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PsychedeliaDokholyan Laboratory
Plate 498 of 545Verified

Salvinorin A

Also known asDivinorin A · Salvinorin · (-)-Salvinorin A · salvinorin-A · herbal ecstasy · Mexican mint · Salvonorin A · Ska Maria Pastora

methyl (2S,4aR,6aR,7R,9S,10aS,10bR)-9-acetyloxy-2-(furan-3-yl)-6a,10b-dimethyl-4,10-dioxo-2,4a,5,6,7,8,9,10a-octahydro-1H-benzo[f]isochromene-7-carboxylate

PubChem CID
128563
Measurements
32
InChIKey
OBSYBRPAKCASQB-AGQYDFLVSA-N

I · Summary

What is known

Published passages, each quoted whole and attributed to the database that published it. Two blocks are written here rather than quoted, and both say so where they stand: the synthesized summary at the top, which may draw only on the passages beneath it, and the history note, which cites the works it came from. Every claim in either carries a marker to its source.

Synthesized summary

written by this site — every other word below is quoted

Salvinorin A is the active constituent of Salvia divinorum, a Mexican plant with a long history of use as an entheogen by Mazatec shamans for ritual divination and healing 1,2. It is the outlier of this archive on two counts. Chemically it carries no nitrogen — the record describes an organic heterotricyclic, organooxygen natural product 7 — and yet it is a potent and selective kappa opioid receptor agonist 2, with other targets such as the CB1 receptor proposed rather than settled 3. Legally it is the other way round from almost everything here: the same passage records that neither Salvia divinorum nor salvinorin A is controlled under the federal Controlled Substances Act, and that neither has an approved medical use in the United States 2. Route governs its pharmacology more than dose does 4,5,6. It is effectively deactivated by the gastrointestinal tract, so traditional use depends on absorption across the oral mucosa from chewed fresh leaves or their juice, where 200–500 µg produces effects described as subjectively identical to the whole herb 4. The controlled studies bracket that from both sides: vaporized doses of 18–21 µg/kg peaked in plasma at two minutes and correlated with the rated effects 5, while sublingual doses up to 4 mg produced nothing significantly greater than placebo and mostly fell below the limit of quantification 6.

Drawn only from the passages printed below, so every claim above can be checked against material on this page. The numbers are those passages. Synthesized by Claude Opus 5 (claude-opus-5), via Claude Code on 2026-08-27.

What it is

  • 7cited by the summary above

    Salvinorin A is a natural product found in Salvia divinorum. It has a role as a oneirogen and a metabolite. It is an organic heterotricyclic compound and an organooxygen compound.

    ChEBI

  • Salvinorin A has been investigated for the basic science of Pharmaceutical Preparations.

    DrugBank

  • salvinorin A has been reported in Salvia divinorum with data available.

    LOTUS - the natural products occurrence database

  • 1cited by the summary above

    Salvinorin A is the main active psychotropic molecule in Salvia divinorum, a Mexican plant which has a long history of use as an entheogen by indigenous Mazatec shamans. Salvinorin A is a hallucinogenic compound with dissociative effects (L1181).

    Toxin and Toxin Target Database (T3DB)

Recognized use

  • /EXPL THER/ Leukotrienes (LTs) are lipid mediators derived from arachidonic acid (AA) involved in a number of autoimmune/inflammatory disorders including asthma, allergic rhinitis and cardiovascular diseases. Salvinorin A (SA), a diterpene isolated from the hallucinogenic plant Salvia divinorum, is a well-established analgesic compound, but its anti-inflammatory properties are under-researched and its effects on LT production is unknown to date. Here, we studied the possible effect of SA on LT production and verified its actions on experimental models of inflammation in which LTs play a prominent role. Peritoneal macrophages (PM) stimulated by calcium ionophore A23187 were chosen as in vitro…

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)PMID 26859523Rossi A et al; Pharmacol Res 106: 64-71 (2016)

  • 3cited by the summary above

    /EXPL THER/ The hallucinogenic compound, salvinorin A, is a potent kappa-opioid receptor (KOR) agonist. However, other target(s) than the KOR, such as the cannabinoid CB1 receptor, have been proposed to explain its multiple pharmacological actions. Here, we have evaluated the effect of salvinorin A in lipopolysaccharide (LPS)-stimulated macrophages as well as in models of inflammation in vivo. Salvinorin A (0.1-10 pM) reduced LPS-stimulated nitrite, TNF-alpha and IL-10 (but not IL-1beta) levels as well as iNOS (but not COX-2) LPS-induced hyperexpression. The effect of salvinorin A on nitrite levels was reverted by the opioid antagonist naloxone, the KOR antagonist nor-binaltorphimine and by…

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)PMID 21499737Aviello G et al; J Mol Med (Berl) 89 (9): 891-902 (2011)

  • /EXPL THER/ Salvinorin A (SA), the main active component of Salvia Divinorum, is a non-nitrogenous kappa opioid receptor (KOR) agonist. It has been shown to reduce acute pain and to exert potent antinflammatory effects. This study assesses the effects and the mode of action of SA on formalin-induced persistent pain in mice. Specifically, the SA effects on long-term behavioral dysfunctions and changes in neuronal activity occurring at spinal level, after single peripheral formalin injection, have been investigated. Moreover, the involvement of microglial and glial cells in formalin-induced chronic pain condition and in SA-mediated effects has been evaluated. Formalin induced a significant dec…

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)PMID 22913292Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3522567

  • /EXPL THER/ Salvinorin A (SA) has a potent inhibitory action on mouse gastrointestinal (GI) motility and ion transport, mediated primarily by kappa-opioid receptors (KOR). The aim of the present study was to characterize possible antiinflammatory and antinociceptive effects of SA in the GI tract of mice. Colonic damage scores and myeloperoxidase activity were determined after intraperitoneal (i.p.), intracolonic (i.c.), and oral (p.o.) administration of SA using the trinitrobenzene sulfonic acid (TNBS) and dextran sodium sulfate (DSS) models of colitis in mice. Additionally, KOR, cannabinoid (CB)1, and CB2 western blot analysis of colon samples was performed. The antinociceptive effect of SA…

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)PMID 21953882Fichna J et al; Inflamm Bowel Dis 18 (6): 1137-45 (2012)

  • One of the most powerful natural hallucinogens; The leaves are used in traditional medicine for divination and for treatment of anemia and excretory disorders; [Merck Index]

    Use Classification

    Haz-Map, Information on Hazardous Chemicals and Occupational DiseasesMerck Index - O'Neil MJ, Heckelman PE, Dobbelaar PH, Roman KJ (eds). The Merck Index, An Encyclopedia of Chemicals, Drugs, and Biologicals, 15th Ed. Cambridge, UK: The Royal Society of Chemistry, 2013.

  • Traditional medicine used by the Mazatec people of Oaxaca, Mexico. /Salvinorins/

    Use Classification

    Hazardous Substances Data Bank (HSDB)O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1554

  • In traditional medicine, the leaves are used for divination and for treatment of anemia and excretory functions.

    Use Classification

    Hazardous Substances Data Bank (HSDB)O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1554

  • 2cited by the summary above

    Salvia divinorum has been used by the Mazatec Indians for its ritual divination and healing. The active constituent of Salvia divinorum has been identified as salvinorin A. Currently, neither Salvia divinorum nor any of its constituents, including salvinorin A, are controlled under the federal Controlled Substances Act (CSA). Neither Salvia divinorum nor its active constituent salvinorin A has an approved medical use in the U.S.; salvinorin A is a potent and selective kappa opioid receptor agonist.

    Use Classification

    Hazardous Substances Data Bank (HSDB)US DEA Office of Diversion Control. Salvia Divinorum and Salvinorin A. Available from, as of September 14, 2017: https://www.deadiversion.usdoj.gov/index.html

How it acts

  • Salvinorin A, the primary psychoactive derivative of the hallucinogenic herb Salvia divinorum, is a potent and highly selective kappa-opioid receptor (KOR) agonist. Several recent studies, however, have suggested endocannabinoid system mediation of some of its effects. This study represents a systematic examination of this hypothesis. Salvinorin A was isolated from S. divinorum and was evaluated in a battery of in vitro and in vivo procedures designed to detect cannabinoid activity, including CB(1) receptor radioligand and [(35)S]GTPgammaS binding, calcium flux assay, in vivo cannabinoid screening tests, and drug discrimination. Salvinorin A did not bind to nor activate CB(1) receptors. In v…

    Hazardous Substances Data Bank (HSDB)PMID 20354680Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3013230

  • Salvinorin A (SalA), a selective kappa-opioid receptor (KOR) agonist, produces dysphoria and pro-depressant like effects. These actions have been attributed to inhibition of striatal dopamine release. The dopamine transporter (DAT) regulates dopamine transmission via uptake of released neurotransmitter. KORs are apposed to DAT in dopamine nerve terminals suggesting an additional target by which SalA modulates dopamine transmission. SalA produced a concentration-dependent, nor-binaltorphimine (BNI)- and pertussis toxin-sensitive increase of ASP(+) accumulation in EM4 cells coexpressing myc-KOR and YFP-DAT, using live cell imaging and the fluorescent monoamine transporter substrate, trans 4-(4…

    Hazardous Substances Data Bank (HSDB)PMID 25107591Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4188751

Behavior carries the pharmacological classes and the acute-effect durations, with plasma half-life kept separate from duration of effect.

In the body

  • 6cited by the summary above

    Salvinorin A (SA) is a highly selective kappa opioid receptor agonist and the putative psychoactive compound in Salvia divinorum (SD), an increasingly abused hallucinogenic plant. The objectives of this study were to characterize the physiological and subjective effects of SA versus placebo and measure drug and metabolite levels. Sublingual SA doses up to 4 mg were administered in dimethyl sulfoxide/polyethylene glycol 400 solution to eight SD-experienced subjects using a placebo-controlled ascending-dose design. No dose of SA produced significantly greater physiological or subjective effects than placebo. Furthermore, effects did not resemble reported "typical" effects of smoked SD. SA was…

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)PMID 21140258Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3063546

  • 5cited by the summary above

    Salvinorin A is a kappa opioid agonist and the principal psychoactive constituent of the Salvia divinorum plant, which has been used for hallucinogenic effects. Previous research on salvinorin A pharmacokinetics likely underestimated plasma levels typically resulting from the doses administered due to inefficient vaporization and not collecting samples during peak drug effects. Six healthy adults inhaled a single high dose of vaporized salvinorin A (n = 4, 21 ug/kg; n = 2, 18 ug/kg). Participant- and monitor-rated effects were assessed every 2 min for 60 min post-inhalation. Blood samples were collected at 13 time points up to 90 min post-inhalation. Drug levels peaked at 2 min and then rapi…

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)PMID 26880225Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5289219

  • 4cited by the summary above

    The diterpene salvinorin A from Salvia divinorum (Epling and Jativa-M), in doses of 200-500 ug produces effects which are subjectively identical to those experienced when the whole herb is ingested. Salvinorin A is effectively deactivated by the gastrointestinal system, so alternative routes of absorption must be used to maintain its activity. Traditionally the herb is consumed either by chewing the fresh leaves or by drinking the juices of freshly crushed leaves. The effects of the herb when consumed this way depend on absorption of salvinorin A through the oral mucosa before the herb is swallowed.

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)PMID 7526076Siebert DJ; J Ethnopharmacol 43 (1): 53-6 (1994)

  • Salvinorin A’s chemical structure suggests that it may be a substrate of CYP450 (oxidative metabolism), UGT (hydrolysis) or carboxylesterases (ChEs) (hydrolysis). In addition, as observed for CYP1A1, CPY2C18 and CYP2E1, Salvinorin A metabolism via UGTB27 appears to be saturable at higher concentrations.

    Metabolism/Metabolites

    Toxin and Toxin Target Database (T3DB)

History, discovery and cultural use

Written by this site · every claim referenced

Salvinorin A is the principal psychoactive constituent of Salvia divinorum, a Mexican plant with a long history of use as an entheogen by Mazatec shamans 1. The plant has been used by the Mazatec for ritual divination and healing, and salvinorin A was subsequently identified as the active constituent 2.

  1. 1Toxin and Toxin Target Database (T3DB), via PubChem
  2. 2Hazardous Substances Data Bank (HSDB), via PubChem

Ref 1 is the T3DB description and ref 2 the HSDB use-class passage, both held in this archive. Nothing above is quoted from Salvinorin A’s own database records; those appear as quotations elsewhere on this plate.

Histories of this field

Scholarship on psychedelics generally, not on Salvinorin A specifically. Whether any of these treats this compound is a question for the book, not for this page.

  • Mescaline: A Global History of the First Psychedelic

    Traces mescaline and the peyote and San Pedro cacti from pre-Columbian ritual use through nineteenth-century chemistry to twentieth-century psychiatry and the counterculture.

    Jay M. Mescaline: A Global History of the First Psychedelic. Yale University Press, New Haven and London; 2019. ISBN 9780300231076.

  • Expanding Mindscapes: A Global History of Psychedelicsopen access

    Essays on the international and cross-cultural history of psychedelic science, deliberately decentring the standard North American and European account.

    Dyck E, Elcock C, editors. Expanding Mindscapes: A Global History of Psychedelics. The MIT Press, Cambridge MA; 2023. ISBN 9780262546935 (paper), 9780262376891 (open access). doi:10.7551/mitpress/14417.001.0001.

  • Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers

    Botany, ethnography and chemistry of the principal hallucinogenic plants, by the founder of modern ethnobotany and the chemist who first synthesized LSD.

    Schultes RE, Hofmann A, Rätsch C. Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers. 2nd ed. Healing Arts Press, Rochester VT; 2001. ISBN 9780892819799.

  • Psychonauts: Drugs and the Making of the Modern Mind

    The tradition of scientific self-experimentation with psychoactive drugs, and its part in the emergence of psychology and of modernism.

    Jay M. Psychonauts: Drugs and the Making of the Modern Mind. Yale University Press, New Haven; 2023. ISBN 9780300257946.

  • Ancient Psychoactive Substances

    Archaeological and bioarchaeological evidence for psychoactive plant use across the ancient world.

    Fitzpatrick SM, editor. Ancient Psychoactive Substances. University Press of Florida, Gainesville; 2018. ISBN 9780813056708.

  • History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders

    A chapter tracing psychedelic and entactogen research from earlier ritual use through the mid-century research period to current clinical trials.

    Stroud C, Posey Norris SM, Matney C, editors. History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders. In: Exploring Psychedelics and Entactogens as Treatments for Psychiatric Disorders: Proceedings of a Workshop. National Academies Press, Washington DC; 2022. NBK587225.

    Workshop proceedings record what participants said; they are not a consensus statement of the National Academies.

  • Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions

    Peer-reviewed review covering the isolation, synthesis, pharmacology and ritual use of peyote and mescaline.

    Dinis-Oliveira RJ, Pereira CL, da Silva DD. Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions. Current Molecular Pharmacology 12(3):184–194; 2019. doi:10.2174/1874467211666181010154139.

Institutional archives

  • Heffter Research Institute Funds and coordinates clinical research on psilocybin, and keeps records of the studies it has supported since 1993. Sponsors the research it archives.
  • Multidisciplinary Association for Psychedelic Studies (MAPS) Sponsors clinical research, chiefly on MDMA-assisted therapy, and publishes an archive of historical and contemporary documents. A sponsor and an advocacy organization, not a disinterested archive; its clinical programme has a commercial arm.

The rest of this dossier

  • Affinity — 32 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — 7 published passages, plus any assay in this archive bearing on toxicity.
  • Legal — no DEA record is held here — which is not a finding that this compound is uncontrolled.
  • Systems — where this compound’s targets are transcribed, by brain region and tissue.

Passages via PubChem descriptive sections, aggregating DrugBank, LiverTox, FDA, DEA, HSDB, EPA. Each is quoted whole and attributed to the database that published it. The only prose written here about Salvinorin A is the history note, which says so on its face and carries a reference for every claim in it.

II · Identity

Structure and descriptors

Descriptors are computed here with RDKit from the structure PubChem returns — not from the archive's stored copy, so an edited local structure cannot reach this table.

2D structural depiction of Salvinorin A
Depiction served by PubChem for CID 128563. Not redrawn here, so the picture and the identity come from the same record.
Formula
C23H28O8R
Molecular weight
432.47g/molR
Exact mass
432.1784DaR
cLogP
3.00R
TPSA
109.1ŲR
H-bond donors
0R
H-bond acceptors
8R
Rotatable bonds
3R
Aromatic rings
1R
Heavy atoms
31R
Fraction sp³
0.652R
Formal charge
0R

Computed with RDKit 2025.09.2 from the SMILES returned by PubChem. Audit run 26/09/2026.

Bemis–Murcko scaffold

O=C1CCCC2CC[C@H]3C(=O)O[C@H](c4ccoc4)CC3[C@@H]12

Shared with Salvinorin B. All families

III · Behavior

Behavioral summary

Class, mechanism, and the duration of acute effects — each quoted from the record or trial that publishes it. Duration of effects and plasma half-life are shown separately, because they are different quantities and diverge by a factor of three or four.

Classification

Duration of acute subjective effects

—

No controlled human trial reporting a duration for this compound is cited here. The archive does hold onset and duration ranges for it, inherited from an earlier build, but their source column is empty and so they cannot be shown. A duration is not inferred from a chemical relative.

Plasma elimination half-life

How fast the body clears the drug — not how long the effects last. The two diverge sharply: LSD is cleared with a half-life of about 2.6 h while its subjective effects run 8–12 h.

~8 min

“In addition, the unique pharmacokinetics of salvinorin A (half-life ~8 min in non-human primates) allowed us to study the residual impact on KOR after the drug had eliminated from the brain”
non-human primatesPlaczek MS et al., Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2015. PMID 26058662

Primary pharmacological drivers

ChEMBL holds no curated mechanism-of-action record for this compound. The measured affinities below are the evidence this archive has for what it binds.

Mechanism, as published

Quoted verbatim from the database named after each passage, never summarized.

  • Salvinorin A, the primary psychoactive derivative of the hallucinogenic herb Salvia divinorum, is a potent and highly selective kappa-opioid receptor (KOR) agonist. Several recent studies, however, have suggested endocannabinoid system mediation of some of its effects. This study represents a systematic examination of this hypothesis. Sal…
    Hazardous Substances Data Bank (HSDB)PMID 20354680Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3013230
  • Salvinorin A (SalA), a selective kappa-opioid receptor (KOR) agonist, produces dysphoria and pro-depressant like effects. These actions have been attributed to inhibition of striatal dopamine release. The dopamine transporter (DAT) regulates dopamine transmission via uptake of released neurotransmitter. KORs are apposed to DAT in dopamine…
    Hazardous Substances Data Bank (HSDB)PMID 25107591Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4188751

IV · Clinical

Clinical description

Where this compound's substance class sits in ICD-11 and DSM-5-TR, and how much of the recorded literature speaks to each domain of a mental status examination.

Filed under Hallucinogens

  • 6C49Disorders due to use of hallucinogens

Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR): Hallucinogen-Related Disorders. Category names only — the manual is in copyright and no diagnostic criterion is reproduced here.

How much has been written about each domain

The clinical domains, and how many of the records this archive holds for this compound say something under each. What the terms mean, and the word list behind every spoke, are set out in the method.

Affect0Mood2Perception6Cognition1Thought process0Thought content0Psychomotor activity0Insight and judgment0
This measures the literature, not the compound. Each spoke counts how many of the 11 records this archive holds for this compound say something under that domain — 6 at the widest ring. A long spoke means the subject has been written about, not that the effect is strong, and a spoke at the center means nothing here discusses it rather than that nothing happens. The terms behind each domain are listed in the method.
Mood 2
matched on “dysphoria” · in PMID 25107591; Toxicology: Hazardous Substances Data Bank (HSDB)
Perception 6
matched on “hallucinogen” · in PMID 20354680; Toxicology: Toxin and Toxin Target Database (T3DB); PMID 26880225; PMID 25691501; PMID 21131142; PMID 23135605
Cognition 1
matched on “concentrat” · in PMID 25107591

V · Systems

Systems physiology

Where the targets this compound binds are transcribed — brain regions on the left, peripheral and autonomic tissues on the right. A join of two measurements, not a claim about what the compound does to either.

Brain

cerebral cortex — 2.7 nTPM, from OPRD1, OPRK1, OPRM1cerebellum — 4.4 nTPM, from OPRM1, OPRK1hippocampal formation — 0.9 nTPM, from OPRD1, OPRK1, OPRM1amygdala — 1.9 nTPM, from OPRK1, OPRD1, OPRM1hypothalamus — 2.6 nTPM, from OPRK1, OPRM1, OPRD1thalamus — no resolved target expressed herebasal ganglia — 3.8 nTPM, from OPRK1, OPRD1, OPRM1medulla oblongata — no resolved target expressed here

basal ganglia: drawn as the caudate nucleus, putamen and globus pallidus.

Measured but not drawn — this anatomogram has no outline for them: retina 0.9, midbrain 0.6, pituitary gland 0.3, spinal cord 0.2.

Body

heart — 0.1 nTPM, from OPRK1, OPRM1smooth muscle — 0.2 nTPM, from OPRM1lung — 0.2 nTPM, from OPRM1, OPRK1, OPRD1liver — 0.2 nTPM, from OPRM1kidney — 0.2 nTPM, from OPRM1stomach — 0.3 nTPM, from OPRM1, OPRD1duodenum — 0.2 nTPM, from OPRM1, OPRD1small intestine — 0.2 nTPM, from OPRM1, OPRD1colon — 0.2 nTPM, from OPRD1, OPRM1adrenal gland — 0.8 nTPM, from OPRM1, OPRD1thyroid gland — 0.4 nTPM, from OPRM1, OPRK1, OPRD1pancreas — 0.2 nTPM, from OPRD1, OPRM1urinary bladder — 0.1 nTPM, from OPRM1skeletal muscle — 1.0 nTPM, from OPRK1, OPRD1, OPRM1spleen — 0.4 nTPM, from OPRM1, OPRD1salivary gland — 0.3 nTPM, from OPRM1, OPRD1
04 nTPM

Square-root ramp · shared scale across both plates

Shading is transcript level — not affinity, and not affinity combined with expression. Outlined but unshaded organs hold none of this compound’s resolved targets above the atlas’s detection threshold. Anatomy from EMBL-EBI Anatomogram (Apache License 2.0); regions identified by Uberon (uberon.org), CC BY 3.0.

Brain regions

Regions where this compound's measured targets are transcribed. Linked from the plate above.

  1. cerebellum

    4.4 nTPM

  2. basal ganglia

    3.8 nTPM

  3. cerebral cortex

    2.7 nTPM

  4. hypothalamus

    2.6 nTPM

  5. amygdala

    1.9 nTPM

  6. hippocampal formation

    0.9 nTPM

  7. retina

    0.9 nTPM

  8. midbrain

    0.6 nTPM

  9. pituitary gland

    0.3 nTPM

  10. spinal cord

    0.2 nTPM

Peripheral & autonomic

Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.

  1. skeletal muscle

    1.0 nTPM

  2. adrenal gland

    0.8 nTPM

  3. thyroid gland

    0.4 nTPM

  4. spleen

    0.4 nTPM

  5. salivary gland

    0.3 nTPM

  6. stomach 1

    0.3 nTPM

  7. lung

    0.2 nTPM

  8. colon

    0.2 nTPM

  9. pancreas

    0.2 nTPM

  10. duodenum

    0.2 nTPM

  11. small intestine

    0.2 nTPM

  12. smooth muscle

    0.2 nTPM

  13. liver

    0.2 nTPM

  14. kidney

    0.2 nTPM

  15. heart muscle

    0.1 nTPM

  16. urinary bladder

    0.1 nTPM

Each row joins two published measurements and nothing else: the affinity this archive holds for the compound at that target, and the transcript level the Human Protein Atlas reports for that target’s gene in that region. Bars scale with expression only. Expression is not activation — a receptor transcribed in a region is a receptor available to be bound there, which is a weaker and more defensible claim than saying the region is affected.

Expression data from Human Protein Atlas (CC BY-SA 3.0), RNA expression, nTPM (normalized transcripts per million), consensus tissue dataset. Uhlén M, et al. Tissue-based map of the human proteome. Science. 2015;347(6220):1260419.

VI · Profile

Affinity rosette

The strongest measurement at each of 3 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.

KOR — Ki 9.12 pXDOR — Ki 5.30 pXMOR — Ki 5.30 pXKORDORMOR579
Fig. Radius is pX = −log₁₀(value in M), that is 9 − log₁₀(value in nM), computed from the normalized measurement. Hatched wedges are equilibrium binding constants (Ki, Kd); dashed outlines are functional readouts (IC₅₀, EC₅₀, AC₅₀, potency), which answer a different question and are not pooled with them. Rings mark whole pX units from 5 to 10, labeled every second ring in the gutter at the top. Where a target carries several measurements, the strongest is drawn.

VII · Toxicology

Toxicological profile

What has been measured, and what has been published — kept apart, and neither scored. There is no risk rating on this page; the archive once carried one, identical for every compound, produced by a stub.

Measured in this archive

Assays that bear on toxicity, drawn from the same ChEMBL records as everything else on this page. They are measurements of what a compound binds or does to cells — not verdicts about what it does to a person.

No hERG, cytochrome, cytotoxicity or transport measurement exists for Salvinorin A in this archive.

As published

Quoted verbatim from the database named after each passage, never summarized — a summary of a toxicology statement is a new claim.

Toxicity Summary

  • IDENTIFICATION AND USE: Salvinorin A forms colorless crystals or white powder. It is a traditional medicine used by the Mazatec people of Oaxaca, Mexico. In traditional medicine, the leaves are used for divination and for treatment of anemia and excretory functions. Currently, neither Salvia divinorum nor any of its constituents, including salvinorin A, are controlled under the federal Controlled Substances Act (CSA)…

    Hazardous Substances Data Bank (HSDB)

  • Salvinorin A, the active component of the hallucinogenic sage Salvia divinorum, is an apparently selective and highly potent kappa-opioid receptor (KOR) agonist. Salvinorin A is unique among ligands for peptidergic G protein-coupled receptors in being nonnitrogenous and lipid-like in character (A647).

    Toxin and Toxin Target Database (T3DB)

Human Toxicity Excerpts

  • /HUMAN EXPOSURE STUDIES/ Salvinorin A is a kappa opioid agonist and the principal psychoactive constituent of the Salvia divinorum plant, which has been used for hallucinogenic effects. Previous research on salvinorin A pharmacokinetics likely underestimated plasma levels typically resulting from the doses administered due to inefficient vaporization and not collecting samples during peak drug effects. Six healthy ad…

    Hazardous Substances Data Bank (HSDB)PMID 26880225Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5289219

  • /HUMAN EXPOSURE STUDIES/ This study examined the overall psychological effects of inebriation facilitated by the naturally-occurring plant hallucinogen Salvia divinorum using a double-blind, randomized, placebo-controlled trial. Thirty healthy individuals self-administered Salvia divinorum via combustion and inhalation in a quiet, comfortable research setting. Experimental sessions, post-session interviews, and 8-wee…

    Hazardous Substances Data Bank (HSDB)PMID 25691501Addy PH et al; J Psychopharmacol 29 (4): 426-35 (2015)

  • /HUMAN EXPOSURE STUDIES/ Salvinorin A is a potent, selective nonnitrogenous kappa opioid agonist and the known psychoactive constituent of Salvia divinorum, a member of the mint family that has been used for centuries by Mazatec shamans of Mexico for divination and spiritual healing. S. divinorum has over the last several years gained increased popularity as a recreational drug. This is a double-blind, placebo contro…

    Hazardous Substances Data Bank (HSDB)PMID 21131142Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3089685

  • /HUMAN EXPOSURE STUDIES/Salvinorin A is a kappa opioid agonist and the principal psychoactive constituent of the plant Salvia divinorum, which has increased in popularity as a recreational drug over the past decade. Few human studies have examined salvinorin A. This double-blind, placebo-controlled study evaluated the dose-related effects of inhaled salvinorin A in individuals with histories of hallucinogen use. Eigh…

    Hazardous Substances Data Bank (HSDB)PMID 23135605Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3581702

  • For more Human Toxicity Excerpts (Complete) data for Salvinorin A (19 total), please visit the HSDB record page.

    Hazardous Substances Data Bank (HSDB)

Published passages via PubChem toxicology sections, aggregating Hazardous Substances Data Bank (HSDB), RTECS, LiverTox. No figure on this page is scored, ranked or combined into a risk level.

VIII · Evidence

Every measurement

One row per published value. The identifier in the last column resolves to the ChEMBL assay record it was read from.

Equilibrium binding constants 28

Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.

TargetClassTypeValue (nM)pXOrganismAssay
KOROpioid receptorsKi0.7509.12Rattus norvegicusCHEMBL887466
KOROpioid receptorsKi0.7509.12HUMANPMID 17303418
KOROpioid receptorsKi0.8009.10UNDEFINEDPMID 19683449
KOROpioid receptorsKi1.908.72Homo sapiensCHEMBL1168405
KOROpioid receptorsKi1.908.72Homo sapiensCHEMBL839506
KOROpioid receptorsKi1.908.72Homo sapiensCHEMBL968095
KOROpioid receptorsKi2.668.58Homo sapiensCHEMBL5578249
KOROpioid receptorsKi2.908.54HUMANPMID 25193297
KOROpioid receptorsKi3.168.50Homo sapiensCHEMBL3106112
KOROpioid receptorsKi3.208.49Homo sapiensCHEMBL3106112
KOROpioid receptorsKi4.008.40RATPMID 15658846
KOROpioid receptorsKi4.008.40Homo sapiensCHEMBL5360970
KOROpioid receptorsKi4.308.37HUMANPMID 20126400
KOROpioid receptorsKi4.308.37GUINEA PIGPMID 12192085
KOROpioid receptorsKi4.608.34HUMANPMID 15383632
KOROpioid receptorsKi6.208.21Homo sapiensCHEMBL2383888
KOROpioid receptorsKi7.408.13Homo sapiensCHEMBL1775888
KOROpioid receptorsKi7.908.10HUMANPMID 15383632
KOROpioid receptorsKi16.007.80UNDEFINEDPMID 12192085
KOROpioid receptorsKi18.407.74Rattus norvegicusCHEMBL887466
KOROpioid receptorsKi31.607.50HUMANPMID 15952771
KOROpioid receptorsKi38.007.42Homo sapiensCHEMBL839506
KOROpioid receptorsKi40.007.40Homo sapiensCHEMBL5360986
KOROpioid receptorsKi45.807.34HUMANPMID 15952771
DOROpioid receptorsKi5,0005.30RATPMID 12192085
MOROpioid receptorsKi5,0005.30RATPMID 12192085
DOROpioid receptorsKi5,7905.24Homo sapiensCHEMBL839505
DOROpioid receptorsKi5,7905.24Homo sapiensCHEMBL968094

Functional readouts 4

IC₅₀, EC₅₀, AC₅₀ and potency. Assay-dependent, and not interchangeable with a binding constant.

TargetClassTypeValue (nM)pXOrganismAssay
KOROpioid receptorsEC502.208.66Homo sapiensCHEMBL5360971
KOROpioid receptorsEC5010.008.00Homo sapiensCHEMBL4371517
KOROpioid receptorsEC5011.807.93Homo sapiensCHEMBL5578253
KOROpioid receptorsEC5040.007.40Homo sapiensCHEMBL3381495
P
PubChem
C
ChEMBL
R
Computed here with RDKit
D
Derived here from the stored measurement

IX · Trials

Registered clinical trials

Studies filed with ClinicalTrials.gov that name this compound as an intervention. A registered trial is a protocol, not a result — status and enrollment are printed beside every row, and withdrawn studies are counted rather than hidden.

4T

Registered studies

0T

Open or ongoing

4T

With a phase recorded

By phase

A study may carry two phase codes at once, so these count studies bearing each phase and do not sum to the total.

  • Early phase 11
  • Phase 12
  • Phase 21
  • Not applicable1

By status

The registry’s own status for each record. Withdrawn and terminated studies are counted here rather than hidden — a stopped trial is part of what is known.

  • Completed4

Every matched study

Newest first by start date. Each identifier opens the registry record it came from; the title is the sponsor’s own, quoted.

  • NCT03418714Completed · Phase 1 / Phase 2

    Effects of Salvinorin A on Brain Function

    Enrollment
    13Tactual
    Started
    2017-12-14
    Sponsor
    Johns Hopkins University

    Conditions Drug Effect

    Matched “Salvinorin A” in the study’s intervention “Salvinorin A”

  • NCT01149824Completed · Not applicable

    Placebo Controlled Study of Sublingual Salvinorin A

    Enrollment
    8Tactual
    Started
    2009-06
    Sponsor
    California Pacific Medical Center Research Institute

    Conditions Pharmaceutical Preparations

    Matched “Salvinorin A” in the study’s intervention “Salvinorin A”

  • NCT00700596Completed · Early phase 1

    Effects of Salvinorin A in Healthy Controls

    Enrollment
    105Tactual
    Started
    2009-02-12
    Sponsor
    Yale University

    Conditions Healthy

    Matched “Salvinorin A” in the study’s intervention “Salvinorin A”

  • NCT00996411Completed · Phase 1

    Human Psychopharmacology of Salvinorin A

    Enrollment
    14Testimated
    Started
    2008-11
    Sponsor
    Johns Hopkins University

    Conditions Healthy

    Matched “Salvinorin A” in the study’s intervention “Salvinorin A”

Records from ClinicalTrials.gov (U.S. National Library of Medicine, NIH), API v2. A study is listed against a compound only when a verified name for that compound appears as a whole word in one of the study's own intervention names. A short code must appear as written, and a name the registry uses for something else (Aleph, a vaccine maker) is not matched. Title matches are not accepted. The matched name and the intervention text it matched are shown with every row.

Searched as Salvinorin A · Divinorin A · Salvinorin. Run this search at the registry — it returns the unfiltered result, including studies this page rejected as belonging to a different molecule.

A registered trial is a protocol somebody filed with the registry. It is not a result, and nothing on this plate says whether Salvinorin A worked.

XI · Literature

Sources behind this dossier

The papers this compound's values were read from, ranked by what each contributed. Not a review of the field.

Every paper below is one some value on this page came from — a binding constant, a passage of pharmacology or toxicology, or a measured duration. Each entry says what this archive took from it. Nothing else is claimed about any of them: the title is the study’s own account of itself, and a summary written here would be an assertion with no source behind it.

  1. 01

    Salvinorin A: a potent naturally occurring nonnitrogenous kappa opioid selective agonist

    Roth BL, Baner K, Westkaemper R et al. · Proceedings of the National Academy of Sciences of the United States of America 2002

    • · 4 measurements at 3 targets (Ki), strongest KOR at 8.37 pX

    PMID 12192085

  2. 02

    Comparison of pharmacological activities of three distinct kappa ligands (Salvinorin A, TRK-820 and 3FLB) on kappa opioid receptors in vitro and their antipruritic and antinociceptive activities in vivo

    Wang Y, Tang K, Inan S et al. · The Journal of pharmacology and experimental therapeutics 2005

    • · 2 measurements at 1 target (Ki), strongest KOR at 8.34 pX

    PMID 15383632

  3. 03

    Identification of the molecular mechanisms by which the diterpenoid salvinorin A binds to kappa-opioid receptors

    Yan F, Mosier PD, Westkaemper RB et al. · Biochemistry 2005

    • · 2 measurements at 1 target (Ki), strongest KOR at 7.50 pX

    PMID 15952771

  4. 04

    Michael acceptor approach to the design of new salvinorin A-based high affinity ligands for the kappa-opioid receptor

    Polepally PR, Huben K, Vardy E et al. · European journal of medicinal chemistry 2014

    • · 1 measurement at 1 target (Ki), strongest KOR at 8.54 pX

    PMID 25193297

  5. 05

    Psychedelics and the human receptorome

    Ray TS · PloS one 2010

    • · 1 measurement at 1 target (Ki), strongest KOR at 8.37 pX

    PMID 20126400

  6. 06

    Synthesis and pharmacological evaluation of 6-naltrexamine analogs for alcohol cessation

    Ghirmai S, Azar MR, Cashman JR · Bioorganic & medicinal chemistry 2009

    • · 1 measurement at 1 target (Ki), strongest KOR at 9.10 pX

    PMID 19683449

  7. 07

    Convenient synthesis and in vitro pharmacological activity of 2-thioanalogs of salvinorins A and B

    Bikbulatov RV, Yan F, Roth BL et al. · Bioorganic & medicinal chemistry letters 2007

    • · 1 measurement at 1 target (Ki), strongest KOR at 9.12 pX

    PMID 17303418

  8. 08

    Studies toward the pharmacophore of salvinorin A, a potent kappa opioid receptor agonist

    Munro TA, Rizzacasa MA, Roth BL et al. · Journal of medicinal chemistry 2005

    • · 1 measurement at 1 target (Ki), strongest KOR at 8.40 pX

    PMID 15658846

  9. 09

    Time course of pharmacokinetic and hormonal effects of inhaled high-dose salvinorin A in humans

    Johnson MW, MacLean KA, Caspers MJ et al. · Journal of psychopharmacology (Oxford, England) 2016

    • · Human Toxicity Excerpts

    PMID 26880225

  10. 10

    Immediate and Persistent Effects of Salvinorin A on the Kappa Opioid Receptor in Rodents, Monitored In Vivo with PET

    Placzek MS, Van de Bittner GC, Wey HY et al. · Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2015

    • · Biological Half-Life
    • · Plasma elimination half-life

    PMID 26058662

  11. 11

    The subjective experience of acute, experimentally-induced Salvia divinorum inebriation

    Addy PH, Garcia-Romeu A, Metzger M et al. · Journal of psychopharmacology (Oxford, England) 2015

    • · Human Toxicity Excerpts

    PMID 25691501

  12. 12

    Salvinorin A regulates dopamine transporter function via a kappa opioid receptor and ERK1/2-dependent mechanism

    Kivell B, Uzelac Z, Sundaramurthy S et al. · Neuropharmacology 2014

    • · Mechanism of Action

    PMID 25107591

  13. 13

    Dose-related effects of salvinorin A in humans: dissociative, hallucinogenic, and memory effects

    MacLean KA, Johnson MW, Reissig CJ et al. · Psychopharmacology 2013

    • · Human Toxicity Excerpts

    PMID 23135605

  14. 14

    Human psychopharmacology and dose-effects of salvinorin A, a kappa opioid agonist hallucinogen present in the plant Salvia divinorum

    Johnson MW, MacLean KA, Reissig CJ et al. · Drug and alcohol dependence 2011

    • · Human Toxicity Excerpts

    PMID 21131142

  15. 15

    Kappa opioid mediation of cannabinoid effects of the potent hallucinogen, salvinorin A, in rodents

    Walentiny DM, Vann RE, Warner JA et al. · Psychopharmacology 2010

    • · Mechanism of Action

    PMID 20354680