Salvia divinorum
Viewing r2 — May 14, 2026 — CURRENT
Back to HistoryInteractions, related substances, and reports reflect the current entry and are not shown for historical revisions.
Salvia divinorum (Lamiaceae) — ska María pastora, seer's sage — is a perennial herb endemic to the cloud forests of Oaxaca, Mexico. Its principal psychoactive constituent, salvinorin A, is the first known non-nitrogenous kappa-opioid receptor agonist.[1] Salvinorin A acts by activating kappa-opioid receptors, suppressing mesolimbic dopamine transmission and disrupting thalamocortical signalling.[2][3]
Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
Formally described in 1962 from specimens collected during Wasson and Hofmann's Sierra Mazateca expedition,[4] the plant has been used in Mazatec divinatory healing ceremonies for centuries. Salvinorin A's 2002 identification as a selective KOR agonist revealed a hallucinogenic mechanism entirely independent of serotonin 5-HT₂A receptors.[1] Not federally scheduled in the United States, the plant is nonetheless banned or restricted in approximately 27 US states, Canada, the United Kingdom, Australia, and other jurisdictions.[5]
Subjective effects include intense dissociation, depersonalisation, spatial disorientation, proprioceptive distortion, and vivid internal hallucinations.[6] Smoked preparations produce rapid, overwhelming immersion lasting under 20 minutes;[7] traditional buccal quids yield subtler effects over 30–90 minutes.[8] Dysphoria, intense fear, and transient amnesia are commonly reported at typical smoked doses.[6]
No human fatalities have been directly attributed to salvinorin A,[9][10] and no dependence syndrome has been described.[3][11] The primary risks are psychological — KOR-mediated dysphoria makes distressing experiences common, and case reports link use to persistent psychosis in psychiatrically vulnerable individuals.[12] No formal human pharmacokinetic study has been published, and no systematic contaminant surveillance of commercial products exists.
History[edit]
Traditional and historical use
The Mazatec people of the Sierra Mazateca in Oaxaca, Mexico, have used Salvia divinorum in divinatory healing ceremonies (veladas) for centuries, where the plant is known as ska María pastora ("leaves of Mary the Shepherdess").[13][8] A curandera (healer) administers the plant to enter a visionary state for diagnostic or therapeutic purposes.[4][8] Field researcher Diaz documented three traditional preparations between 1973 and 1983: a fresh-leaf quid held in the mouth for buccal absorption, a cold-water infusion of crushed leaves, and direct chewing with juice retained sublingually.[8]
The exact antiquity of Mazatec use remains uncertain — while centuries of practice are commonly cited, the earliest documented ethnographic accounts date to the mid-20th century, and no pre-colonial archaeological or documentary evidence has been identified.citation needed
Western discovery and research
The plant was first brought to Western attention through R. Gordon Wasson's ethnomycological expeditions to the Sierra Mazateca beginning in the late 1930s. In 1962, Wasson and Albert Hofmann collected the first flowering specimen, enabling Epling and Játiva to publish the formal botanical description.[4][14] The active compound was isolated independently by Ortega et al. in 1982 (as "salvinorin") and Valdes et al. in 1984 (as "divinorin A"); these were later confirmed identical.[4]
The landmark discovery came in 2002, when Roth et al. identified salvinorin A as a potent, selective kappa-opioid receptor agonist — the first non-nitrogenous compound found to produce hallucinogenic effects through this mechanism.[1] Controlled human studies at Johns Hopkins,[7][6] Yale,[15] and California Pacific Medical Center[16] subsequently characterised dose-response pharmacology between 2009 and 2016, with antagonist challenge confirming the κ-opioid mechanism in humans.[17]
Modern era
During the 1990s and 2000s, S. divinorum gained popularity as a legal hallucinogen alternative, with internet sales driving international awareness.[13][18] A wave of US state-level bans followed in the mid-2000s.[19] The DEA listed the plant as a "Drug and Chemical of Concern" in 2009 but has not pursued federal scheduling.[19]
The United Kingdom banned S. divinorum under the Psychoactive Substances Act 2016,[5] Canada added it to Schedule IV in 2017,[5] and the plant remains absent from UN international drug control conventions.[20] Research interest has shifted in the 2020s toward salvinorin A analogues as potential therapeutics for pain, addiction, and gastrointestinal disease,[21][22] though none have entered clinical trials.
Botanical Overview[edit]
Taxonomy and family
Salvia divinorum Epling & Játiva is a perennial herb in the genus Salvia, the largest genus in the family Lamiaceae (mint family).[14] It is among the very few Salvia species with documented psychoactive properties. The species was formally described in 1962 from the first flowering specimen collected during Wasson and Hofmann's expedition to the Sierra Mazateca.[4] No subspecies or chemotype variants are recognised in the botanical literature.
Native range and habitat
The plant is endemic to the cloud forests of the Sierra Mazateca in Oaxaca, Mexico, where it grows in humid, shaded ravines at elevations between approximately 300 and 1,800 metres.citation needed It favours dark, moist conditions under forest canopy and does not tolerate direct sunlight or frost. Wild populations are considered rare; the plant is primarily propagated vegetatively through stem cuttings, as seed production is extremely limited.citation needed
Identification
S. divinorum is a sprawling herb that can reach 1–1.5 metres in height. Its stems are square in cross-section — characteristic of the mint family — hollow, and brittle. Leaves are large (10–30 cm), ovate, green, with serrated margins. Flowers appear rarely in cultivation; when present, they are white with purple calyces, arranged in racemes.citation needed The plant is most readily distinguished from other Salvia species by its unusually large leaf size, hollow square stems, and sprawling growth habit.
Harvesting and processing
Traditional Mazatec harvesting involves picking fresh leaves immediately before preparation.[8] In modern commercial contexts, leaf material is dried and sold as plain leaf or processed into concentrated extracts via solvent extraction. Drying and storage conditions affect salvinorin A content variably, and commercial extract potency labelling does not reliably correspond to measured concentration.[23]
Alkaloid Profile[edit]
Dominant compound
The principal — and essentially sole — psychoactive constituent of Salvia divinorum is salvinorin A (salvinorin A), a neoclerodane diterpenoid. Unlike virtually all other known naturally occurring hallucinogens, salvinorin A contains no nitrogen atom, placing it outside conventional alkaloid classification.[1] It is nonetheless discussed alongside plant alkaloids due to its psychoactive potency. Salvinorin A is a highly selective full agonist at the κ-opioid (KOR) with no significant activity at serotonin 5-HT₂A receptors or over 50 other screened molecular targets.[1]
Binding characteristics
Salvinorin A engages KOR through an unconventional binding mode — interacting with residues in transmembrane domains II and VII rather than the transmembrane III aspartate used by classical opioid ligands.[21] It displays pronounced β-arrestin-biased signalling, which produces rapid receptor desensitisation and distinguishes its pharmacological profile from that of endogenous dynorphins and classical KOR agonists.[3] Full agonist efficacy at the cloned human KOR was confirmed by Chavkin et al. in 2004.[24]
Minor diterpenoids
Several structurally related diterpenoids — including salvinorins B, C, D, E, and F — have been isolated from S. divinorum, but none have demonstrated significant pharmacological activity at psychoactive-relevant targets. Salvinorin A accounts for the entirety of the plant's known psychoactive effects.
Variability
Salvinorin A concentration varies across individual plants, cultivation conditions, and preparation methods. Commercial products show substantial deviation between labelled and measured salvinorin A content.[23] Extract products are labelled with strength multipliers (5×, 10×, 20×) that do not reliably correspond to measured concentration, making dose calibration from product labelling unreliable.
Neuroscience[edit]
Where it acts
Salvinorin A is a selective full agonist at the κ-opioid with no activity at serotonin 5-HT₂A — the primary target of classical psychedelics.[1] This was confirmed in a human antagonist-challenge study: naltrexone fully blocked salvinorin A's subjective and neuroendocrine effects, while the 5-HT₂A antagonist ketanserin did not.[17] KOR activation suppresses dopamine release in the nucleus accumbens[2] and disrupts thalamocortical circuits,[3] producing dissociation and hallucination without euphoria or positive reinforcement.
What it changes
KOR activation engages the brain's endogenous stress-response system — the same dynorphin circuits that counter-modulate reward.[11][3] Dopaminergic suppression in mesolimbic pathways explains the characteristically aversive quality and low abuse potential. Disruption of large-scale cortical network connectivity has been proposed as the substrate for dissolution of self-referential processing during the experience.[3] Dose-related increases in plasma prolactin and cortisol have been documented in humans.[15]
- No human pharmacokinetic data with plasma sampling exist for any route of administration.
- The mechanism by which the traditional quid produces effects via buccal absorption — while a controlled sublingual liquid formulation did not[16] — remains unresolved.
- No neuroimaging studies of salvinorin A in humans have been published.
Subjective Effects[edit]
The Salvia divinorum experience resists classification within established psychedelic, dissociative, or opioid frameworks. Smoked preparations produce a sudden, total immersion — complete loss of awareness of the physical environment, vivid internal hallucinations including entity contact and immersive scenario experiences, and profound spatial and temporal disorientation.[6] The traditional fresh-leaf quid yields a subtler perceptual shift: light-headedness, altered proprioception, amplified auditory perception, and depersonalisation without full hallucinatory breakthrough.[8] Set and setting strongly modulate experience quality, with unfamiliar or chaotic environments consistently associated with distressing outcomes.[25]
Pharmacologically, S. divinorum occupies a unique niche — κ-opioid agonism produces perceptual disruption without the euphoric valence of serotonergic psychedelics or the anaesthetic dissociation of NMDA antagonists like ketamine.[1][3] Dysphoria is the modal affective tone, not a side effect — a direct consequence of the kappa-opioid mechanism that distinguishes it from virtually every other hallucinogenic substance.
Effect Grid
The full dissociative-hallucinogenic experience. Vivid internal hallucinations dominate — immersive scenario experiences, entity contact, and revisiting of childhood memories are frequently reported. Spatial disorientation is pronounced, and awareness of the physical environment may be lost entirely. Depersonalisation and derealisation are intense. Temporal disorientation distorts the perceived passage of time.
Motor control impairment is severe — users are typically unable to stand or walk safely. Bodily dissociation, body schema distortion, vestibular distortion, and sensations of being pulled or compressed are common. Dysphoria is more frequently reported than euphoria. Amnesia for portions of the experience is typical.
When smoked, the full experience lasts approximately 15–20 minutes with onset and peak coinciding at roughly 2 minutes. Post-acute cognitive fatigue and mild confusion may persist for hours. This is the tier described in most controlled human studies (Johnson 2011, MacLean 2013).
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Depth perception distortion · Vestibular distortion · Visual morphing · Visual drifting · Color alteration · Geometry · Visual acuity suppression · Visual melting · Auditory suppression · Brightness alteration · Visual haze / noise · Auditory distortion · Environmental patterning · Synesthesia · Visual breathing · Visual magnification · Internal hallucinations · External hallucinations · Object transformations · Perspective hallucinations · Visual processing suppression · Object activation · Visual scenery slicing · Visual flipping · Auditory hallucinations
Color alteration · Geometry · Visual acuity suppression · Visual melting · Auditory suppression · Brightness alteration · Visual haze / noise · Auditory distortion · Environmental patterning · Synesthesia · Visual breathing · Visual magnification · Internal hallucinations · External hallucinations · Object transformations · Perspective hallucinations · Visual processing suppression · Object activation · Visual scenery slicing · Visual flipping · Auditory hallucinations
Pupil constriction · Physical fatigue · Spontaneous body sensations · Bodily heaviness · Laughter fits · Muscle relaxation · Nystagmus (eye wobbles) · Tingling / electric sensations · Trembling · Vibrations / buzzing · Nausea · Vomiting · Bodily dissociation · Tactile hallucination
Laughter fits · Muscle relaxation · Nystagmus (eye wobbles) · Tingling / electric sensations · Trembling · Vibrations / buzzing · Nausea · Vomiting · Bodily dissociation · Tactile hallucination
Thought disorganization · Focus suppression · Information processing suppression · Memory suppression · Novelty enhancement · Analysis suppression · Cognitive dysphoria · Language suppression · Cognitive fatigue · Motivation suppression · Thought loops · Delirium · Delusions
Memory suppression · Novelty enhancement · Analysis suppression · Cognitive dysphoria · Language suppression · Cognitive fatigue · Motivation suppression · Thought loops · Delusions
Euphoria
Automaticity · Sociability suppression · Cognitive disconnection · Boundary dissolution · Ego dissolution · Identity alteration
Ego dissolution · Identity alteration
Existential realization · Noetic insight · Transpersonal feelings · Voidness · Death-rebirth sequence · Near-death experience
Death-rebirth sequence · Near-death experience
Timeline · by preparation
Preparations[edit]
Fresh-leaf quid (buccal)
Fresh-leaf quid is the traditional Mazatec preparation. Freshly picked leaves are rolled or crushed into a bolus and held in the mouth, with juice retained for buccal and sublingual absorption.[8] Onset is gradual (10–20 minutes), with effects lasting 30–90 minutes.[8] The experience is markedly milder than smoked preparations — light-headedness, altered proprioception, depersonalisation, and enhanced imagery without full hallucinatory breakthrough. This preparation requires fresh plant material, limiting availability outside cultivation regions.
Dried leaf (smoked)
Dried leaf (plain, non-enhanced) is smoked in a pipe or water pipe. Onset occurs within approximately 2 minutes, with effects resolving within 15–20 minutes.[7] The experience is considerably more intense than the quid — complete dissociation from the physical environment is possible even with plain leaf at higher amounts. Potency varies by plant source, drying method, and storage conditions.
Concentrated extract (smoked/vaporised)
Concentrated extracts are produced by solvent extraction of dried leaf material and sold with strength multipliers (5×, 10×, 20×, 60×+). These preparations are most commonly associated with intense, overwhelming experiences and adverse psychological reactions. Labelled potency frequently does not reflect measured salvinorin A content.[23] Onset and duration mirror dried leaf (approximately 2 minutes onset, 15–20 minutes duration), but intensity at equivalent mass is dramatically higher. The unpredictability of extract potency makes dose calibration from product labelling unreliable.
Water infusion (oral)
Water infusion — crushed fresh leaves mixed with cold water — is a documented traditional preparation.[8] Effects were described as mild and short-lasting in ethnographic field research. This preparation is rarely encountered outside traditional Mazatec contexts.
Per-preparation dose tiers, timelines, and bioavailability data are in the Dose · by preparation card on this page.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Negligible
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- —
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- —
Toxicity
No human fatalities have been directly attributed to salvinorin A.[9][10] No formal LD50 has been established. The most recent systematic review of preclinical data found no evidence of significant physiological toxicity at psychoactive doses.[26]
Controlled human studies found no significant increase in heart rate or blood pressure across inhaled doses from 0.375 to 21 μg/kg.[7] This distinguishes salvinorin A from classical psychedelics, which reliably elevate heart rate.
Salvinorin A (160–640 μg/kg, s.c.) impaired spatial long-term memory, episodic memory, and aversive memory in rats while sparing short-term memory; these effects were blocked by the selective κ-opioid antagonist nor-BNI, confirming KOR mediation.[27] Amnesia for portions of the acute experience is also documented in human studies.[6]
Commercial S. divinorum products carry labelling accuracy concerns — measured salvinorin A content deviates substantially from labelled potency.[23] No published systematic surveillance of pesticide residues, heavy metals (lead, cadmium, arsenic, mercury), mycotoxins, or microbial contamination in commercial products was identified. No ISO/IEC-accredited testing programmes or Certificate of Analysis requirements specific to S. divinorum products exist in any jurisdiction.
safety citation needed The absence of contaminant surveillance data does not indicate absence of contamination — it reflects a gap in the published evidence base.
Psychological Risks
Intense fear, panic, and extreme disorientation are common at typical smoked doses, particularly with concentrated extracts or in uncontrolled settings.[25] Dysphoria is more frequently reported than euphoria.[8] Complete loss of awareness of the physical environment constitutes the primary acute risk — users may fall, walk into hazards, or injure themselves without recognising danger.
Case reports have linked S. divinorum use to persistent psychotic episodes in individuals with possible pre-existing psychiatric vulnerability.[12] One report described a psychotic episode following unintentional consumption, resistant to two pharmacological treatments before resolving with brexiprazole.[28] Multiple reviews flag elevated psychiatric risk in adolescents, users of other substances, and individuals with underlying psychotic disturbances.[13][29]
The causal relationship between S. divinorum and persisting psychosis is not established — all published cases involve individuals with potential pre-existing vulnerability, and no prospective psychiatric outcome data exist.
Tolerance & Dependence
Tachyphylaxis — rapid loss of effect with repeated dosing within a single session — is commonly reported.[25] No formal tolerance study exists in humans.
No dependence syndrome has been described in the clinical literature.[29] The aversive phenomenology and KOR-mediated dopaminergic suppression underlie the substance's low abuse potential.[3][2] Survey data indicate over 52% of users reduced or ceased use within 12 months, citing dislike of effects (33%) and loss of interest (29%).[13]
No withdrawal has been characterised. Multiple reviews conclude that salvinorin A has low abuse potential based on aversive phenomenology, dopaminergic suppression, and absence of positive reinforcement in animal self-administration paradigms.[3][11]
Drug Interactions
Salvinorin A is metabolised by CYP2D6, CYP1A1, CYP2E1, and CYP2C18, with additional glucuronidation via UGT2B7, and is a P-glycoprotein substrate.[30] Drugs that inhibit CYP2D6 (fluoxetine, paroxetine, quinidine) or CYP2E1 (disulfiram) could theoretically increase salvinorin A plasma levels and prolong effects. P-glycoprotein inhibitors (verapamil, cyclosporine) could alter CNS distribution.
- CNS depressants (opioids, benzodiazepines, alcohol, cannabis): Additive CNS depression, disorientation, and impaired motor control are theoretically possible.safety citation needed
- Lithium: seizure risk has been reported anecdotally with lithium in combination with psychedelics. No specific case report with salvinorin A exists.safety citation needed
- MAOIs and SSRIs: Theoretical pharmacodynamic concern given KOR–SERT interactions. No clinical case reports.safety citation needed
Contraindications
Absolute:
- Personal or family history of psychotic disorders (schizophrenia, schizoaffective disorder, bipolar disorder with psychotic features) — case reports document persistent psychotic episodes in individuals with possible pre-existing vulnerability[12][28]
Relative:
- Adolescence — elevated risk flagged in multiple reviews; developing brain vulnerability to KOR-mediated dopaminergic suppression is a mechanistic concern[13][29]
- Pregnancy and breastfeeding — no published safety data existsafety citation needed
- Hepatic impairment — CYP enzyme involvement in salvinorin A metabolism suggests possible altered metabolism in liver disease[30]
- Concurrent use of CYP2D6 or CYP2E1 inhibitors — theoretical risk of increased salvinorin A exposure
- Unsupervised settings or environments with fall risk — motor control impairment and complete loss of environmental awareness at typical smoked doses create physical injury risk[25]
Standard immunoassay drug screens do not detect salvinorin A. Detection requires specific LC-MS/MS methodology.[31]
Harm Reduction[edit]
Forms & Identification
Salvia divinorum products range from plain dried leaf to highly concentrated extracts labelled with strength multipliers (5×, 10×, 20×, and higher). Labelled potency does not reliably correspond to measured salvinorin A content,[23] and no ISO/IEC-accredited testing programme or Certificate of Analysis standard exists for these products.
When purchasing commercial products, lower-strength preparations (plain leaf or 5×) offer more predictable dosing than high-concentration extracts. Starting with plain dried leaf before attempting extracts allows calibration of individual sensitivity. No reagent testing kit reliably quantifies salvinorin A content in home settings.
Guidelines
Practical Guidance
- Begin with plain dried leaf before attempting any concentrated extract
- Use the smallest amount possible for a first experience — salvinorin A is active at microgram doses
- Ensure a sober sitter is present throughout the experience and for at least 15 minutes after apparent offset
- Sit or lie down before administration — never stand during onset
- Remove all fire sources, sharp objects, and fall hazards from the immediate environment
- Do not drive or operate machinery for at least one hour after effects resolve
- Do not redose within the same session — tachyphylaxis makes repeated dosing unpredictable
- Avoid use in unfamiliar environments, at social gatherings, or in any setting where uncontrolled movement poses a risk
- Avoid combining with CNS depressants, alcohol, or other psychoactive substances
Set & Setting
Set and setting exert unusually strong influence on the S. divinorum experience.[25] The substance's capacity to obliterate awareness of the physical environment makes controlled, familiar settings essential.
A quiet, dimly lit indoor space with soft surfaces and no sharp edges or hazards is strongly recommended. A sober, trusted sitter is considered essential — not optional — at any dose above threshold. The sitter's role is physical safety: preventing falls, contact with flame, and wandering into dangerous areas. The sitter should not attempt to interact with or redirect the user's experience unless physical safety is at risk.
Aftercare & integration.
Post-Experience Processing
The intensity and alien quality of the S. divinorum experience frequently leaves users shaken, confused, or emotionally unsettled even after acute effects resolve. Allow 30–60 minutes of quiet recovery before returning to normal activities.
Amnesia for portions of the experience is common.[6] Writing or recording impressions shortly after can help with processing. Persistent dysphoria, anxiety, or derealization lasting more than 24 hours warrants professional consultation.
Hydration and a light meal after the experience may ease physical discomfort. Avoid further psychoactive substance use for the remainder of the day.
Recovery & Support
Cessation and Support Resources
Compulsive S. divinorum use is rare due to the substance's aversive phenomenology and low reinforcement potential.[3] However, any pattern of use that causes distress or impairment warrants professional attention.
If S. divinorum use has triggered or worsened psychiatric symptoms — particularly psychotic features, persistent anxiety, or depersonalisation — seek evaluation from a mental health professional experienced with substance-related presentations.
- SAMHSA National Helpline: 1-800-662-4357 (free, confidential, 24/7)
- Crisis Text Line: Text HOME to 741741
- Emergency services: Call 911 (US) or local emergency number for acute psychiatric crisis
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognising an emergency
- Complete unresponsiveness lasting more than 5 minutes after smoking
- Attempts to stand, walk, or run while unaware of physical surroundings
- Severe panic with agitation that does not begin to resolve within 10–15 minutes
- Self-harm attempts or violent behaviour
- Psychotic symptoms (paranoia, delusions, disorganised speech) persisting beyond 30 minutes after smoking
Immediate steps
- Ensure the person is in a safe position (seated or lying on their side) and cannot fall or contact hazards
- Speak calmly and reassuringly — do not physically restrain unless they are in immediate danger
- If panic is present, reassure them the effects are temporary and will pass within minutes
- Call emergency services if psychotic symptoms persist beyond 30 minutes, if there is any injury, or if the person remains unresponsive
What to tell the dispatcher
State the substance (Salvia divinorum or salvinorin A), the approximate amount and preparation used, time of administration, and current symptoms. Good Samaritan laws exist in many jurisdictions and provide legal protection for reporting drug-related emergencies.
No pharmacological reversal agent for salvinorin A is available outside clinical settings. Naltrexone blocks κ-opioid effects but is not carried by first responders and is not indicated for acute field management.
Legal Status[edit]
Salvia divinorum and salvinorin A are not listed under any of the three UN international drug control conventions.[20][5] This absence from international scheduling has produced a fragmented global legal landscape, with control measures implemented piecemeal at national and sub-national levels. In the United States, S. divinorum is not federally scheduled but is banned or restricted in approximately 27 states; internationally, it is controlled in Canada, the United Kingdom, Australia, Germany, Japan, and several other jurisdictions.
| Jurisdiction | Status | Notes |
|---|---|---|
| United States (federal) | Not scheduled | DEA lists S. divinorum as a "Drug and Chemical of Concern" but has not initiated formal scheduling[19] |
| United States (states — banned) | Controlled substance (~27 states) | Outright bans in Delaware, Florida, Illinois, Kansas, Kentucky, Louisiana, Mississippi, Missouri, Nebraska, North Dakota, Ohio, Oklahoma, Pennsylvania, South Dakota, Tennessee, Texas, Virginia, and others[19] |
| United States (states — age-restricted) | Age restriction only | California (18+), Maine[19] |
| United States (states — unrestricted) | No state-level restriction | ~22 states including Alaska, Arizona, Idaho, Massachusetts, Montana, Nevada, New Hampshire, New Jersey, New Mexico, New York, Oregon, South Carolina, Utah, Washington, West Virginia, and DC[19] |
| Canada | Schedule IV | Controlled since 2017 under the Controlled Drugs and Substances Act[5] |
| United Kingdom | Banned | Prohibited since 26 May 2016 under the Psychoactive Substances Act 2016; salvinorin A is not individually named[5] |
| Australia | Schedule 9 — Prohibited | Most restrictive schedule under the Therapeutic Goods Act; live plants also prohibited[5] |
| Germany | Controlled | Controlled since approximately 2015 under narcotics law[5] |
| EU member states (selected) | Domestic restrictions vary | Belgium, Denmark, Estonia, Finland, Iceland (EEA), Ireland, Italy, Romania, Slovakia, Spain, and Sweden have enacted domestic restrictions[20][5] |
| Japan | Controlled | Controlled since 2007[5] |
| Brazil, South Korea, Norway, Poland | Domestic restrictions | Various domestic controls in effect[5] |
citation needed US state-level legal status is subject to frequent change. The classifications above are based on 2024 secondary sources and require verification against current state statutes.
Because salvinorin A is a diterpenoid with no nitrogen atom, it does not fall within the structural definitions used by many structural analog acts or blanket scheduling frameworks designed around nitrogenous psychoactive compounds. Jurisdictions that control S. divinorum have done so by specifically naming the plant, the compound, or by applying broad psychoactive-substance legislation (as in the United Kingdom's Psychoactive Substances Act 2016).
references
- [1]
- [2] ^abcCarlezon WA, Beguin C, DiNieri JA, Baumann MH, Richards MR, Todtenkopf MS, Rothman RB, Ma Z, Lee DY, Cohen BM (2006) Depressive-like effects of the kappa-opioid receptor agonist salvinorin A on behavior and neurochemistry in rats — Journal of Pharmacology and Experimental Therapeutics PMID:16223871
- [3]
- [4]
- [5]
- [6]