kappa-opioid activation. The clinical significance of this brief hormonal change following occasional use is not established.
Psychological risks
Kappa-opioid activation inherently produces dysphoria, anxiety, and aversive psychological states — the endogenous dynorphin/KOR system encodes the dysphoric component of the stress response.[5]
At high inhaled doses, salvinorin A produces complete disconnection from external reality, loss of body awareness, confusion, amnesia, and complete ego dissolution.[1][4] The extreme rapidity of onset (15–60 seconds[24]) means incapacitation can occur before the user can respond — creating risk of falls, burns from smoking equipment, and injury from uncontrolled movement.
Rare case reports document psychotic episodes following use.[29][6] These are uncommon relative to estimated prevalence of use,[30] but the association with psychosis in predisposed individuals warrants caution.
Tolerance and dependence
Tolerance develops rapidly through receptor desensitization. Brain imaging in rodents demonstrated that higher doses induce a sustained 40–49% reduction in kappa-opioid receptor availability persisting up to 2.5 hours after the drug is eliminated from the brain.[31] At lower doses, no prolonged receptor changes were observed.[31]
Cross-tolerance is expected with other kappa-opioid agonists but not with serotonergic psychedelics (LSD, psilocybin), which operate through an entirely independent receptor system.[19]
Dependence liability is negligible. Salvinorin A does not produce positive reinforcement — it functions as a punisher rather than a reward in animal studies.[5] Its aversive phenomenology and suppression of reward-circuit dopamine limit compulsive use.[5] Recreational use is characteristically intermittent and curiosity-driven rather than habitual.[12] No physical withdrawal has been documented.
Drug interactions
No controlled human drug interaction studies have been published for salvinorin A. All interaction assessments below are based on mechanistic reasoning.safety citation needed
Opioid antagonists (naltrexone, naloxone): Fully reverse all effects of salvinorin A — confirmed in humans.[19] Clinically relevant for emergency management of severe reactions.
Other opioid agonists: Concurrent kappa- and μ-opioid activation would produce unpredictable additive effects. Not characterized in published literature.
Serotonergic psychedelics (LSD, psilocybin, mescaline): No cross-tolerance exists between KOR and 5-HT₂A mechanisms.[19] Combination would represent two independent hallucinogenic mechanisms acting simultaneously, with unpredictable results.
MAO inhibitors: Salvinorin A is a terpenoid, not an amine, and is not a substrate for monoamine oxidase. MAOI potentiation is not expected, though additive CNS effects remain theoretically possible.citation needed
SSRIs and SNRIs: The KOR system modulates SERT activity, and preclinical models suggest serotonin transporter blockade can attenuate some effects of salvinorin A. Clinical significance is unknown.citation needed
Other medications: Salvinorin A is primarily metabolized by esterases rather than cytochrome P450 enzymes,[16] reducing the expected risk of interactions with CYP-metabolized drugs, though this has not been systematically confirmed.
Contraindications
No controlled studies have evaluated contraindications. The following are based on mechanistic reasoning and case report data.
Psychotic disorders: Individuals with a personal or family history of schizophrenia or other psychotic disorders face elevated risk. Case reports associate use with psychotic episodes.[29][6]
Bipolar disorder: The intense, rapidly fluctuating affective states — from profound dysphoria to confusion and ego dissolution — represent a theoretical risk for mood episode destabilization.citation needed
Concurrent opioid use: Pharmacodynamic interactions with opioid agonists are expected. Combination introduces unpredictable additive effects.citation needed
Hazardous physical environments: The near-instantaneous onset (15–60 seconds[24]) and complete incapacitation at higher doses[1] create acute danger near fall hazards, open flames, water, or moving vehicles.
Vehicle operation: Complete motor and cognitive incapacitation during peak effects precludes safe operation of vehicles or machinery.
Harm Reduction[edit]
Forms & Identification
Salvinorin A cannot be detected by standard alkaloid reagent tests (Marquis, Mecke, Simon's).[32][33] For extract products, concentration labels (5×, 10×, etc.) are unregulated and unreliable — actual salvinorin A content may differ significantly from what is stated. When using extract products, treat every new batch as an unknown potency and start with the smallest possible amount.
Guidelines
- Test every new batch at the lowest possible dose — potency varies between products and sources
- Use a reclining position — lie down or sit in a supported chair before inhaling
- Always have a sober sitter present who understands the rapid onset and short duration
- Clear the environment of hazards: open flames, sharp objects, hard surfaces within falling distance, bodies of water
- Secure all smoking materials — have the sitter hold the pipe or vaporizer after the dose is inhaled, as the user will lose motor control
- Start with plain leaf before trying extracts — move to concentrated extracts only after establishing individual sensitivity
- Allow at least 30 minutes of quiet time following the experience before standing, walking, or leaving the setting
- Do not combine with other psychoactive substances — drug interactions are uncharacterized
Set & Setting
The salvinorin A experience is exceptionally sensitive to environment. Onset is near-instantaneous, leaving no time to adjust once the dose is inhaled. A quiet, familiar, physically safe space is essential — remove sharp objects, open flames, and anything breakable from the immediate area. A reclining position (sitting or lying down) is strongly recommended, as motor control is lost rapidly at active doses.
A sober, trusted sitter is not optional for smoked or vaporized use. The sitter's role is to prevent physical harm (falls, contact with hot surfaces, wandering) and to provide calm, minimal verbal reassurance if the user shows distress. The sitter should not attempt to physically restrain the user unless there is immediate danger of serious injury.
Aftercare & integration. The salvinorin A experience is often disorienting and difficult to process. Many users report difficulty articulating what happened, and amnesia for portions of the experience is common. Allow time in a quiet setting before attempting to describe or analyze the experience.
Journaling soon after return to baseline — even fragmented impressions — can help anchor memories before they fade. Discussing the experience with the sitter or a trusted person in the hours or days following may aid processing. If the experience produced lasting distress, confusion about reality, or persistent anxiety, professional support from a therapist experienced with altered states is appropriate.
Recovery & Support
Compulsive salvinorin A use is rare — the experience is more commonly abandoned than sought repeatedly.[12] No physical dependence or withdrawal has been documented. If a pattern of repeated use develops despite negative experiences, this may reflect an underlying psychological need rather than pharmacological compulsion, and professional support is warranted.
The Fireside Project (psychedelic peer support line), MAPS integration resources, and local harm reduction organizations can provide guidance and referrals.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Most salvinorin A experiences, even distressing ones, resolve within 20 minutes. Seek emergency help if the person attempts self-harm, becomes physically combative, does not return to baseline awareness within 30 minutes, sustains a fall or burn injury, or shows signs of a psychotic break (persistent delusions, inability to recognize surroundings or people after effects should have resolved).
Immediate steps:
- 1. Ensure physical safety — gently guide the person away from hazards. Do not physically restrain unless there is immediate danger of serious injury.
- 2. Stay calm and speak in short, quiet sentences. Do not attempt to reason with someone in peak dissociation.
- 3. If the person is lying down and unresponsive, place them in the recovery position.
- 4. Call emergency services if the person is injured, if distress does not resolve within 30 minutes, or if psychotic symptoms persist.
What to tell the dispatcher: Name the substance (salvinorin A or Salvia divinorum), approximate amount and form used, time of use, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help.
Reversal agent: Naltrexone and naloxone fully reverse all effects of salvinorin A.[19] Emergency medical personnel carrying naloxone can administer it if needed.
Legal Status[edit]
Legal status
Salvinorin A and Salvia divinorum are not listed under the United Nations 1961 Single Convention on Narcotic Drugs or the 1971 Convention on Psychotropic Substances.[33] Regulatory status varies by jurisdiction, producing a fragmented international landscape.
In the United States, salvinorin A remains unscheduled at the federal level. The Drug Enforcement Administration lists it as a "Drug and Chemical of Concern" but has not initiated formal scheduling. Approximately 27 states have enacted state-level bans or restrictions.[34] Australia was the first country to ban the substance, classifying it as Schedule 9 (prohibited) in 2002.
Because salvinorin A is a terpenoid containing no nitrogen, it does not fall under alkaloid-specific structural analog legislation. However, broad psychoactive substance bans (such as the UK Psychoactive Substances Act) capture it regardless of chemical class.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States (federal) | Unscheduled | DEA lists as "Drug and Chemical of Concern"; no federal scheduling[34] |
| United States (states) | Varies | Approximately 27 states have enacted bans or restrictions |
| Australia | Schedule 9 (Prohibited) | Banned since June 1, 2002; first country to prohibit[34] |
| United Kingdom | Prohibited | Covered under Psychoactive Substances Act 2016[34] |
| Canada | Schedule IV (CDSA) | Sale and manufacture prohibited since approximately 2015[34] |
| Germany | Appendix I (BtMG) | Controlled under Narcotics Act since March 1, 2008[34] |
| Sweden | Prohibited | Illegal since April 1, 2006 |
| France | Controlled | Listed as poisonous substance since August 2010; illegal for human consumption |
| Italy | Prohibited | Prohibited since January 2005 |
| Netherlands | Unscheduled | No scheduling as of available data |
| New Zealand | Controlled | Psychoactive Substances Act 2014 |
references
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- [2]
- [3] ^abcdCasselman I, Nock CJ, Wohlmuth H, Weatherby RP, Heinrich M (2014) From local to global-fifty years of research on Salvia divinorum. — Journal of ethnopharmacology doi:10.1016/j.jep.2013.11.032
- [4] ^abcMacLean KA, Johnson MW, Reissig CJ, Prisinzano TE, Griffiths RR (2013) Dose-related effects of salvinorin A in humans: dissociative, hallucinogenic, and memory effects. — Psychopharmacology doi:10.1007/s00213-012-2912-9
- [5]
- [6] ^abcEl-Khoury J, Sahakian N (2015) The Association of Salvia divinorum and Psychotic Disorders: A Review of the Literature and Case Series. — Journal of psychoactive drugs doi:10.1080/02791072.2015.1073815