{"schemaVersion":"cwiki-fiche-1.0","identifiers":{"inchiKey":"YDKZOUNVEIGJPO-UHFFFAOYSA-N","prefName":"11-Hydroxycannabinol","symbol":"11-OH-CBN","iupacName":"9-(hydroxyméthyl)-6,6-diméthyl-3-pentylbenzo[c]chromén-1-ol","aliases":["11-hydroxycannabinol","11-OH-CBN","11-hydroxy-CBN","hydroxyméthyl-cannabinol"],"cas":"30432-08-7","pubchemCid":"3082311","chebiId":null,"smiles":"CCCCCC1=CC(=C2C(=C1)OC(C3=C2C=C(C=C3)CO)(C)C)O","molecularFormula":"C21H26O3","molecularWeight":326.4,"xrefs":{"pubchem":"https://pubchem.ncbi.nlm.nih.gov/compound/3082311"}},"classification":{"family":"semisynthetique","familyLabel":"Semi-synthetic cannabinoid","origin":"semisynthetic","originLabel":"Semi-synthétique","structuralClassFr":"Dérivé hydroxylé du cannabinol, lui-même homologue entièrement aromatisé du Δ9-THC. Le squelette benzo[c]chromène porte ici un cycle aromatique là où le THC présente un cyclohexène, ce qui supprime les centres stéréogènes 6a et 10a et rend la molécule plane. La modification métabolique porte sur le méthyle en position 11, transformé en alcool primaire, seule différence avec le cannabinol."},"originSynthesis":{"heading":"Route of preparation (chemical process)","summaryFr":"There is no plant route for this molecule. It forms in the liver by hydroxylation of the methyl borne by carbon 11 of cannabinol, a reaction analogous to the one that turns Δ9-THC into 11-hydroxy-THC. The skeleton of cannabinol being entirely aromatised on its terpene ring, the resulting molecule retains that planar character, unlike the hydroxylated metabolites of the tetrahydrocannabinols.","originNote":"No notable natural occurrence in the plant. The molecule forms in the body as a hepatic phase I metabolite of cannabinol, and it is prepared chemically for the purposes of research and analysis. It should be recalled here that the cannabinol from which it comes is not itself a biosynthetic product of hemp: it results very largely from the oxidation of THC during drying and storage, which the reference literature regards as a conservation artefact rather than as a native constituent.","discovered":"Décrit dans les travaux japonais sur le métabolisme du cannabinol menés dans les années 1980, notamment par Yamamoto et Watanabe, qui en font le métabolite majeur du CBN et comparent son activité pharmacologique à celle de la molécule mère. Sa pharmacologie de réception est ensuite quantifiée en 1997 par l'équipe de Mechoulam et Vogel, dans une série consacrée aux dérivés du cannabinol."},"pharmacology":{"summaryFr":"11-hydroxycannabinol is the major metabolite of cannabinol, formed in the liver by hydroxylation of the methyl at position 11. It illustrates a rule that holds throughout the cannabinoid series: that hydroxylation does not destroy affinity for the receptors, it increases it. Where cannabinol is a mediocre ligand, its metabolite binds CB1 with an inhibition constant of 38.0 nanomolar and CB2 with 26.6 nanomolar, in the measurements of Rhee and colleagues. Its functional profile is more singular: an agonist on the CB1 pathway, where it inhibits adenylyl cyclase with a median effective concentration of 58.1 nanomolar, it fails to activate the CB2 pathway and behaves there as an antagonist. The same study showed that moving to the dimethylheptyl side chain turns this modest compound into a very potent agonist of both receptors, with affinities falling below the nanomolar, a result that fed all the subsequent medicinal chemistry of substituted cannabinols. One caveat must accompany the reading of this entry: the cannabinol from which the molecule derives is very largely an oxidation product of THC occurring in storage, and not a biosynthetic constituent of hemp, so that the whole cannabinol class belongs more to conservation chemistry than to botany.","receptorSummaryFr":"An agonist of both cannabinoid receptors, with an affinity markedly higher than that of the cannabinol from which it derives. Rhee and colleagues measured inhibition constants of 38.0 nanomolar at CB1 and 26.6 nanomolar at CB2. Its functional behaviour is, however, dissociated according to the receptor: it inhibits CB1-coupled adenylyl cyclase with a median effective concentration of 58.1 nanomolar, whereas it produces only 20 per cent inhibition on the CB2 pathway at 10 micromolar. The authors describe it for that reason as a specific though not very potent CB2 antagonist, an unusual profile for a cannabinoid metabolite.","binding":[{"target":"CB1","efficacy":"full_agonist","relativeActivity":62,"reported":"Ki = 38,0 ± 7,2 nM","confidence":"medium"},{"target":"CB2","efficacy":"antagonist","relativeActivity":55,"reported":"Ki = 26,6 ± 5,5 nM","confidence":"medium"}],"references":[{"label":"Rhee et coll. 1997 : dérivés du cannabinol, liaison aux récepteurs CB1 et CB2 et inhibition de l'adénylylcyclase","pmid":"9379442","doi":null,"url":"https://pubmed.ncbi.nlm.nih.gov/9379442/"},{"label":"Yamamoto et coll. 1987 : activité pharmacologique du cannabinol et de son métabolite majeur le 11-hydroxycannabinol","pmid":"3664823","doi":null,"url":"https://pubmed.ncbi.nlm.nih.gov/3664823/"}]},"pharmacokinetics":"Aucune donnée de pharmacocinétique humaine n'est publiée pour ce métabolite pris isolément : il n'a jamais été administré à l'humain et n'existe dans l'organisme qu'en aval d'une exposition au cannabinol. Sa formation a été caractérisée chez le rongeur, où il constitue le produit majeur de la transformation hépatique du CBN. Les paramètres d'absorption, de distribution et de demi-vie restent indéterminés.","metabolism":"Le composé est un produit de phase I, issu de l'hydroxylation microsomale du cannabinol par les cytochromes P450 hépatiques. Comme les autres cannabinoïdes hydroxylés, il est ensuite susceptible d'être oxydé en acide carboxylique correspondant et conjugué à l'acide glucuronique avant élimination. Le détail des isoformes impliquées chez l'humain n'a pas fait l'objet d'une caractérisation aussi précise que pour le métabolisme du Δ9-THC.","detection":"La molécule est recherchée en laboratoire de recherche par chromatographie liquide couplée à la spectrométrie de masse en tandem, à partir d'étalons de synthèse. Elle ne fait partie d'aucun panel de dépistage courant : les immunoessais cannabis ciblent l'acide 11-nor-9-carboxy-THC, et les méthodes de confirmation en toxicologie clinique n'incluent généralement pas les métabolites du cannabinol.","subjectiveEffects":{"profile":[{"key":"calm","label":"Calm","description":"Relaxation of body and mind; reduced mental noise without marked drowsiness.","intensity":40},{"key":"focus","label":"Clarity","description":"Sustained attention and clear thinking; functional lucidity, not euphoria.","intensity":15},{"key":"sleep","label":"Sleep","description":"Sedative effect: aids sleep onset and the continuity of deep sleep.","intensity":45},{"key":"appetite","label":"Appetite","description":"Stimulation of hunger and of taste appreciation (the “munchies” effect).","intensity":30},{"key":"uplift","label":"High","description":"Euphoria and sensory intensity; altered perception of time and space.","intensity":30}],"doseRanges":null,"humanDataCharacterised":false},"indications":{"approvedMedicines":[]},"harmProfile":{"unstudiedBanner":true,"bannerTextFr":"Aucune dose humaine caractérisée : données animales / in vitro uniquement. Profil d'effet, marge de sécurité et toxicité aiguë non documentés en clinique humaine.","toxicologyFr":"Aucun événement toxique documenté n'est attribuable à cette molécule, qui n'est pas commercialisée et n'a pas d'usage humain. Aucune dose humaine n'est caractérisée. Son affinité élevée pour le récepteur CB1 laisse supposer une activité psychotrope si elle était administrée, mais cette hypothèse n'a pas été vérifiée chez l'humain, et rien n'autorise à extrapoler une posologie à partir des données de liaison."},"legal":{"scheduleStatus":"unscheduled","scheduleLabel":"Unscheduled","frScheduleStatus":"unscheduled","tiers":[{"jurisdiction":"international","jurisdictionLabel":"International","label":"Non inscrit aux conventions de contrôle","reference":null,"url":null,"effectiveDate":null,"lastVerified":"2026-05-01","supersededBy":null},{"jurisdiction":"eu","jurisdictionLabel":"Union européenne","label":"Non contrôlé au niveau de l'Union ; usage de recherche","reference":null,"url":null,"effectiveDate":null,"lastVerified":"2026-05-01","supersededBy":null},{"jurisdiction":"fr","jurisdictionLabel":"France","label":"Non inscrit nommément ; sans usage commercial autorisé","reference":null,"url":null,"effectiveDate":null,"lastVerified":"2026-05-01","supersededBy":null}],"sourcesFr":"EUR-Lex, UNODC, CND, ANSM, IUPHAR/BPS, ChEBI, EUDA."},"references":[{"label":"Rhee et coll. 1997 : dérivés du cannabinol, liaison aux récepteurs CB1 et CB2 et inhibition de l'adénylylcyclase","pmid":"9379442","doi":null,"url":"https://pubmed.ncbi.nlm.nih.gov/9379442/"},{"label":"Yamamoto et coll. 1987 : activité pharmacologique du cannabinol et de son métabolite majeur le 11-hydroxycannabinol","pmid":"3664823","doi":null,"url":"https://pubmed.ncbi.nlm.nih.gov/3664823/"}],"meta":{"slug":"11-oh-cbn","url":"https://en.phytogrammes.com/wiki/11-oh-cbn","lastVerified":"2026-05-01","dataUpdatedAt":"2026-08-16","confidence":"medium","dataCompletenessPct":90,"disclaimerFr":"Contenu éditorial informatif, sans valeur d'avis médical ni juridique. Sources primaires citées par fiche. Réservé aux adultes."}}