JNJ-1661010

Synthetic FAAH inhibitor, studied in rats, with no human clinical data identified.

C₁₉H₁₉N₅OS

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.

Data sheet

Names

IUPAC name: N-phenyl-4-(3-phenyl-1,2,4-thiadiazol-5-yl)piperazine-1-carboxamide
Other names: JNJ1661010

Identifiers

Formula: C₁₉H₁₉N₅OS
Molar mass: 365.50 g/mol
PubChem CID: 2809273(new tab)
InChIKey: BHBOSTKQCZEAJM-UHFFFAOYSA-N

Class

Family: ECS modulator (research)

Legal status

Status: Unscheduled

See the legal framework

Updated on 13 October 2026

Receptors and activity

FAAHModulator75 out of 100
CI50 33 nM sur FAAH humaine après 20 min de préincubation (Keith et coll., 2008)

Bar length shows the relative strength of the interaction, as an indication.

Subjective signature

Calm: 5 out of 100; Relaxation of body and mind; reduced mental noise without marked drowsiness.
Clarity: 5 out of 100; Sustained attention and clear thinking; functional lucidity, not euphoria.
High: 5 out of 100; Euphoria and sensory intensity; altered perception of time and space.
Appetite: 5 out of 100; Stimulation of hunger and of taste appreciation (the “munchies” effect).
Sleep: 5 out of 100; Sedative effect: aids sleep onset and the continuity of deep sleep.

Editorial estimate, not clinical.

Pharmacology

JNJ-1661010 is an inhibitor of FAAH, the enzyme that breaks down anandamide and other fatty acid amides. Described in 2008 in a medicinal chemistry series, then characterised in 2009 by pharmacology work carried out at Johnson & Johnson, the molecule forms a covalent bond with the enzyme that slowly breaks down. In rats, it raises brain levels of anandamide, OEA and PEA and reduces experimental pain of neuropathic, inflammatory and acute origin (Karbarz et al., 2009). Other work in mice reports a reduction of spontaneous contractions of isolated uterus, an attenuation of haloperidol-induced catalepsy and an amelioration of collagen-induced arthritis (Pagano et al., 2017; Celorrio et al., 2016; Lowin et al., 2015). The data are exclusively preclinical: no therapeutic indication is established and no human clinical data were identified in the sources consulted.

Key sources.

History

Source: Fully synthetic molecule, from pharmaceutical chemistry work on FAAH inhibitors. The reference data used for this entry record no natural occurrence, either in hemp or in any other living organism.

Origin (research tool)

No biosynthetic pathway: a chemically synthesised molecule of the aryl piperazine urea class, carrying a 1,2,4-thiadiazole ring.

Legal framework

European Union: Not listed in the 1961 and 1971 international conventions (INCB Green List, 2026 edition). No harmonised control measure at European Union level was identified in the sources consulted for this entry: the status therefore falls under the national law of each member state.
France: Not named in the consolidated list of narcotics published by ANSM (update of 16 February 2026), either under its code or its chemical name; its structure meets none of the generic family definitions of that list (notably indole and indazole methanones, carboxylates and carboxamides, naphthoylpyrroles, naphthylmethylindoles, naphthylidene indenes, cyclohexylphenols, pyrrolo[3,2-c]pyridine carboxamides and thiazolyl indoles), nor the clauses covering benzofurans, cathinones or phenethylamines. Not classified in France on that basis, subject to legal review.

Sources: EUR-Lex, UNODC, CND, ANSM, IUPHAR/BPS, ChEBI, EUDA. Our method.

References

Structured data

SMILES: C1CN(CCN1C2=NC(=NS2)C3=CC=CC=C3)C(=O)NC4=CC=CC=C4
InChIKey: BHBOSTKQCZEAJM-UHFFFAOYSA-N

Machine-readable entry (JSON)

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