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Semi-synthetic cannabinoid

HU-345

Quinone derived from cannabinol, with no measurable binding to the CB1 and CB2 receptors: a research tool.

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.

Receptors and activity

  1. CB1Modulator2 out of 100

    Aucune liaison mesurable jusqu'à 15 µM pour l'ensemble des quinones du brevet, dont HU-345 (brevet US 8 497 299, Mechoulam et coll.)

  2. CB2Modulator2 out of 100

    Aucune liaison mesurable jusqu'à 15 µM pour l'ensemble des quinones du brevet, dont HU-345 (brevet US 8 497 299, Mechoulam et coll.)

  3. PPAR-γAgonist5 out of 100

    CE50 de 23,1 µM (activation de PPAR-γ en test luciférase, Caprioglio et coll., 2020)

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

Subjective signature

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

Pharmacology

HU-345, or cannabinolquinone (CBNQ), is a quinone derivative of cannabinol (CBN), obtained by chemical oxidation and described in a patent application from the Hebrew University of Jerusalem filed in 2005. The patent, which groups HU-345 with other cannabinoid quinones, reports that they do not bind the CB1 and CB2 receptors up to 15 µM and that no measurable psychotropic effect is observed. In cell culture, growth of Raji lymphoma cells is inhibited by more than 50% at 6.25 µg/mL, and that of Jurkat and DU-145 cell lines at 12.5 µg/mL. In a 2020 study of phytocannabinoid oxidation, its EC50 at PPAR-γ is 23.1 µM, whereas cannabinol exceeds 25 µM. No pharmacokinetic, metabolic or human toxicology data are published in the sources consulted.

History

Source
Semi-synthetic molecule: it derives from cannabinol (CBN) by oxidation of its phenol ring. It is not described as a constituent of cannabis in the sources consulted.

Route of preparation (chemical process)

No biosynthetic pathway: the molecule is obtained by chemical synthesis, through oxidation of cannabinol. No living organism is reported to produce it in the sources consulted.

References

Structured data

SMILES
CCCCCC1=CC(=O)C2=C(C1=O)OC(C3=C2C=C(C=C3)C)(C)C
InChIKey
UFDYTRQMIXJHTH-UHFFFAOYSA-N

Machine-readable entry (JSON)

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