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Merck
CN

SML4230

Cannabigerol

new

≥98% (HPLC)

Synonym(s):

2-[(2E)-3,7-dimethyl-2,6-octadien-1-yl]-5-pentyl-1,3-benzenediol, 2-((2E)-3,7-Dimethylocta-2,6-dienyl)-5-pentylbenzene-1,3-diol, CBG

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About This Item

Empirical Formula (Hill Notation):
C21H32O2
CAS Number:
Molecular Weight:
316.48
MDL number:
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Quality Level

Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

-10 to -25°C

SMILES string

OC1=C(C(O)=CC(CCCCC)=C1)C/C=C(C)/CCC=C(C)C

Biochem/physiol Actions

Partial agonist against of cannabinoid receptors CB1 and CB2; non-psychotropic phytocannabinoid.
Cannabigerol is a non-psychoactive phytocannabinoid. Cannabigerol binds CB1 and CB2 receptors with Ki values of 440 and 337 nM, respectively and acts as a partial agonist against both receptor subtypes. The compound is a potent a2-adrenoceptor agonist (EC50 = 0.2 nM). Cannabigerol modulates the expression of expression of proinflammatory proteins, such as TNF-α, IL-1β, IL-6, IL-10, interferon-γ, and prostaglandin E2.

Regulatory Information

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Rahul Nachnani et al.
The Journal of pharmacology and experimental therapeutics, 376(2), 204-212 (2020-11-11)
Medical cannabis and individual cannabinoids, such as Δ9-tetrahydrocannabinol (Δ9-THC) and cannabidiol (CBD), are receiving growing attention in both the media and the scientific literature. The Cannabis plant, however, produces over 100 different cannabinoids, and cannabigerol (CBG) serves as the precursor
M G Cascio et al.
British journal of pharmacology, 159(1), 129-141 (2009-12-17)
Cannabis is the source of at least seventy phytocannabinoids. The pharmacology of most of these has been little investigated, three notable exceptions being Delta(9)-tetrahydrocannabinol, cannabidiol and Delta(9)-tetrahydrocannabivarin. This investigation addressed the question of whether the little-studied phytocannabinoid, cannabigerol, can activate
Agnieszka Gęgotek et al.
The Journal of pharmacology and experimental therapeutics, 387(2), 170-179 (2023-09-01)
Excessive daily exposure of human skin to natural UVA radiation leads to impaired redox homeostasis in epidermal keratinocytes, resulting in changes in their proteome. Commonly used antioxidants usually exhibit protection in a narrowed range, which makes it necessary to combine

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