CBG
The 'mother' cannabinoid
Cannabinoid
What is CBG?
CBG stands for Cannabigerol. CBG is the decarboxylated version of CBGA, which is the mother cannabinoid to most other cannabinoids.
Neuro-protective properties
In mouse studies, CBG showed an effective ability to increase motor function control in mice with Huntington's disease. On top of this, CBG has high anti-oxidant properties, and as oxidative stress is a significant factor in neurological diseases, it has shown high potential benefits.
CBG protects against Aβ toxicity, though the exact mechanism by which it provides this protection has not been further researched as far as I am aware.
CBG also lowered MS-induced cytokines, adding the ability to help slow symptom progression along with other treatments.
Inflammation and immune regulation
Recent studies showed that cannabinoids downregulate cytokine and chemokine production and, in some models, upregulate T-regulatory cells (Tregs) as a mechanism to suppress inflammatory responses. This can help with controlling tumours from becoming metastatic. It is important to remember that these cannabinoids should be used in tandem with current treatments, NOT AS A SUBSTITUTE!
One of the biggest benefits of CBG is its high level of anti-inflammatory as well as immuno-regulatory processes. It was shown to help heavily in patients with IBD, allergic asthma, and other chronic inflammatory conditions. Specifically, its binding with CB2 was the main contributor to this anti-inflammatory response. Remember, CB2 is most active when inflammation is present in the body.
Anti-bacterial
From an anti-bacterial standpoint, CBG has shown to be fairly wide-ranged in its anti-bacterial effects compared to CBD or other cannabinoids. The exact mechanism as to why it affects these more is theorized to be due to weakening the bacterial cell membrane and allowing cellular collapse of the bacteria. CBG has also been shown to inhibit activities like biofilm formation and virulence.
Blood pressure
CBG has shown an affinity to α2AR. Activation of α2AR inhibits the release of norepinephrine, causing vasodilation (relaxation of blood vessels), bradycardia (slower heart rate), and decreased contractility (weaker heart contractions), ultimately resulting in lower blood pressure. It seems like this effect was greatly increased with chronic use of CBG, not short-term use.
Study: CBG and cancer
Accumulating evidence has substantiated the anti-tumorigenic properties of CBG, showcasing its efficacy in reducing cell proliferation, migration, and survival in various tumor types, including prostate cancer, glioblastoma, colorectal carcinoma, pancreatic cancer, and breast cancer. Cannabinoids have been well-researched in cancer, with the bulk of the research focused on THC and CBD, both of which increase the survival of glioblastoma patients. These two agents have progressed to clinical trials, coupling chemotherapy with phytocannabinoids to assess breast and colon cancer patient recovery. CBG, whilst not at the clinical trial stage as of yet, has shown much promise with regard to treating glioblastoma. CBG, like many other cannabinoids, is lipid-soluble. This property allows it to easily pass through the lipid bilayer of cell membranes, including the blood–brain barrier, and it was found to reduce C6-rat glioma cell proliferation.
A study in 2021 found that CBG alone and in combination with CBD effectively promoted apoptosis in glioblastoma stem cells. CBG inhibited the invasive behavior of glioblastoma cells, in a similar way as CBD combined with temozolomide, a chemotherapeutic. The CBG plus CBD combination was found to be more effective than CBD with THC in inducing cytotoxicity and reducing invasion in a 3D spheroid assay.
The inhibitory effects of CBG and CBD on glioblastoma stem cells are likely primarily involved in the modulation of GPR55 and TRPV1 signaling. As solid tumors progress, the tumor microenvironment (TME) undergoes changes that transform into a highly immunosuppressive milieu. Regulatory myeloid cells play key roles in the immunosuppressive environment and activate tumor-secreted cytokines. It was found that CBG decreased the CSF-1 secretion by melanoma cells. CBG significantly reduces the expansion and macrophage transition of the monocytic-myeloid-derived suppressor cells (MDSCs) subpopulation. It is a promising treatment for tumors with elevated CSF-1 expression.
In a study of minor phytocannabinoids on Multiple myeloma (MM), CBG was found to inhibit MM cell growth in a dose-dependent manner and reduce the invasion of MM cells toward osteoblast cells. During tumor progression, genetic and epigenetic alterations can enable tumors to evade immune detection, a phenomenon known as immune escape. The adaptive immune system's ability to detect and eliminate emerging tumors relies on immune surveillance by cytotoxic T lymphocytes (CTLs). CTLs recognize tumor cells by binding to major histocompatibility complex class I (MHC-I) molecules, which present fragments of tumor-derived proteins. Dada et al. demonstrated that CBG can reverse this immune escape phenotype in vitro by upregulating MHC-I expression on various metastatic tumor cells, thereby rendering them susceptible to T cell recognition. The mechanism of anti-tumor effects of CBG involved the Hippo-YAP, TRP channels, EGFR-RAS pathways, and targeted tumor-secreted cytokines. The Hippo-YAP pathway is a crucial cellular signaling pathway that regulates organ size, cell proliferation, and apoptosis. When this pathway is dysregulated, it can contribute to tumorigenesis.
Recently, a paper evaluated the cytotoxic and cytostatic effects of CBG alone or in combination with curcumin and piperine in colon carcinoma cell lines HCT116 and HT29. Both mono and combination treatments demonstrated a notable reduction in the expression of the YAP oncogene in cell lines. Cannabinoid compounds, along with curcumin/piperine, effectively inhibit the proliferation of HCT116 cells by activating the Hippo signaling pathway. In contrast, the suppression of proliferation in the HT29 cell line appears to be mediated by a decrease in YAP expression independent of Hippo signaling. These findings underscore CBG's multifaceted potential in modulating critical pathways, presenting it as a noteworthy candidate for therapeutic interventions in various cancers.
In a study conducted by Lamtha and coworkers, the kinase-inhibition activity of CBG to tyrosine-kinase of EGFR, which is involved in over 70% of all cancers, was evaluated. The binding kinetics information indicated that CBG had a high binding affinity and kinase inhibitory activity against EGFR-TK. In addition, CBG significantly induced cell apoptosis in the EGFR-positive cancer A431 line. Zeppa et al. investigated the effects of CBG on pancreatic ductal adenocarcinoma (PDAC) cell lines PANC-1 and MIAPaCa-1. Their findings demonstrated that CBG reduced mTOR protein expression and suppressed EGFR expression in both of the two cell lines. Moreover, the data supported that CBG reduces downstream RAS signaling.
The combination of CBG and conventional chemotherapy agents holds promise for enhancing treatment efficacy. Potentiation of chemotherapy and reduction of chemotherapy side effects are the potential ways by combining CBG with chemotherapy. CBG alone was found to suppress hormone-refractory prostate cancer (HRPC) development in a mouse model of prostate cancer (TRAMP mice) via reprogramming metabolic and oncogenic signaling, although this effect was less pronounced than CBD. However, the two in combination exhibited potent anti-cancer effects even in mice unresponsive to enzalutamide (androgen receptor antagonist) treatment. As such, combination therapy may be an attractive adjuvant therapeutic option for prostate cancer patients.
Further studies in pre-clinical in vivo models on CBG are necessary to better understand its role in cancer progression and immune escape. In vivo studies would be particularly useful to more deeply investigate its anticancer effects. More research is needed to fully understand the interactions between CBG and chemotherapy drugs. However, the potential benefits of this combination warrant further investigation.
Conditions that cite this compound
These condition guides point here — they cover the same compound from the patient side.