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AM-381

A covalent FAAH inhibitor, a laboratory molecule with no human data found.

Unscheduled
Level of detail

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.

C₁₈H₃₇FO₂S

CID 10131877

Family
ECS pharmacological toolEnzyme inhibitor
Molar mass
336.60 g/mol

Updated on

In plain terms

AM-381 is a laboratory molecule, not a hemp component. It is used to block the enzyme that destroys anandamide, a substance the body makes itself and that binds to the same receptors as THC. No study in humans was found.

Receptors and activity

Target network

FAAH (fatty acid amide hydrolase)InhibitorIC50 = 4 nM · not specified (ChEMBL: human)irreversible FAAH inhibition, value reported by a review (Lambert and Fowler 2005) from ChEMBL; Deutsch 1997: nanomolar IC50 values for the C12-C18 series
  • Blocks or inhibits
  • Binds or modulates

The lower the cited value, the closer the target sits to AM-381: 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 AM-381.

Brain, side view
Body, front view
Blood

FAAHFAAH found in 7 regions of the body

  1. CortexpresentCortical pyramidal neurons1
  2. Basal gangliapresentStriatal neurons1
  3. HypothalamuspresentPresent in hypothalamic nuclei1
  4. CerebellumpresentPurkinje cells and cerebellar layers1
  5. BrainstempresentInferior olivary nuclei1
  6. Adipose tissuepresentExpressed in mature adipocytes2
  7. BonepresentPresent on osteoclasts3

Map sources

  1. Romero J et al. Fatty acid amide hydrolase localization in the human central nervous system: an immunohistochemical study. Brain Res Mol Brain Res, 2002 (new tab)
  2. Engeli S et al. Activation of the peripheral endocannabinoid system in human obesity. Diabetes, 2005 (new tab)
  3. Rossi F et al. The endovanilloid/endocannabinoid system in human osteoclasts: possible involvement in bone formation and resorption. Bone, 2009 (new tab)

Cited values

  1. FAAH (fatty acid amide hydrolase)InhibitorIC50 = 4 nM · not specified (ChEMBL: human)73 out of 100

    Lambert and Fowler, J Med Chem 2005 (value from ChEMBL, document CHEMBL1140350) (new tab) · irreversible FAAH inhibition, value reported by a review (Lambert and Fowler 2005) from ChEMBL; Deutsch 1997: nanomolar IC50 values for the C12-C18 series

  2. CB1Binding (function not established)no measured value cited

    CB1 affinity decreasing with the chain length of the fatty sulfonyl fluorides; C14, C16 and C18 selective for the amidase; value specific to AM-381 not taken from the abstract (Deutsch et al. 1997)

Bar length follows the measured value (Ki, Kd, EC50 or IC50), on one scale shared by every entry, from 100 µM to 0.1 nM. A target with no cited value has no bar.

Pharmacology

AM-381, or stearylsulfonyl fluoride, belongs to the first generation of FAAH inhibitors developed in the late 1990s. In the series published in 1997, the C12 to C18 analogues inhibited anandamide amidase at nanomolar concentrations, and those at C14, C16 and C18, including the C18 one, proved clearly more selective for the enzyme than for the CB1 receptor (Deutsch et al. 1997). Sulfonyl fluorides are known esterase inhibitors, and their action on FAAH is covalent and irreversible for the later analogues of the series (Alapafuja et al. 2012). A 2005 review reports, for stearylsulfonyl fluoride, an IC50 of 4.0 nM at FAAH (irreversible inhibition), a value picked up by ChEMBL. No behavioural study, pharmacokinetic data or human data concerning AM-381 itself were found; the animal results often cited in this field concern the C16 analogue, AM-374. Selectivity against other serine hydrolases has not been characterised for this molecule.

Key sources.

History

Source
An entirely synthetic molecule. It exists neither in hemp nor in any known living organism: it is a reagent designed in the laboratory to block an enzyme (Deutsch et al. 1997).

Origin

Research tool

No biosynthetic pathway exists for this molecule: it is a synthetic compound of the alkanesulfonyl fluoride class with an octadecyl chain, whose sulfonyl fluoride function is the chemically reactive part.

Classification

Family, origin and source verification

Family

ECS pharmacological tool › Enzyme inhibitor

Verification

Classification, sources and binding values checked on 20 October 2026; text read against its sources and Wikipedia.

Wikipedia (English)

No dedicated article.

References

  1. Deutsch DG et al. Fatty acid sulfonyl fluorides inhibit anandamide metabolism and bind to the cannabinoid receptor. Biochem Biophys Res Commun, 1997 (new tab)PMID 9070252
  2. Alapafuja SO et al. Sulfonyl fluoride inhibitors of fatty acid amide hydrolase. J Med Chem, 2012 (new tab)PMID 23083016
  3. Lambert DM, Fowler CJ. The endocannabinoid system: drug targets, lead compounds, and potential therapeutic applications. J Med Chem, 2005 (new tab)PMID 16078824
  4. PubChem, Stearylsulfonyl fluoride (AM-381), CID 10131877 (identifiers and properties) (new tab)

Identifiers

Names

IUPAC name
octadecane-1-sulfonyl fluoride
Other names
Stearylsulfonyl fluoride · 1-Octadecanesulfonyl fluoride · Octadecanesulfonyl fluoride

Identifiers

Formula
C₁₈H₃₇FO₂S
PubChem CID
10131877(new tab)
InChIKey
SZXIBISKCHYMAR-UHFFFAOYSA-N
SMILES
CCCCCCCCCCCCCCCCCCS(=O)(=O)F

Machine-readable entry (JSON)

LLM ingestion format: a structured superset of the entry (identifiers, binding, versioned legal status). Full corpus.