Salvinorin A

methyl (2S,4aR,6aR,7R,9S,10aS,10bR)-9-(acetyloxy)-2-(furan-3-yl)-6a,10b-dimethyl-4,10-dioxo-dodecahydro-2H-naphtho[2,1-c]pyran-7-carboxylate

Overview

Salvinorin A belongs to Psychedelics.

Key safety note: Salvinorin A is extraordinarily potent (active from ~200 µg smoked) and produces brief but overwhelming, disorienting effects, a hallmark being complete loss of awareness of one's real surroundings, so the dominant hazard is behavioural: falls, burns (from the smoking implement) and injury during the peak.[3][5]
Effects
Subjective effects vary. What a substance feels like depends on dose, individual physiology, mindset, and setting. The points below describe commonly reported effects, not guaranteed, uniform, or desirable outcomes.
  • A brief, extremely intense and disorienting hallucinogenic state: often strongly dissociative: depersonalisation, a sense of merging with or becoming objects, contact with entities, and revisiting places or memories, with frequent loss of awareness of the real environment.
  • The character is usually described as alien and unsettling rather than pleasurable. Dysphoria, fear, confusion and uncontrollable movement or laughter are common, and recall/recognition memory is temporarily impaired.
  • When smoked, onset is almost immediate (<30 s), effects peak at ≈1–2 minutes and largely resolve within ≈20–30 minutes. The buccal/sublingual route is slower (onset 10–15 min) and lasts about an hour.
  • Physical effects can include incoordination, dizziness, sweating and a heavy, sedated body feeling.
Dosing & duration
Harm-reduction note: These are commonly cited reference ranges, not a recommendation or a “safe” dose. Potency, purity, body chemistry, tolerance, and drug combinations vary widely. Start low, go slow, wait for full effects before redosing, and never assume an unknown product matches these figures. Missing data is not evidence of safety.

Smoked / vaporised, Buccal / sublingual (quid). Not a recommendation. Salvinorin A is one of the most potent naturally occurring psychoactives and is dosed in micrograms: the figures below are for pure, smoked salvinorin A and are extremely sensitive to small changes. It is orally inactive (destroyed in the gut), so it is smoked/vaporised or held in the mouth. The buccal route needs substantially more. Plant leaf and '×5/×10/×20' standardised extracts vary enormously in potency and are far harder to gauge.

Dose ranges

Threshold

≈100–200 µg (smoked)

Common

≈200–750 µg (smoked pure)

Strong

≈0.75–2 mg (smoked)

Duration

onset

<30 s (smoked), 10–15 min (buccal)

peak

≈1–2 min (smoked)

total

≈20–30 min (smoked), ≈1 h (buccal)

Chemical & Physical Properties
FormulaC23H28O8
Molar mass432.46 g/mol
StateSolid
Melting point238–240 °C, also reported as 242–244 °C
Boiling pointNot reported
DensityNot reported
Vapor pressureNot reported
pKaNot reported
LogP2.5 (predicted, XLogP3)
SolubilitySoluble in ethanol and acetone. Poorly soluble in water (~25 mg/L)
Refractive indexNot reported
Identifiers & Synonyms
CAS83729-01-5
CAS (enantiomer)
PubChem CID128563
InChIKeyOBSYBRPAKCASQB-AGQYDFLVSA-N
InChIInChI=1S/C23H28O8/c1-12(24)30-16-9-15(20(26)28-4)22(2)7-5-14-21(27)31-17(13-6-8-29-11-13)10-23(14,3)19(22)18(16)25/h6,8,11,14-17,19H,5,7,9-10H2,1-4H3/t14-,15-,16-,17-,19-,22-,23-/m0/s1
SMILESCC(=O)O[C@H]1C[C@H]([C@@]2(CC[C@H]3C(=O)O[C@@H](C[C@@]3([C@H]2C1=O)C)C4=COC=C4)C)C(=O)OC

Synonyms

  • Salvinorin A
  • Active principle of Salvia divinorum
  • Sally-D
Pharmacodynamics & Biochemistry

Salvinorin A is the main active constituent of the sage Salvia divinorum and is pharmacologically unique: a highly potent, highly selective full agonist at the κ-opioid receptor (KOR, Kᵢ ≈2.4 nM, EC50 ≈1.8 nM). It is the first known KOR agonist that is not an alkaloid: a trans-neoclerodane diterpenoid containing no nitrogen atom, so it cannot form a salt. Crucially, it has no activity at the 5-HT2A receptor, the target of 'classical' serotonergic psychedelics such as LSD, psilocin and mescaline, so its hallucinogenic effect is mechanistically distinct. Its effects in humans are blocked by the opioid antagonist naltrexone but not by the 5-HT2A antagonist ketanserin, confirming the KOR mechanism. It is additionally a dopamine D2 partial agonist (affinity ~5–10 nM, ~40–60% intrinsic activity) and has some cannabinoid CB1 activity, and it modulates the dopamine and serotonin transporters. KOR-driven suppression of striatal dopamine release underlies its characteristic dysphoria.

Biological targets

  • KOR
  • D2

Binding & functional measurements

TargetMeasurementSpecies
κ receptorKi 2.4 nMHuman
D2Ki 5.0 nMHuman
Pharmacokinetics
BioavailabilityOrally inactive (degraded in the GI tract), absorbed via oral mucosa or lungs. Plasma protein binding ≈83%
TmaxSmoked: onset <30 s, peak ≈1–2 min, buccal: onset 10–15 min
Half-life≈50 min (human plasma, ≈8 min in non-human primates): subjective effects much shorter
VdNot reported
Protein bindingNot reported
MetabolismEster hydrolysis (esterases/CYP450) to inactive salvinorin B. Delactonation. Glucuronidation (UGT2B7) to salvinorin A glucuronide
ExcretionUrine and bile
Toxicology & Safety
Harm-reduction note: Toxicity and risk depend on dose, route, purity, combinations, setting, and individual health factors. Missing harms should never be interpreted as evidence of safety.

Not reported

Salvinorin A is extraordinarily potent (active from ~200 µg smoked) and produces brief but overwhelming, disorienting effects, a hallmark being complete loss of awareness of one's real surroundings, so the dominant hazard is behavioural: falls, burns (from the smoking implement) and injury during the peak. Unlike serotonergic psychedelics the experience is frequently dysphoric, frightening or unpleasant rather than euphoric, reflecting its κ-opioid pharmacology (sedation, dysphoria, anhedonia, psychotomimesis). Physiological toxicity appears low and no lethal dose is established, but a sober sitter and a safe, hazard-free setting are essential. Limited human data must never be read as evidence of safety.[3][5]

Legal Status
Legal note: Legal status can change over time and may vary by country, region, formulation, analogue status, prescription context, and enforcement practice. Always confirm with current official sources before relying on this section.
Interactions & Contraindications

Drug interactions

Alcohol Additive sedation and dissociation with alcohol and other CNS depressants.[3]

Contraindications

Personal or family history of psychosis, schizophrenia or bipolar disorder personal or family history of psychosis, schizophrenia or bipolar disorder.
Settings where impairment or dissociation risks injury (driving, water, heights) use without a sober sitter, or near heat, water, heights or roads.[3]
History of significant depression κ-opioid agonism can be strongly dysphoric.[5]
Pregnancy or breastfeeding
Usage & Context
  • Traditional entheogenic and healing use of Salvia divinorum leaves by the Mazatec people of Oaxaca, Mexico: chewed as a quid or drunk as a crushed-leaf infusion.
  • Modern recreational and psychonautic use, usually of dried leaf or standardised extracts smoked for the short, intense effect. Deterred for many by its dysphoric character.
  • A significant research tool as the prototypical non-alkaloid, highly selective κ-opioid agonist, used to probe KOR pharmacology and dissociation.
Sources & Evidence

Further Information