|CBD,CBG||ovarian cancer in vitro via experiment||Evaluation of the effects of cannabinoids CBD and CBG on human ovarian cancerc ells in vitro||Jan 2019|
Action Pathway: GPR55|
CBD and CBG induced dose-dependent and time-dependent cytotoxic effects on the ovarian cancer cells tested with activity at micromolar concentrations towards the A2780 and A2780/CP70 cancer cells whilst displaying less activity against the non-cancer cells. CBD was the more potent of the two cannabinoids. However, the difference observed was not significant compared to CBG. CBD and CBG in combination with the established chemotherapeutic drug carboplatin showed synergistic effects in the cancer cells but importantly, CBD and CBG did not synergise with carboplatin in the non-cancer ARPE19 cells.
|CBG||hungtingtons disease,neuroprotective in mice via experiment||Neuroprotective Properties of Cannabigerol in Huntingtons Disease: Studies in R6/2 Mice and 3-Nitropropionate-lesioned Mice||Jan 2015|
|CBG was extremely active as neuroprotectant in mice intoxicated with 3-nitropropionate (3NP), improving motor deficits and preserving striatal neurons against 3NP toxicity.|
|CBG||appetite boost in rats via placebo trial||Cannabigerol is a novel, well-tolerated appetite stimulant in pre-satiated rats||Aug 2016|
Ingestion Method: 30-120 mg/kg, per ora (p.o.)|
CBG produced no adverse effects on any parameter in the neuromotor tolerability test battery. In the feeding assay, 120-240 mg/kg CBG more than doubled total food intake and increased the number of meals consumed, and at 240 mg/kg reduced latency to feed. However, the sizes or durations of individual meals were not significantly increased.
|CBG||anti-inflamatory in vitro||In Vitro Model of Neuroinflammation: Efficacy of Cannabigerol, a Non-Psychoactive Cannabinoid||Jun 2018|
Ingestion Method: 1, 2.5, 5, 7.5, 10, 12.5, 15 and 20 uM|
Furthermore, CBG pre-treatment counteracted not only inflammation, as demonstrated by the reduction of IL-1beta-, TNF-alpha-, IFN-? and PPAR? protein levels assessed by immunocytochemistry, but also oxidative stress in NSC-34 cells treated with the medium of LPS-stimulated RAW 264.7.
|CBD,CBG,CBC||cancer,breast cancer in vitro||Antitumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma.||May 2006|
|Results obtained in a panel of tumor cell lines clearly indicate that, of the five natural compounds tested, cannabidiol is the most potent inhibitor of cancer cell growth (IC(50) between 6.0 and 10.6 microM), with significantly lower potency in noncancer cells. The cannabidiol-rich extract was equipotent to cannabidiol, whereas cannabigerol and cannabichromene followed in the rank of potency.|
|CBG,CBD||anti-inflamatory in vitro||Evaluation of the cyclooxygenase inhibiting effects of six major cannabinoids isolated from Cannabis sativa.||Jan 2011|
Action Pathway: COX-1/2|
In the present work, the six cannabinoids tetrahydrocannabinol (delta-?-THC), tetrahydrocannabinolic acid (delta-?-THC-A), cannabidiol (CBD), cannabidiolic acid (CBDA), cannabigerol (CBG) and cannabigerolic acid (CBGA), isolated from Cannabis sativa, were evaluated for their effects on prostaglandin production. For this purpose an in vitro enzyme based COX-1/COX-2 inhibition assay and a cell based prostaglandin production radioimmunoassay were used.
|CBG||neuroprotective,hungtingtons disease in mice||Neuroprotective properties of cannabigerol in Huntington's disease: studies in R6/2 mice and 3-nitropropionate-lesioned mice.||Jan 2015|
|CBG was extremely active as neuroprotectant in mice intoxicated with 3-nitropropionate (3NP), improving motor deficits and preserving striatal neurons against 3NP toxicity. In addition, CBG attenuated the reactive microgliosis and the upregulation of proinflammatory markers induced by 3NP, and improved the levels of antioxidant defenses that were also significantly reduced by 3NP.|
|CBG||colon cancer in vitro||Colon carcinogenesis is inhibited by the TRPM8 antagonist cannabigerol, a Cannabis-derived non-psychotropic cannabinoid.||Dec 2014|
|In vivo, CBG inhibited the growth of xenograft tumours as well as chemically induced colon carcinogenesis. CBG hampers colon cancer progression in vivo and selectively inhibits the growth of CRC cells, an effect shared by other TRPM8 antagonists. CBG should be considered translationally in CRC prevention and cure.|
|THCV,CBG||bladder in vitro||Effect of Non-psychotropic Plant-derived Cannabinoids on Bladder Contractility: Focus on Cannabigerol.||June 2015|
|The rank order of efficacy was CBG=THCV>CBD>CBDV. In depth studies on CBG showed that the effect of this phytocannabinoid on acetylcholine-induced contractions was not affected by CB1 or CB2 receptor antagonists. Additionally, CBG also reduced acetylcholine-induced contractions in the human bladder.|
|CBG||appetite boost in rats via experiment (n=16)||A cannabigerol-rich Cannabis sativa extract, devoid of d9-tetrahydrocannabinol, elicits hyperphagia in rats.||Jun 2017|
Ingestion Method: 30-240 mg/kg|
Positive The total food intake was increased by 120 and 240 mg/kg CBG-BDS (1.53 and 1.36 g, respectively, vs. 0.56 g in vehicle-treated animals). Latency to feeding onset was dose dependently decreased at all doses, and 120 and 240 mg/kg doses increased both the number of meals consumed and the cumulative size of the first two meals.
|CBG||cancer,oral cancer in vitro||Boron trifluoride etherate on silica-A modified Lewis acid reagent (VII). Antitumor activity of cannabigerol against human oral epitheloid carcinoma cells.||Jun 1998|
|Cannabigerol (3) exhibited the highest growth-inhibitory activity against the cancer cell lines.|