HU-210
PubChem records this structure as HU 210.
Also known asA1H66
(6aR,10aR)-9-(hydroxymethyl)-6,6-dimethyl-3-(2-methyloctan-2-yl)-6a,7,10,10a-tetrahydrobenzo[c]chromen-1-ol
- PubChem CID
- 9821569
- ChEMBL
- CHEMBL41721
- Measurements
- 11
- InChIKey
- SSQJFGMEZBFMNV-WOJBJXKFSA-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.
— No descriptive record. PubChem holds no attributed passage about HU-210 under any heading this site reads, and ChEMBL curates no mechanism for it. That is the common case for the research chemicals in this archive: they have structures and binding measurements, and nobody has written a monograph. The measurements are still on the plates that follow.
History, discovery and cultural use
— Not in this archive. PubChem, ChEMBL and the Human Protein Atlas publish pharmacology, regulation and toxicology, and none of them publishes a heading for when HU-210 was first made, by whom, or how it has been used. That is a gap in the databases this site reads and not a gap in the literature — the history of these compounds is written, at length and under peer review, in the works below. This site does not summarize them; it says where they are. Where a published passage above happens to touch origin or traditional use, it appears inside the entry that carries it.
Histories of this field
Scholarship on psychedelics generally, not on HU-210 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.
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.
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 — 11 measurements in this archive, equilibrium constants kept apart from functional readouts.
- Toxicology — nothing published for HU-210. An absent record is an absence of study, not evidence of safety.
- 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 HU-210 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.
- Formula
- C25H38O3R
- Molecular weight
- 386.58g/molR
- Exact mass
- 386.2821DaR
- cLogP
- 6.22R
- TPSA
- 49.7ŲR
- H-bond donors
- 2R
- H-bond acceptors
- 3R
- Rotatable bonds
- 7R
- Aromatic rings
- 1R
- Heavy atoms
- 28R
- Fraction sp³
- 0.680R
- Formal charge
- 0R
Computed with RDKit 2025.09.2 from the SMILES returned by PubChem. Audit run 26/09/2026.
Bemis–Murcko scaffold
C1=CC[C@H]2c3ccccc3OC[C@@H]2C1
Shared with Delta-8-tetrahydrocannabinol. 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 holds no other record of one either. 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.
No half-life is published for this compound in the sources this site reads.
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.
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.
No diagnostic chapter is shown for this compound. Either PubChem records no MeSH pharmacological class for it, or the class it records is not one of the substance classes ICD-11 gives a chapter to. Inferring a chapter from the compound’s name or its binding profile would be a diagnosis this archive is in no position to make.
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.
None of the 0 records this archive holds for this compound uses a term from any of the clinical domains. That is a statement about the literature recorded here, not about the compound.
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
basal ganglia: drawn as the caudate nucleus, putamen and globus pallidus.
Measured but not drawn — this anatomogram has no outline for them: pituitary gland 17.3, midbrain 2.1, spinal cord 1.7, retina 1.1.
Body
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.
cerebral cortex
18.6 nTPM- CB1CNR19.7 pX18.6
cerebellum
18.3 nTPM- CB1CNR19.7 pX18.3
pituitary gland
17.3 nTPM- CB1CNR19.7 pX17.3
basal ganglia
15.1 nTPM- CB1CNR19.7 pX15.1
amygdala
13.3 nTPM- CB1CNR19.7 pX13.3
hippocampal formation
13.2 nTPM- CB1CNR19.7 pX13.2
hypothalamus
9.0 nTPM- CB1CNR19.7 pX9.0
midbrain
2.1 nTPM- CB1CNR19.7 pX2.1
spinal cord
1.7 nTPM- CB1CNR19.7 pX1.7
retina
1.1 nTPM
Peripheral & autonomic
Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.
colon
10.0 nTPMspleen
8.4 nTPMsmall intestine
8.1 nTPMadrenal gland
4.6 nTPM- CB1CNR19.7 pX4.6
thyroid gland
3.9 nTPMstomach 1
3.4 nTPMurinary bladder
3.4 nTPMlung
2.8 nTPMsmooth muscle
2.3 nTPM- CB1CNR19.7 pX2.3
skeletal muscle
1.8 nTPMsalivary gland
1.8 nTPMpancreas
1.2 nTPM- CB1CNR19.7 pX1.2
heart muscle
0.8 nTPM- CB1CNR19.7 pX0.8
duodenum
0.6 nTPMkidney
0.6 nTPM- CB1CNR19.7 pX0.6
liver
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.
1 of this compound’s targets could not be resolved to a gene and are absent from both columns: NMDA.
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.
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 HU-210 in this archive.
Published toxicology
— None. The toxicology databases this site reads — HSDB, RTECS and LiverTox, by way of PubChem — hold no record for HU-210. They index compounds that have been studied for decades, so most of this archive has no entry. An absent record is an absence of study, not evidence of safety.
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 10
Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.
| Target | Class | Type | Value (nM) | pX | Organism | Assay |
|---|---|---|---|---|---|---|
| CB2 | Cannabinoid receptors | Ki | 0.140 | 9.85 | HUMAN | PMID 12065738 |
| CB2 | Cannabinoid receptors | Ki | 0.150 | 9.82 | HUMAN | PMID 17942307 |
| CB1 | Cannabinoid receptors | Ki | 0.180 | 9.74 | HUMAN | PMID 17942307 |
| CB1 | Cannabinoid receptors | Ki | 0.410 | 9.39 | HUMAN | PMID 12065738 |
| CB1 | Cannabinoid receptors | Ki | 0.730 | 9.14 | RAT | PMID 11408610 |
| CB1 | Cannabinoid receptors | Ki | 1.50 | 8.82 | HUMAN | PMID 18511157 |
| CB1 | Cannabinoid receptors | Ki | 2.32 | 8.63 | Zebra Finch | PMID 11259544 |
| CB2 | Cannabinoid receptors | Ki | 4.10 | 8.39 | HUMAN | PMID 16392793 |
| CB2 | Cannabinoid receptors | Ki | 7.30 | 8.14 | HUMAN | PMID 16392793 |
| CB2 | Cannabinoid receptors | Ki | 150 | 6.82 | RAT | PMID 16279794 |
Functional readouts 1
IC₅₀, EC₅₀, AC₅₀ and potency. Assay-dependent, and not interchangeable with a binding constant.
| Target | Class | Type | Value (nM) | pX | Organism | Assay |
|---|---|---|---|---|---|---|
| NMDA | Glutamate receptors | IC50 | 10,000 | 5.00 | Rattus norvegicus | CHEMBL751628 |
- 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.
— No registered study names HU-210 as an intervention. That is an absence of registered research, not evidence about the compound. Most of this archive has never been the subject of a registered trial.
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 HU-210. Run this search at the registry.
A registered trial is a protocol somebody filed with the registry. It is not a result, and nothing on this plate says whether HU-210 worked.
X · Legal
Controlled-substance status
United States federal scheduling, read from the DEA records this archive holds. Not legal advice, and an absent record is not a finding that a compound is uncontrolled.
An absent DEA record is not a finding that HU-210 is legal. It means this archive holds no DEA passage for it. The Controlled Substances Analogue Enforcement Act reaches substances that appear on no schedule by name, and many compounds here are ring-substituted analogues of scheduled drugs. Nothing on this plate should be read as saying a compound may lawfully be made, held or supplied.
United States federal status only. State law differs, and so does the law of every other country — none of it is represented here. Scheduling changes, and this reflects the DEA records held by PubChem descriptive sections when the monograph was last harvested, not necessarily today. This is a record of what a database publishes, not legal advice.
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.
- 01
New 1,8-naphthyridine and quinoline derivatives as CB2 selective agonists
Manera C, Cascio MG, Benetti V et al. · Bioorganic & medicinal chemistry letters 2007
- · 2 measurements at 2 targets (Ki), strongest CB2 at 9.82 pX
- 02
Stern E, Muccioli GG, Millet R et al. · Journal of medicinal chemistry 2006
- · 2 measurements at 1 target (Ki), strongest CB2 at 8.39 pX
- 03
Mauler F, Mittendorf J, Horváth E et al. · The Journal of pharmacology and experimental therapeutics 2002
- · 2 measurements at 2 targets (Ki), strongest CB2 at 9.85 pX
- 04
Fan H, Kotsikorou E, Hoffman AF et al. · European journal of medicinal chemistry 2009
- · 1 measurement at 1 target (Ki), strongest CB1 at 8.82 pX
- 05
Design, synthesis, and binding studies of new potent ligands of cannabinoid receptors
Brizzi A, Brizzi V, Cascio MG et al. · Journal of medicinal chemistry 2005
- · 1 measurement at 1 target (Ki), strongest CB2 at 6.82 pX
- 06
Evidence for a new G protein-coupled cannabinoid receptor in mouse brain
Breivogel CS, Griffin G, Di Marzo V et al. · Molecular pharmacology 2001
- · 1 measurement at 1 target (Ki), strongest CB1 at 9.14 pX
- 07
Zebra finch CB1 cannabinoid receptor: pharmacology and in vivo and in vitro effects of activation
Soderstrom K, Johnson F · The Journal of pharmacology and experimental therapeutics 2001
- · 1 measurement at 1 target (Ki), strongest CB1 at 8.63 pX