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Research tools

BIA 10-2474

An experimental FAAH inhibitor, involved in the fatal accident of a phase 1 trial in Rennes in 2016.

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.

C₁₆H₂₀N₄O₂

CAS 1233855-46-3

Family
ECS pharmacological toolEnzyme inhibitor
Molar mass
300.40 g/mol

Updated on

In plain terms

BIA 10-2474 is a laboratory molecule with no link to hemp or CBD. It was designed to block an enzyme in the human body that breaks down anandamide, a natural substance close to cannabinoids. During a phase 1 trial held in Rennes in 2016, one volunteer died (brain death) and four others had neurological problems, from mild to severe; the exact cause remains unknown.

Receptors and activity

Target network

FAAHInhibitorno measured value
  • Blocks or inhibits

The lower the cited value, the closer the target sits to BIA 10-2474: 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 BIA 10-2474.

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. FAAHInhibitorno measured value cited
  2. ABHD6Inhibitorno measured value cited
  3. Off-target lipid serine hydrolases (ABHD11, PNPLA6, PLA2G15, PLA2G6, AIG1)Inhibitorno measured value cited
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

BIA 10-2474 is an inhibitor of FAAH (fatty acid amide hydrolase), the enzyme that hydrolyses anandamide, given by mouth. By blocking this enzyme, the molecule indirectly raises anandamide concentrations; no direct binding to CB1 or CB2 receptors is documented. In mice it inhibits brain and liver FAAH at doses of the order of a microgram per kilogram (ED50 of 13.5 and 6.2 µg/kg) and is about 10 times less potent than PF-04457845 on human FAAH in situ; its main targets are FAAH and ABHD6, then, at higher exposure, ABHD11, PNPLA6, PLA2G15, PLA2G6 and AIG1 (Bonifácio et al. 2020). Proteomic profiling published in Science in 2017 showed that it inhibits several lipases not hit by PF-04457845, a selective inhibitor tested in the clinic, and that it alters lipid networks in human cortical neurons (van Esbroeck et al. 2017). In the phase 1 trial held in Rennes in 2016, in the cohort receiving 50 mg a day (six treated participants, two on placebo), an acute neurological syndrome appeared from the fifth day in three of the four participants whose data were published, with brain lesions of the pons and hippocampi; one participant had brain death (Kerbrat et al., N Engl J Med 2016, PMID 27806235). The exact mechanism of this neurotoxicity remains unknown, and the molecule never had an established therapeutic indication.

Key sources.

History

Source
A wholly synthetic molecule from the FAAH-inhibitor research programme of the Portuguese pharmaceutical company Bial. It is found neither in cannabis nor in any living organism, and it has never received a marketing authorisation.

Origin

Research tool

No known biological pathway: the molecule is not formed in any living organism. It is obtained by medicinal chemistry, within the class of imidazole carboxamides, with no relation whatsoever to the biosynthetic pathway of plant cannabinoids.

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)

BIA 10-2474 (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. Kerbrat et al., N Engl J Med 2016: acute neurological disorder during a phase 1 trial (new tab)PMID 27806235
  2. van Esbroeck et al., Science 2017: non-FAAH targets of BIA 10-2474 (new tab)PMID 28596366
  3. Bonifácio et al., Br J Pharmacol 2020: preclinical pharmacological evaluation (new tab)PMID 31901141
  4. Hayes et al., Crit Rev Toxicol 2021: non-clinical toxicological evaluation (new tab)PMID 33528291
  5. Peck et al., Clin Pharmacol Ther 2022: lessons from the accident (new tab)PMID 35007339
  6. PubChem, BIA 10-2474, CID 46831476 (new tab)

Identifiers

Names

IUPAC name
N-cyclohexyl-N-methyl-4-(1-oxidopyridin-1-ium-3-yl)imidazole-1-carboxamide
Other names
BIA-10-2474 · BIA-102474

Identifiers

Formula
C₁₆H₂₀N₄O₂
CAS
1233855-46-3
PubChem CID
46831476(new tab)
InChIKey
DOWVMJFBDGWVML-UHFFFAOYSA-N
SMILES
CN(C1CCCCC1)C(=O)N2C=C(N=C2)C3=C[N+](=CC=C3)[O-]

Machine-readable entry (JSON)

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