BAY 38-7271
A synthetic full CB1 and CB2 agonist, a neuroprotective candidate abandoned after a phase II trial.
Harm-reduction warning
No characterised human dose: animal / in vitro data only. Effect profile, safety margin and acute toxicity are not documented in human clinical practice. Extremely potent compound: severe effects, seizures and deaths reported in the literature.
C₂₀H₂₁F₃O₅S
CAS 212188-60-8
- Family
- Synthetic CB receptor agonistResearch ligand or medicine
- Molar mass
- 430.40 g/mol
Updated on
In plain terms
BAY 38-7271 is a laboratory molecule, developed by the pharmaceutical company Bayer (described in 2002) and entirely absent from hemp. It binds to the same receptors as THC and, in the rat, produces the same cannabinoid-type effects at markedly lower doses (about twenty times lower in a discrimination test). It was trialled in hospital in patients in a coma after head trauma, and no further development was then found: outside that medical setting, nobody knows what it produces in a waking person.
Receptors and activity
Target network
- Activates
The lower the cited value, the closer the target sits to BAY 38-7271: one ring per factor of 100. A target with no measured value stays on the edge.
Where these targets live
Where each target has been found in humans, according to the cited studies. The map shows the target, not an effect of BAY 38-7271.
CB1CB1 found in 7 regions of the body
- Basal gangliadenseMost dense in basal ganglia outflow nuclei1
- CerebellumdenseVery dense in the cerebellum1
- HippocampusdenseVery high concentrations in the hippocampus2
- AmygdaladenseHigh concentrations in the amygdala2
- CortexpresentPresent throughout the neocortex2
- Adipose tissuepresentExpressed in adipose tissue3
- GutpresentColonic epithelium, smooth muscle and plexus4
Map sources
- Herkenham M et al. Cannabinoid receptor localization in brain. Proc Natl Acad Sci U S A, 1990 (new tab)
- Glass M et al. Cannabinoid receptors in the human brain: a detailed anatomical and quantitative autoradiographic study in the fetal, neonatal and adult human brain. Neuroscience, 1997 (new tab)
- Engeli S et al. Activation of the peripheral endocannabinoid system in human obesity. Diabetes, 2005 (new tab)
- Wright K et al. Differential expression of cannabinoid receptors in the human colon: cannabinoids promote epithelial wound healing. Gastroenterology, 2005 (new tab)
Cited values
- CB1AgonistKi = 0.5 nM · rat/human89 out of 100
Mauler et al. 2002, J Pharmacol Exp Ther (new tab) · binding on rat brain membranes, human cortex or recombinant human CB1 (Ki of 0.46 to 1.85 nM depending on the preparation); agonist in [35S]GTPγS binding
- CB2AgonistKi = 4.3 nM · human73 out of 100
Brogi et al. 2011, Eur J Med Chem (new tab) · [3H]CP55,940 displacement, human CB2 (literature value taken from ChEMBL)
Pharmacology
BAY 38-7271 is an agonist at the CB1 and CB2 cannabinoid receptors, described as a full agonist, with no structural kinship to THC: it is a sulfonic ester of a diaryl ether, from a neuroprotection programme at Bayer AG. Its affinity for CB1 is nanomolar (Ki of 0.46 to 1.85 nM) and it was characterised as a CB1 agonist in [35S]GTPγS binding. In the rat, hypothermia (minimal effective dose of 6 µg/kg intravenously) and substitution for CP 55,940 in drug discrimination appear at amounts far lower than those of THC (ED50 of 0.018 mg/kg intraperitoneally against 0.34 mg/kg for THC in the discrimination test), and rimonabant abolishes them. In animal models of subdural haematoma and cerebral ischaemia, the molecule reduced infarct volume, intracranial pressure and oedema, with a therapeutic window of several hours. A phase II trial conducted in 97 comatose patients after severe head trauma reported better one-month survival than under placebo in both treated groups, an advantage no longer found at six months; no further development was found. Outside that hospital setting, human data are entirely lacking: no study describes the subjective effects, tolerance, dependence or toxicity of non-medical exposure.
Key sources.
- Mauler F et al., characterisation of BAY 38-7271 as a potent cannabinoid agonist with neuroprotective properties, J Pharmacol Exp Ther 2002;302:359-368 (new tab)PMID 12065738
- De Vry J, Jentzsch KR, discriminative effects of BAY 38-7271, Eur J Pharmacol 2002 (new tab)PMID 12464360
- Mauler F et al., neuroprotective efficacy and reduction of brain oedema by BAY 38-7271, Brain Research 2003 (new tab)PMID 14519516
- Mauler F et al., review of BAY 38-7271, pharmacology, toxicology and phase I, CNS Drug Reviews 2003;9:343-358 (new tab)PMID 14647528
- Firsching R et al., Early survival of comatose patients after severe traumatic brain injury with the dual cannabinoid CB1/CB2 receptor agonist KN38-7271: randomised placebo-controlled phase II trial (97 patients, 14 centres), J Neurol Surg A Cent Eur Neurosurg 2012 (new tab)PMID 22696266
- Brogi S et al., Eur J Med Chem 2011: Ki of BAY 38-7271 at human CB2 (4.3 nM, value curated in ChEMBL; full text not consulted) (new tab)PMID 21183257
- Peripheral analogues of BAY 59-3074, confirming the full agonism of BAY 38-7271 at CB1 and CB2 (PMC9457575) (new tab)
- PubChem, record of compound CID 9845561 (BAY 38-7271) (new tab)
- Légifrance, Annex IV of the order of 22 February 1990 setting the list of substances classified as narcotics (new tab)
History
- Source
- An entirely synthetic molecule: it exists neither in hemp nor in any living organism, and has never been isolated from a plant. It arose from a pharmaceutical programme devoted to neuroprotection after head trauma. No source consulted reports it on the recreational market.
Origin
Laboratory synthesis
No biosynthetic pathway leads to this molecule. It is obtained exclusively by chemical synthesis. No living organism produces it.
Legal framework
- European Union
At European Union level, the molecule has never been the subject of a risk assessment by the EUDA (formerly EMCDDA) or of a common control measure, unlike many synthetic agonists of the JWH, AM, MDMB or FUBINACA series. It is listed in no schedule of the 1961 and 1971 United Nations conventions. Its only regulated use in Europe was as an investigational medicinal product, in a multicentre clinical trial conducted in fourteen neurosurgical centres.
- France
In France, BAY 38-7271 (KN38-7271) is not named in the decree of 22 February 1990 setting the list of substances classified as narcotics. The molecule is neither an ester nor an ether of tetrahydrocannabinol: the generic clause covering “tetrahydrocannabinols, their esters, ethers, salts as well as the salts of the aforementioned derivatives” (in annex III since the decision of 6 February 2026) therefore does not capture it. Its skeleton, a sulfonic ester of a diaryl ether, likewise does not correspond to the generic families of synthetic cannabinoids described in that annex (notably indole or indazole methanones, indole or indazole carboxamides, naphthoylpyrroles, cyclohexylphenols). It is therefore unscheduled to date, which in no way makes it lawful for human use: it has no marketing authorisation, appears on no list of authorised food or cosmetic ingredients, and cannot be sold for consumption. The Director General of ANSM may add it to the list by decision, as has been done for a great many synthetic agonists.
Sources: EUR-Lex, UNODC, CND, ANSM, IUPHAR/BPS, ChEBI, EUDA. Our method.
Classification
Family, origin and source verification
- Family
Synthetic CB receptor agonist › Research ligand or medicine
- Class
non-classical (diaryl ether sulfonic ester, indane)
- Verification
Classification, sources and binding values checked on 20 October 2026; text read against its sources and Wikipedia.
- Wikipedia (English)
Article paired by the molecule's structure (InChIKey), revision read on 19 October 2026. Read as a second opinion, never cited as a source.
References
- Mauler F et al., characterisation of BAY 38-7271 as a potent cannabinoid agonist with neuroprotective properties, J Pharmacol Exp Ther 2002;302:359-368 (new tab)PMID 12065738
- De Vry J, Jentzsch KR, discriminative effects of BAY 38-7271, Eur J Pharmacol 2002 (new tab)PMID 12464360
- Mauler F et al., neuroprotective efficacy and reduction of brain oedema by BAY 38-7271, Brain Research 2003 (new tab)PMID 14519516
- Mauler F et al., review of BAY 38-7271, pharmacology, toxicology and phase I, CNS Drug Reviews 2003;9:343-358 (new tab)PMID 14647528
- Firsching R et al., Early survival of comatose patients after severe traumatic brain injury with the dual cannabinoid CB1/CB2 receptor agonist KN38-7271: randomised placebo-controlled phase II trial (97 patients, 14 centres), J Neurol Surg A Cent Eur Neurosurg 2012 (new tab)PMID 22696266
- Brogi S et al., Eur J Med Chem 2011: Ki of BAY 38-7271 at human CB2 (4.3 nM, value curated in ChEMBL; full text not consulted) (new tab)PMID 21183257
- Peripheral analogues of BAY 59-3074, confirming the full agonism of BAY 38-7271 at CB1 and CB2 (PMC9457575) (new tab)
- PubChem, record of compound CID 9845561 (BAY 38-7271) (new tab)
- Légifrance, Annex IV of the order of 22 February 1990 setting the list of substances classified as narcotics (new tab)
Identifiers
Names
- IUPAC name
- [3-[[(2R)-2-(hydroxymethyl)-2,3-dihydro-1H-inden-4-yl]oxy]phenyl] 4,4,4-trifluorobutane-1-sulfonate
- Other names
- KN38-7271 · KN 38-7271 · BAY-38-7271 · KN-387271 · 3-(2-hydroxymethylindanyl-4-oxy)phenyl-4,4,4-trifluoro-1-sulfonate
Identifiers
- Formula
- C₂₀H₂₁F₃O₅S
- CAS
- 212188-60-8
- PubChem CID
- 9845561(new tab)
- InChIKey
- XJURALZPEJKKOV-CQSZACIVSA-N
- SMILES
- C1[C@H]
(CC2= C1C= CC= C2OC3= CC(= CC= C3) OS(= O) (= O) CCCC(F) (F) F) CO
LLM ingestion format: a structured superset of the entry (identifiers, binding, versioned legal status). Full corpus.