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Research tools

abn-CBDAbnormal cannabidiol

Synthetic regioisomer of CBD, a vasodilator in animals through a still unidentified target, with no cannabinoid-type behavioural effect.

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.

C₂₁H₃₀O₂

CAS 22972-55-0

Family
ECS pharmacological toolOther target
Molar mass
314.50 g/mol

Updated on

In plain terms

Abnormal cannabidiol is a laboratory-made « evil twin » of CBD: same atoms, but one fragment is attached somewhere else. It does not exist in the plant and turns up as a manufacturing residue in synthetic CBD. In animals it lowers blood pressure without causing any cannabinoid-type behavioural effect; the data cited here come from experiments on animals and cells.

Receptors and activity

Target network

GPR55AgonistEC50 = 2 nM · humanrecombinant human GPR55, HEK293T cell membranes, GTPγS activity (value « about 2 nM » from the abstract)
  • Activates

The lower the cited value, the closer the target sits to abn-CBD: 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 abn-CBD.

Brain, side view
Body, front view
Blood

GPR55GPR55 found in 4 regions of the body

  1. Basal gangliapresentmRNA found in the caudate nucleus and putamen1
  2. BonepresentOsteoclasts and osteoblasts2
  3. Adipose tissuepresentExpressed in visceral adipose tissue3
  4. LiverpresentExpressed in the liver3

Map sources

  1. Sawzdargo M et al. Identification and cloning of three novel human G protein-coupled receptor genes GPR52, PsiGPR53 and GPR55: GPR55 is extensively expressed in human brain. Brain Res Mol Brain Res, 1999 (new tab)
  2. Whyte LS et al. The putative cannabinoid receptor GPR55 affects osteoclast function in vitro and bone mass in vivo. Proc Natl Acad Sci U S A, 2009 (new tab)
  3. Moreno-Navarrete JM et al. The L-α-lysophosphatidylinositol/GPR55 system and its potential role in human obesity. Diabetes, 2012 (new tab)

Cited values

  1. GPR55AgonistEC50 = 2 nM · human78 out of 100

    Johns et al., Br J Pharmacol 2007 (new tab) · recombinant human GPR55, HEK293T cell membranes, GTPγS activity (value « about 2 nM » from the abstract)

  2. GPR18AgonistEC50 = 836 nM35 out of 100

    McHugh et al., Br J Pharmacol 2012 (new tab) · p44/42 MAPK phosphorylation in HEK293-GPR18 cells, full agonist; migration of BV-2 microglia and of HEK293-GPR18 cells, blocked by O-1918 (McHugh 2010)

  3. Atypical endothelial target (unidentified)AgonistIC50 = 3 µM · mouse25 out of 100

    Johns et al., Br J Pharmacol 2007 (new tab) · vasodilation of isolated mesenteric arteries (myography), value « about 3 µM » identical in wild-type and GPR55-/- mice

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

Abnormal cannabidiol is the synthetic regioisomer of CBD: the terpene fragment is attached at position 4 of the resorcinol ring, not position 2. Described in 1977 as lacking overt behavioural effects but hypotensive in anaesthetised dogs (Adams et al. 1977), it does not bind CB1 and causes hypotension and mesenteric vasodilation in wild-type mice as well as in mice lacking CB1 and CB2, effects inhibited by CBD; Járai et al. (1999) inferred a distinct, unidentified endothelial receptor. GPR55 is activated by the molecule (EC50 of about 2 nM in GTPγS on the human recombinant receptor) but does not mediate the vascular effect in mice (Johns et al. 2007); GPR18, of which it is a full agonist (EC50 of 835.7 nM, McHugh et al. 2012) and at which it drives the migration of microglial cells (McHugh et al. 2010), remains a candidate. Bondarenko's review (2014) notes that Gi/o protein-independent targets have been described for the agonists and antagonists of the presumed endothelial receptor, which calls for caution in reading vascular studies. In mice, Krohn et al. (2016) reported that intraperitoneal abn-CBD attenuated the scores of TNBS-induced colitis, an effect inhibited by O-1918 but not by AM630. All these data come from experiments on animals and cells.

Key sources.

History

Source
A synthetic molecule, a regioisomer of cannabidiol, absent from hemp. It is described as the main by-product of the chemical synthesis of CBD (Brighenti et al. 2024) and therefore turns up as an impurity in CBD of synthetic origin; it is also used as a laboratory reagent.

Origin

Research tool

No plant biosynthetic pathway: hemp does not produce this molecule. It is a synthetic regioisomer of CBD, with the terpene fragment attached at position 4 of the resorcinol instead of position 2.

Classification

Family, origin and source verification

Family

ECS pharmacological tool › Other target

Verification

Classification, sources and binding values checked on 20 October 2026; text read against its sources and Wikipedia.

Wikipedia (English)

Abnormal cannabidiol (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. Adams MD et al., A cannabinoid with cardiovascular activity but no overt behavioral effects, Experientia 1977 (marked hypotension in the anaesthetised dog, no behavioural effect) (new tab)PMID 891878
  2. Járai Z et al., Cannabinoid-induced mesenteric vasodilation through an endothelial site distinct from CB1 or CB2 receptors, PNAS 1999 (new tab)PMID 10570211
  3. Johns DG et al., The novel endocannabinoid receptor GPR55 is activated by atypical cannabinoids but does not mediate their vasodilator effects, Br J Pharmacol 2007 (new tab)PMID 17704827
  4. McHugh D et al., N-arachidonoyl glycine drives directed cellular migration through GPR18, the putative abnormal cannabidiol receptor, BMC Neuroscience 2010 (new tab)PMID 20346144
  5. McHugh D et al., Δ9-Tetrahydrocannabinol and N-arachidonyl glycine are full agonists at GPR18 receptors and induce migration in human endometrial HEC-1B cells, Br J Pharmacol 2012 (new tab)PMID 21595653
  6. Krohn RM et al., Abnormal cannabidiol attenuates experimental colitis in mice, promotes wound healing and inhibits neutrophil recruitment, J Inflamm 2016 (new tab)PMID 27418880
  7. Bondarenko AI, Endothelial atypical cannabinoid receptor: do we have enough evidence?, Br J Pharmacol 2014 (new tab)PMID 25073723
  8. Brighenti V et al., A new HPLC method with multiple detection systems for impurity analysis and discrimination of natural versus synthetic cannabidiol, Anal Bioanal Chem 2024 (new tab)PMID 38940871
  9. Citti C et al., Origin of Δ9-Tetrahydrocannabinol Impurity in Synthetic Cannabidiol, Cannabis and Cannabinoid Research 2021 (abnormal cannabidiol, one of the two main by-products of the chemical route) (new tab)
  10. ANSM, Consolidated list of substances classified as narcotics, updated 16 February 2026, annex IV (benzo[c]chromene heading; H2-CBD, H4-CBD) (new tab)
  11. PubChem, compound CID 89949 (abnormal cannabidiol) (new tab)

Identifiers

Names

Common name
Abnormal cannabidiol
IUPAC name
4-[(1R,6R)-3-methyl-6-prop-1-en-2-ylcyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol
Other names
Abn-CBD · Cannabidiol anormal · CBD anormal

Identifiers

Formula
C₂₁H₃₀O₂
CAS
22972-55-0
PubChem CID
89949(new tab)
InChIKey
YWEZXUNAYVCODW-RBUKOAKNSA-N
SMILES
CCCCCC1=CC(=CC(=C1[C@@H]2C=C(CC[C@H]2C(=C)C)C)O)O

Machine-readable entry (JSON)

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