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Research tools

AM-374

An irreversible FAAH inhibitor used in the laboratory: it raises anandamide.

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.

C₁₆H₃₃FO₂S

CID 3572

Family
ECS pharmacological toolEnzyme inhibitor
Molar mass
308.50 g/mol

Updated on

In plain terms

AM-374 is a laboratory molecule, made by chemists, absent from hemp and from any plant. It does not mimic cannabis: it blocks an enzyme, FAAH, that normally destroys anandamide, a cannabinoid the body produces itself. In animals, this blockade raises the level of anandamide in the brain; no study in humans was found.

Receptors and activity

Target network

FAAHInhibitorIC50 = 6.3 nM · ratrecombinant rat FAAH, coumarin ester substrate (fluorescence); 13 nM on rat brain FAAH with [14C]anandamide (ChEMBL, review by Tuo et al. 2017); irreversible inhibition
  • Blocks or inhibits
  • Binds or modulates

The lower the cited value, the closer the target sits to AM-374: 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-374.

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. FAAHInhibitorIC50 = 6.3 nM · rat70 out of 100

    Johnston et al., Bioorg Med Chem Lett 2012 (value from ChEMBL, document CHEMBL2169869) (new tab) · recombinant rat FAAH, coumarin ester substrate (fluorescence); 13 nM on rat brain FAAH with [14C]anandamide (ChEMBL, review by Tuo et al. 2017); irreversible inhibition

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

    CB1 affinity decreasing with the chain length of the fatty sulfonyl fluorides (C12: IC50 18 nM; C20: 78 µM); C14, C16 and C18 selective for the amidase; value specific to AM-374 not taken from the abstract (Deutsch et al. 1997)

  3. DAGLα (humaine)Inhibitorno measured value cited

    94% inhibition at 10 µM (value from ChEMBL, Johnston et al. 2012)

  4. MAGL (humaine)Inhibitorno measured value cited

    82% inhibition at 10 µM (value from ChEMBL, Johnston et al. 2012)

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-374, or palmitylsulfonyl fluoride, is an irreversible inhibitor of FAAH, the enzyme that hydrolyses anandamide into arachidonic acid and ethanolamine. Described in 1997 by the team of Deutsch and Makriyannis, it proved about twenty times more potent than PMSF at preventing the breakdown of anandamide in brain homogenates, and more than a thousand times more effective than PMSF in cultured cells (Deutsch et al. 1997). Its mode of action is indirect: in rat hippocampal slices, at 0.1 µM, it allowed anandamide to inhibit acetylcholine release (Gifford et al. 1999); injected into the ventricles, it did not alone change lever-pressing behaviour in rats, but strengthened the effect of a low dose of anandamide (Arizzi et al. 2004). In rats, given intraperitoneally, it crosses the blood-brain barrier, durably raises anandamide in several brain regions, activates the ERK/MAPK pathway and reduced seizures and damage induced by kainic acid (Karanian et al. 2007); combined with AM404, it produced a neuroprotection blocked by a selective CB1 antagonist (Karanian et al. 2005). Two limits must be stated: the molecule also binds CB1 receptors depending on chain length, and its sulfonyl fluoride function exposes it to off-target reactions on other serine hydrolases, which is why more selective analogues were developed (Alapafuja et al. 2012). No study in humans was found.

Key sources.

History

Source
An entirely synthetic molecule. AM-374 exists neither in hemp nor in any known living organism: it is a laboratory pharmacological tool of the AM series of codes, whose saturated sixteen-carbon fatty chain, like that of palmitic acid, ends in a sulfonyl fluoride group, the reactive part of the molecule.

Origin

Research tool

No biosynthetic pathway. AM-374 is produced by no plant or living organism: it is a synthetic compound of the long-chain alkyl sulfonyl fluoride class.

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. Gifford AN et al. Potentiation of the action of anandamide on hippocampal slices by the fatty acid amide hydrolase inhibitor, palmitylsulphonyl fluoride (AM 374). Eur J Pharmacol, 1999 (new tab)PMID 10556675
  3. Arizzi MN et al. Behavioral effects of inhibition of cannabinoid metabolism: the amidase inhibitor AM374 enhances the suppression of lever pressing produced by exogenously administered anandamide. Life Sci, 2004 (new tab)PMID 14672756
  4. Karanian DA et al. Dual modulation of endocannabinoid transport and fatty acid amide hydrolase protects against excitotoxicity. J Neurosci, 2005 (new tab)PMID 16120783
  5. Karanian DA et al. Endocannabinoid enhancement protects against kainic acid-induced seizures and associated brain damage. J Pharmacol Exp Ther, 2007 (new tab)PMID 17545313
  6. Alapafuja SO et al. Sulfonyl fluoride inhibitors of fatty acid amide hydrolase. J Med Chem, 2012 (new tab)PMID 23083016
  7. Johnston M et al. Assay and inhibition of diacylglycerol lipase activity. Bioorg Med Chem Lett, 2012 (new tab)PMID 22738638
  8. PubChem, AM-374, CID 3572 (identifiers and properties) (new tab)

Identifiers

Names

IUPAC name
hexadecane-1-sulfonyl fluoride
Other names
AM374 · AM 374 · palmitylsulfonyl fluoride · palmitylsulphonyl fluoride · PSF · hexadecanesulfonyl fluoride · hexadecyl sulfonyl fluoride · HDSF

Identifiers

Formula
C₁₆H₃₃FO₂S
PubChem CID
3572(new tab)
InChIKey
QIVFMUVBIHIZAM-UHFFFAOYSA-N
SMILES
CCCCCCCCCCCCCCCCS(=O)(=O)F

Machine-readable entry (JSON)

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