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Research tools

AACOCF3Arachidonoyl trifluoromethyl ketone

Arachidonic acid analogue: inhibits cPLA2 and FAAH, binds CB1 (Ki 0.65 µM).

Unscheduled
Level of detail

C₂₁H₃₁F₃O

CAS 149301-79-1

Family
ECS pharmacological toolEnzyme inhibitor
Molar mass
356.50 g/mol

Updated on

In plain terms

AACOCF3 is a laboratory-made molecule modelled on a common fatty acid, arachidonic acid; it is absent from hemp and is not consumed. Researchers use it as a tool to slow two enzymes, including the one that destroys anandamide, a cannabinoid the body makes itself. It has been studied in rats; no study in humans was found.

Receptors and activity

Target network

FAAH (amidase de l'anandamide)InhibitorInhibition of anandamide hydrolysis close to 100% in vitro at 7.5 µM inhibitor; cellular anandamide content increased twelvefold at 12 µM in neuroblastoma cells; no IC50 in the abstract (Koutek et al. 1994)
  • Blocks or inhibits
  • Binds or modulates

The lower the cited value, the closer the target sits to AACOCF3: 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 AACOCF3.

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. cPLA2 (phospholipase A2 cytosolique de 85 kDa)Inhibitorno measured value cited

    Slow- and tight-binding inhibitor; upper limit of the dissociation constant of the Ca2+·AACOCF3·cPLA2 complex of 5 × 10⁻⁵ in mole fraction, with no value in nM in the abstract (Street et al. 1993)

  2. FAAH (amidase de l'anandamide)Inhibitorno measured value cited

    Inhibition of anandamide hydrolysis close to 100% in vitro at 7.5 µM inhibitor; cellular anandamide content increased twelvefold at 12 µM in neuroblastoma cells; no IC50 in the abstract (Koutek et al. 1994)

  3. iPLA2 (calcium-independent phospholipase A2)InhibitorIC50 = 15 µM · mouse14 out of 100

    Ackermann et al., J Biol Chem 1995 (new tab) · enzyme purified from the P388D1 macrophage line (0.028 in mole fraction); palmitoyl trifluoromethyl ketone about 4-fold more potent (3.8 µM)

  4. CB1Binding (function not established)Ki = 650 nM36 out of 100

    Koutek et al., J Biol Chem 1994 (new tab) · [3H]CP-55940 displacement (abstract: 0.65 µM); species and preparation not specified in the abstract; intrinsic efficacy not reported

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.

Measured effects

Not characterised. No placebo-controlled human trial has measured the effects of AACOCF3, so no level is shown.

Levels computed from placebo-controlled human trials: difference from placebo on 100, at the dose and route stated. Read the method

Pharmacology

AACOCF3 is an analogue of arachidonic acid in which the carboxylic acid group is replaced by a trifluoroacetyl group. Street and colleagues described it in 1993 as a slow- and tight-binding inhibitor of the 85-kDa human cytosolic phospholipase A2: inhibition is detectable at one inhibitor molecule per several thousand substrate molecules, whereas analogues in which the acid group is replaced by COCH3, CH(OH)CF3, CHO or CONH2 did not inhibit the enzyme. In 1994, Koutek and colleagues tested it among anandamide analogues designed as putative transition-state inhibitors: the trifluoromethyl ketones and α-keto esters inhibited anandamide hydrolysis almost completely in vitro at 7.5 µM, and AACOCF3 was the most effective in intact neuroblastoma cells (cellular anandamide raised 12-fold at 12 µM). It was also the only compound of the series to displace [3H]CP-55940 from CB1 (Ki 0.65 µM), the abstract reporting no intrinsic efficacy. It also inhibits the calcium-independent phospholipase A2 of murine macrophages (IC50 15 µM; Ackermann et al. 1995): this accumulation of targets limits the attribution of an observed effect to a single pathway. MAFP, described in 1997, was about 800 times more potent on anandamide amidase in rat brain homogenates, AACOCF3 being described as a reversible inhibitor (Deutsch et al. 1997). In rats, given intravenously 30 minutes after spinal cord compression (7.13 mg/kg), it increased the number of surviving neurons and oligodendrocytes at 7 days and improved the locomotor score (Huang et al. 2009); given by gavage 2 hours after cauda equina compression (7.5 mg/kg), it reduced cPLA2 phosphorylation and the levels of free fatty acids, lysophosphatidylcholine, PGE2 and LTB4, and improved locomotor function (Khan et al. 2015). These results are preclinical; no study in humans was found.

Key sources.

History

Source
An entirely synthetic molecule, an analogue of arachidonic acid; no natural occurrence was found in the sources consulted. No clinical development was found: it is known as a research tool, designated AACOCF3, ATK or Arach-CF3 depending on the authors.

Origin

Research tool

No known biosynthetic pathway: AACOCF3 is a synthetic compound of the class of trifluoromethyl ketones derived from arachidonic acid, not described in any living organism.

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)

Arachidonyl trifluoromethyl ketone (new tab)

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

  1. Street IP et al. Slow- and tight-binding inhibitors of the 85-kDa human phospholipase A2. Biochemistry, 1993 (new tab)PMID 8018213
  2. Koutek B et al. Inhibitors of arachidonoyl ethanolamide hydrolysis. J Biol Chem, 1994 (new tab)PMID 8083191
  3. Ackermann EJ, Conde-Frieboes K, Dennis EA. Inhibition of macrophage Ca2+-independent phospholipase A2 by bromoenol lactone and trifluoromethyl ketones. J Biol Chem, 1995 (new tab)PMID 7814408
  4. Deutsch DG et al. Methyl arachidonyl fluorophosphonate: a potent irreversible inhibitor of anandamide amidase. Biochem Pharmacol, 1997 (new tab)PMID 9065728
  5. Huang W et al. Arachidonyl trifluoromethyl ketone is neuroprotective after spinal cord injury. J Neurotrauma, 2009 (new tab)PMID 19371144
  6. Khan M et al. Oral administration of cytosolic PLA2 inhibitor arachidonyl trifluoromethyl ketone ameliorates cauda equina compression injury in rats. J Neuroinflammation, 2015 (new tab)PMID 25971887
  7. PubChem, AACOCF3, CID 5280436 (identifiers and properties) (new tab)

Identifiers

Names

Common name
Arachidonoyl trifluoromethyl ketone
IUPAC name
(6Z,9Z,12Z,15Z)-1,1,1-trifluorohenicosa-6,9,12,15-tetraen-2-one
Other names
AACOCF3 · AACOCF₃ · ATK · ATFMK · Arach-CF3 · Arachidonyl trifluoromethyl ketone · arachidonyltrifluoromethane · (6Z,9Z,12Z,15Z)-1,1,1-trifluorohenicosa-6,9,12,15-tetraen-2-one · 1,1,1-trifluoro-6,9,12,15-heneicosatetraen-2-one

Identifiers

Formula
C₂₁H₃₁F₃O
CAS
149301-79-1
PubChem CID
5280436(new tab)
InChIKey
PLWROONZUDKYKG-DOFZRALJSA-N
SMILES
CCCCC/C=C\C/C=C\C/C=C\C/C=C\CCCC(=O)C(F)(F)F

Machine-readable entry (JSON)

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