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Research tools

SSR411298

A reversible FAAH inhibitor developed by Sanofi, with no direct action at CB1, discontinued after phase 2.

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.

C₂₁H₂₆N₂O₆

CID 44482551

Family
ECS pharmacological toolEnzyme inhibitor
Molar mass
402.40 g/mol

Updated on

In plain terms

SSR411298 is a synthetic molecule developed by a French pharmaceutical company, with no connection to hemp. It does not bind to the cannabis receptors: it slows an enzyme that destroys anandamide, a substance the body makes itself. It was tested in two phase 2 trials (depression in older adults, cancer pain); no results were filed in the registry and the second trial was stopped after five enrolments for strategic reasons.

Receptors and activity

Target network

FAAH (fatty acid amide hydrolase)InhibitorIC50 = 62.5 nM · mouse[3H]anandamide hydrolysis, mouse brain homogenate; reversible inhibition (dialysis); ex vivo 50% inhibitory dose of 0.17 mg/kg orally
  • Blocks or inhibits

The lower the cited value, the closer the target sits to SSR411298: 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 SSR411298.

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 = 62.5 nM · mouse53 out of 100

    Griebel et al., Sci Rep 2018 (new tab) · [3H]anandamide hydrolysis, mouse brain homogenate; reversible inhibition (dialysis); ex vivo 50% inhibitory dose of 0.17 mg/kg orally

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

SSR411298 is a reversible inhibitor of FAAH, the enzyme that hydrolyses anandamide. Its IC50 is 62.5 nM on mouse brain, with reversibility shown by dialysis; given orally to mice, the dose inhibiting half of brain FAAH activity is 0.17 mg/kg (0.10 mg/kg intraperitoneally), with inhibition stable up to 6 hours then declining until 24 hours. The result is a rise in anandamide, PEA and OEA in the hippocampus, with no change in 2-AG; the molecule does not interact with CB1 or CB2 up to 10 µM and acts by letting the endogenous mediators accumulate (Griebel et al. 2018). In rodents it was not recognised as WIN 55,212-2 in a discrimination test up to 500 mg/kg and did not produce a rimonabant-precipitated withdrawal syndrome, unlike Δ9-THC. The authors describe anxiolytic-like effects limited to highly aversive conditions and antidepressant-like effects in rodent models. In humans, two Sanofi phase 2 trials were registered: one in 527 older patients with major depression (10, 50 and 200 mg per day for 8 weeks, completed in February 2010, no results filed), the other in persistent cancer pain (200 mg per day), stopped in 2012 after five enrolments for strategic reasons. No published clinical results were found.

Key sources.

History

Source
An entirely synthetic compound, found in no plant and derived from no plant cannabinoid: a FAAH inhibitor developed by Sanofi (Griebel et al. 2018).

Origin

Research tool

No biological pathway produces this molecule: it is a synthetic compound, a carbamate derived from a 1,3-dioxane bearing a methoxynaphthyl group.

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. Griebel G et al. The selective reversible FAAH inhibitor, SSR411298, restores the development of maladaptive behaviors to acute and chronic stress in rodents. Sci Rep, 2018 (new tab)PMID 29403000
  2. Kerbrat A et al. Acute neurologic disorder from an inhibitor of fatty acid amide hydrolase. N Engl J Med, 2016 (new tab)PMID 27806235
  3. ClinicalTrials.gov NCT00822744, phase 2 trial of SSR411298 (10, 50 and 200 mg) in major depression in the elderly, Sanofi, 527 participants, started 12/2008, completed 02/2010, no results posted (new tab)
  4. ClinicalTrials.gov NCT01439919, phase 2 trial of SSR411298 (200 mg) in persistent cancer pain, Sanofi, terminated 02/2012 for strategic reasons after 5 participants (new tab)
  5. PubChem, SSR411298, CID 44482551 (identifiers and properties) (new tab)

Identifiers

Names

IUPAC name
(2-amino-2-oxoethyl) N-[3-[5-(6-methoxynaphthalen-1-yl)-1,3-dioxan-2-yl]propyl]carbamate
Other names
SSR 411298 · SA72

Identifiers

Formula
C₂₁H₂₆N₂O₆
PubChem CID
44482551(new tab)
InChIKey
OGKKHZMANPWMSD-UHFFFAOYSA-N
SMILES
COC1=CC2=C(C=C1)C(=CC=C2)C3COC(OC3)CCCNC(=O)OCC(=O)N

Machine-readable entry (JSON)

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