I didn't completely rub all the purple skin off the bottom section from this orientation in the photo, but it's basically a yin yang of two smaller seeds fused together. I wonder if these don't normally show up on the market because they are too heavy and the sorting machines discard them? This came out of the last 2 grams of seeded bud from my personal breeding project.
https://www.mdpi.com/1424-8247/19/4/560
Background/Objectives: Rheumatoid arthritis (RA) is a chronic, inflammatory, autoimmune disease that primarily affects the joints. Current treatments aim to relieve pain and limit joint damage; however, many are associated with significant side effects or high costs. Neutrophils play a critical role in RA development and progression by driving synovial inflammation and tissue damage, yet no approved therapies directly target neutrophil-mediated pathogenic mechanisms. Cannabinoids have demonstrated anti-inflammatory potential. Although cannabinoids have been studied in RA, the direct modulation of neutrophil-driven mechanisms by purified CBG has not been systematically addressed. To harness the cannabinoid potential, we investigated the effects of the purified cannabinoid Cannabigerol (CBG) on neutrophil-mediated immune responses in RA. Methods: We assessed the effects of CBG on human blood isolated neutrophil cytokine secretion, signal transduction and migration as ex vivo models. In addition, collagen antibody-induced arthritis (CAIA) was applied in C57BL/6 wt mice, and immune-cell recruitment and cytokine secretion were examined after CBG treatment. Results: Ex vivo experiments demonstrated that CBG hampered the secretion of pro-inflammatory cytokines from human neutrophils in a dose-dependent manner (TNF-α and IL-6 by 68% and 72%, respectively). Furthermore, CBG downregulated inflammatory signal transduction, such as P38-MAPK, ERK1/2 and Akt phosphorylationpost neutrophil activation by 41%, 54% and 78%, respectively. Importantly, 60% of the CBG downregulation of IL-6 was consistent with the CB2 receptor axis in a selective way. In addition, CBG attenuated neutrophil migration toward IL-8 by 67%. To further evaluate CBG therapeutic capacity, we used CAIA as an in vivo model. CBG treatment resulted in improving mice arthritis clinical scores and body weight in comparison to RA-diseased mice. Moreover, CBG reduced leukocyte recruitment to the inflamed joints by 48%, primarily through the inhibition of neutrophil and monocyte cells to 27% and 49%, respectively. Additionally, CBG showed its anti-inflammatory effect by decreasing inflammatory cytokines like IL-6 and IL-1β by 98% and 60% in the blood. Also, CBG reduced MCP-1 and IL-1β cytokines in the joints by 22% and 38%, respectively. Conclusions: These results show that CBG has anti-inflammatory capacity and therapeutic potential in regulating neutrophil-mediated immunity in RA. These findings are preclinical and require further validation before therapeutic positioning.
. . .
Cannabinoids produce more than 100 naturally occurring chemicals, the most abundant of which are Δ-9-tetrahydrocannabinol (THC), cannabidiol (CBD), terpenes and flavonoids. THC and CBD bind with cannabinoid receptors (CB1 and CB2), which are present in the brain, immune system and many organs [20]. THC and CBD help to manage conditions ranging from chronic pain persistent inflammation, cancer, inflammatory bowel disease, and neurological disorders to even viral diseases such as Human Immunodeficiency virus (HIV) and SARS-CoV-2 [21]. Both THC and CBD exhibit promising therapeutic properties; however, impairments and the increased incidence of mental health diseases are associated with acute and chronic THC use, respectively, and significant side effects are associated with the chronic use of high-dose CBD [22]. Preclinical in vitro and in vivo studies show promising results regarding the anti-arthritic properties of cannabinoids, psychoactive and non-psychoactive alike [23]. Our previous studies demonstrated that a high-CBD extract (CBD-X) significantly reduced pro-inflammatory cytokine secretion in human-derived PBMCs, neutrophils and T cells [24]. More recent findings further show that CBD-X exerts anti-inflammatory effects in rheumatoid arthritis by inhibiting pro-inflammatory cytokine secretion, limiting immune-cell recruitment and attenuating inflammatory signal transduction [25]. However, CBD-X is an extract that has 37% CBD, 1.7% THC, 0.3% CBG and other unknown terpenes and flavonoids [25]. Therefore, we decided to focus our research on purified cannabinoids.
Cannabigerol (CBG) serves as the precursor molecule for the most abundant cannabinoids. While THC and CBD have been more widely studied than CBG, it has had increased attention due to the wide range of potential health benefits [26]. Studies indicate that CBG may have therapeutic potential in treating neurologic disorders (e.g., Huntington disease, Parkinson disease and multiple sclerosis) and inflammatory bowel disease, as well as having antibacterial activity [27]. Moreover, there are anti-inflammatory effects of CBG in rheumatoid arthritis synovial fibroblasts and peripheral blood mononuclear cell cultures [28]. Furthermore, research showed CBG has potential anti-inflammatory properties, including the diabetic kidney disease progression of rats subjected to a high-fat, high-sucrose diet [29].
CBG is a multi-target player that interacts with the endocannabinoid system and other key signaling pathways, such as CB1, CB2, transient receptor potential (TRP) channels and α2-adrenoceptor, potentially influencing inflammation, pain, neurodegeneration and other ailments. CB1 and CB2 are the two main types of cannabinoid receptors. Unlike THC and CBD, CBG does not bind directly to the CB1 receptors in the brain, which are responsible for the psychoactive effects of cannabis. CBG weakly agonizes the action of CB1 and partially acts as an agonist on CB2 receptor agonists [26]. Cannabinoid receptor 2 deficiency exacerbates inflammation and neutrophil recruitment [30]. The expression of the CB2 mRNA can be detected in neutrophils [31]. The CB2 receptor is primarily expressed only when there is active inflammation. Accordingly, CBG’s interaction with CB2 downregulates the inflammation [32]. Furthermore, CBG interacts with TRP channels, which play a crucial role in regulating the cytoplasmic calcium concentration from the extracellular sources as well as the calcium stored within the endoplasmic reticulum (ER). CBG serves as a strong agonist of TRPA1 and a weaker agonist of TRPV1, TRPV2 and TRPV4 while antagonizing TRPM8 (TRP melastatin type 8) [26]. CBG acts as a potent agonist of Peroxisome proliferator-activated receptor gamma (PPARγ), a transcription factor that suppresses NFκB or MAP kinases [33]. In addition, CBG is a potent serotonin 1A receptor (5-HT1A) antagonist, which is known to reduce the activity of NF-κB and the phosphorylation of its inhibitor α (IκB- α), resulting in a decrease in cytokine secretion [29].
Recent computational modeling indicates that CBG possesses a unique 3D conformational flexibility, characterized by ‘coiled’ and ‘stapled’ poses that are sterically distinct from the rigid bicyclic structure of CBD [34]. In addition, CBG exhibits affinity and activity characteristics between Δ9-THC and CBD at the cannabinoid receptors but appears to be unique in its interactions with the α-2 adrenoceptors, PPARγ and 5-HT1A [27].
However, CBG shows anti-inflammatory effects, but due to the lack of research, it is not widely used. Its physicochemical properties lead to considerable challenges, such as poor intestinal absorption, extensive first-pass metabolism, low bioavailability and variable brain penetration, all of which limit its effective application in clinical settings [35]. In addition, the regulatory status of cannabis, sources for cannabis and funding to support studies are difficult barriers to navigate [36].
There is growing interest in CBG and its promising therapeutic potential in treating immune-related diseases. Our aim in this study is to examine the regulatory effect of CBG in mitigating inflammatory RA disease severity through regulating neutrophil activity. We hypothesized that CBG through CB2 receptor mediation directly suppresses neutrophil activation and recruitment, thereby attenuating RA severity.
https://www.mdpi.com/1424-8247/19/4/560
Background/Objectives: Rheumatoid arthritis (RA) is a chronic, inflammatory, autoimmune disease that primarily affects the joints. Current treatments aim to relieve pain and limit joint damage; however, many are associated with significant side effects or high costs. Neutrophils play a critical role in RA development and progression by driving synovial inflammation and tissue damage, yet no approved therapies directly target neutrophil-mediated pathogenic mechanisms. Cannabinoids have demonstrated anti-inflammatory potential. Although cannabinoids have been studied in RA, the direct modulation of neutrophil-driven mechanisms by purified CBG has not been systematically addressed. To harness the cannabinoid potential, we investigated the effects of the purified cannabinoid Cannabigerol (CBG) on neutrophil-mediated immune responses in RA. Methods: We assessed the effects of CBG on human blood isolated neutrophil cytokine secretion, signal transduction and migration as ex vivo models. In addition, collagen antibody-induced arthritis (CAIA) was applied in C57BL/6 wt mice, and immune-cell recruitment and cytokine secretion were examined after CBG treatment. Results: Ex vivo experiments demonstrated that CBG hampered the secretion of pro-inflammatory cytokines from human neutrophils in a dose-dependent manner (TNF-α and IL-6 by 68% and 72%, respectively). Furthermore, CBG downregulated inflammatory signal transduction, such as P38-MAPK, ERK1/2 and Akt phosphorylationpost neutrophil activation by 41%, 54% and 78%, respectively. Importantly, 60% of the CBG downregulation of IL-6 was consistent with the CB2 receptor axis in a selective way. In addition, CBG attenuated neutrophil migration toward IL-8 by 67%. To further evaluate CBG therapeutic capacity, we used CAIA as an in vivo model. CBG treatment resulted in improving mice arthritis clinical scores and body weight in comparison to RA-diseased mice. Moreover, CBG reduced leukocyte recruitment to the inflamed joints by 48%, primarily through the inhibition of neutrophil and monocyte cells to 27% and 49%, respectively. Additionally, CBG showed its anti-inflammatory effect by decreasing inflammatory cytokines like IL-6 and IL-1β by 98% and 60% in the blood. Also, CBG reduced MCP-1 and IL-1β cytokines in the joints by 22% and 38%, respectively. Conclusions: These results show that CBG has anti-inflammatory capacity and therapeutic potential in regulating neutrophil-mediated immunity in RA. These findings are preclinical and require further validation before therapeutic positioning.
. . .
Cannabinoids produce more than 100 naturally occurring chemicals, the most abundant of which are Δ-9-tetrahydrocannabinol (THC), cannabidiol (CBD), terpenes and flavonoids. THC and CBD bind with cannabinoid receptors (CB1 and CB2), which are present in the brain, immune system and many organs [20]. THC and CBD help to manage conditions ranging from chronic pain persistent inflammation, cancer, inflammatory bowel disease, and neurological disorders to even viral diseases such as Human Immunodeficiency virus (HIV) and SARS-CoV-2 [21]. Both THC and CBD exhibit promising therapeutic properties; however, impairments and the increased incidence of mental health diseases are associated with acute and chronic THC use, respectively, and significant side effects are associated with the chronic use of high-dose CBD [22]. Preclinical in vitro and in vivo studies show promising results regarding the anti-arthritic properties of cannabinoids, psychoactive and non-psychoactive alike [23]. Our previous studies demonstrated that a high-CBD extract (CBD-X) significantly reduced pro-inflammatory cytokine secretion in human-derived PBMCs, neutrophils and T cells [24]. More recent findings further show that CBD-X exerts anti-inflammatory effects in rheumatoid arthritis by inhibiting pro-inflammatory cytokine secretion, limiting immune-cell recruitment and attenuating inflammatory signal transduction [25]. However, CBD-X is an extract that has 37% CBD, 1.7% THC, 0.3% CBG and other unknown terpenes and flavonoids [25]. Therefore, we decided to focus our research on purified cannabinoids.
Cannabigerol (CBG) serves as the precursor molecule for the most abundant cannabinoids. While THC and CBD have been more widely studied than CBG, it has had increased attention due to the wide range of potential health benefits [26]. Studies indicate that CBG may have therapeutic potential in treating neurologic disorders (e.g., Huntington disease, Parkinson disease and multiple sclerosis) and inflammatory bowel disease, as well as having antibacterial activity [27]. Moreover, there are anti-inflammatory effects of CBG in rheumatoid arthritis synovial fibroblasts and peripheral blood mononuclear cell cultures [28]. Furthermore, research showed CBG has potential anti-inflammatory properties, including the diabetic kidney disease progression of rats subjected to a high-fat, high-sucrose diet [29].
CBG is a multi-target player that interacts with the endocannabinoid system and other key signaling pathways, such as CB1, CB2, transient receptor potential (TRP) channels and α2-adrenoceptor, potentially influencing inflammation, pain, neurodegeneration and other ailments. CB1 and CB2 are the two main types of cannabinoid receptors. Unlike THC and CBD, CBG does not bind directly to the CB1 receptors in the brain, which are responsible for the psychoactive effects of cannabis. CBG weakly agonizes the action of CB1 and partially acts as an agonist on CB2 receptor agonists [26]. Cannabinoid receptor 2 deficiency exacerbates inflammation and neutrophil recruitment [30]. The expression of the CB2 mRNA can be detected in neutrophils [31]. The CB2 receptor is primarily expressed only when there is active inflammation. Accordingly, CBG’s interaction with CB2 downregulates the inflammation [32]. Furthermore, CBG interacts with TRP channels, which play a crucial role in regulating the cytoplasmic calcium concentration from the extracellular sources as well as the calcium stored within the endoplasmic reticulum (ER). CBG serves as a strong agonist of TRPA1 and a weaker agonist of TRPV1, TRPV2 and TRPV4 while antagonizing TRPM8 (TRP melastatin type 8) [26]. CBG acts as a potent agonist of Peroxisome proliferator-activated receptor gamma (PPARγ), a transcription factor that suppresses NFκB or MAP kinases [33]. In addition, CBG is a potent serotonin 1A receptor (5-HT1A) antagonist, which is known to reduce the activity of NF-κB and the phosphorylation of its inhibitor α (IκB- α), resulting in a decrease in cytokine secretion [29].
Recent computational modeling indicates that CBG possesses a unique 3D conformational flexibility, characterized by ‘coiled’ and ‘stapled’ poses that are sterically distinct from the rigid bicyclic structure of CBD [34]. In addition, CBG exhibits affinity and activity characteristics between Δ9-THC and CBD at the cannabinoid receptors but appears to be unique in its interactions with the α-2 adrenoceptors, PPARγ and 5-HT1A [27].
However, CBG shows anti-inflammatory effects, but due to the lack of research, it is not widely used. Its physicochemical properties lead to considerable challenges, such as poor intestinal absorption, extensive first-pass metabolism, low bioavailability and variable brain penetration, all of which limit its effective application in clinical settings [35]. In addition, the regulatory status of cannabis, sources for cannabis and funding to support studies are difficult barriers to navigate [36].
There is growing interest in CBG and its promising therapeutic potential in treating immune-related diseases. Our aim in this study is to examine the regulatory effect of CBG in mitigating inflammatory RA disease severity through regulating neutrophil activity. We hypothesized that CBG through CB2 receptor mediation directly suppresses neutrophil activation and recruitment, thereby attenuating RA severity.
One of the world's biggest seedbanks, NASC, has a series of interview Q/A with the breeders they carry. One thing that stood out to me was how many breeders were talking about how they moved to Maine for the better laws. They didn't explain in the videos what they meant so I had to look it up myself.
Level I
| Application Fee | $20,000 |
|---|---|
| Initial Fee (Certificate of Operation) | $180,000 |
| Annual License Renewal Fee | $200,000 |
Level II
| Application Fee | $2,000 |
|---|---|
| Initial Fee (Certificate of Operation) | $18,000 |
| Annual License Renewal Fee | $20,000Level I Application Fee $20,000Initial Fee (Certificate of Operation) $180,000Annual License Renewal Fee $200,000Level IIApplication Fee $2,000Initial Fee (Certificate of Operation) $18,000Annual License Renewal Fee $20,000 |
https://mainecannabis.org/licensing/cultivation
A Tier 1 cultivation facility license comprises two subcategories: plant-count-based Tier 1 cultivation facility license and plant-canopy-based Tier 1 cultivation facility license. The plant-count-based Tier 1 cultivation facility license permits the licensee to cultivate a specified number (up to 30) of mature marijuana plants and an unlimited number of immature marijuana plants and seedlings. The plant-canopy-based Tier 1 cultivation facility license allows the cultivation of not more than 500 square feet of plant canopy area of mature marijuana plants.
A Tier 2 cultivation facility license authorizes the licensee to cultivate up to 2,000 square feet of plant canopy of mature plants. A Tier 3 cultivation facility licensee can cultivate up to 7,000 square feet of plant canopy of mature plants, while a Tier 4 cultivation facility licensee is permitted to cultivate no more than 20,000 square feet of plant canopy of mature plants, unless allowed to do so by the DAFS (Department of Administrative and Financial Services) under 28-B MRS §304. A nursery cultivation facility license authorizes the licensee to cultivate up to a 1,000-square foot plant canopy area, subject to the provisions and limitations of 28-B MRS §501(3).
| License Type | Annual License Fee (Outdoor Only) | Annual License Fee (Indoor/both) | Application Fee |
|---|---|---|---|
| Tier 1 Cultivation Facility (Plant-Count-Based) | $9 per mature plant | $17 per mature plant | $100 |
| Tier 1 Cultivation Facility (Plant-Canopy-Based) | $250 | $500 | $100 |
| Tier 2 Cultivation Facility | $1,500 | $3,000 | $500 |
| Tier 3 Cultivation Facility | $5,000 | $10,000 | $500 |
| Tier 4 Cultivation Facility (for each increase in canopy size) | $15,000 (+$5,000) | $30,000 (+$10,000) | $500 |
| Nursery Cultivation Facility | $350 | $350 | $60License Type Annual License Fee (Outdoor Only) Annual License Fee (Indoor/both) Application FeeTier 1 Cultivation Facility (Plant-Count-Based) $9 per mature plant $17 per mature plant $100Tier 1 Cultivation Facility (Plant-Canopy-Based) $250 $500 $100Tier 2 Cultivation Facility $1,500 $3,000 $500Tier 3 Cultivation Facility $5,000 $10,000 $500Tier 4 Cultivation Facility (for each increase in canopy size) $15,000 (+$5,000) $30,000 (+$10,000) $500Nursery Cultivation Facility $350 $350 $60 |
So you see a massive gulf between the states like ours and Maine in their layout of cultivation tiers. Maine offers two lightweight tiers at the bottom that are quite affordable for a breeder or hobbyist to grow for the purpose of the seed/clone market. The way these breeders work is they do they primary work with a small license like this, and then send bulk seed off to friends in California or other places to do larger phenotype hunts and dial down the genetics.
If there is literally a pattern of one type of business saying we moved to X state because the laws there are better, doesn't it warrant other states looking at their own laws? We already had a Tier III Cultivation License available in Ohio that was smaller than what we have now... And they removed it to focus on only the big players with more money. Who's idea was it to make Ohio less business friendly? Is that the kind of decision politicians are too full of ego to ever unmake when they realize it was a mistake?
https://marijuana.school/minnesotas-new-2026-cannabis-omnibus-bill/
The newly minted Ratio Hemp-Infused Cannabis Product category explicitly allows businesses holding low-potency licenses to cross over and sell significantly stronger formulations—provided they balance the intoxicating THC content with therapeutic, non-intoxicating secondary cannabinoids like CBD, CBG, CBN, or CBC.
The Golden Rule for Higher Potency: To unlock the expanded milligram allowances, products must maintain a structured ratio. Manufacturers are permitted to include up to 100 mg of secondary cannabinoids per serving alongside the increased THC counts.
This is for people age 40+ without Parkinsons, or 30+ with a diagnosis.
Michael J. Fox has been advertising this on Instagram as part of his Parkinsons research. After signing up and answering basic questions about yourself you will get a package in the mail. This has a pencil and 4 booklets each with 10 scratch and sniff multiple choice questions. You log back into the website and enter the data as you scratch and sniff each page. Trust me when I say many of these questions are very pertinent to whether or not you are identifying the same smells as other cannabis breeders.
I don't want to give away any of the choices because that would influence other people. Let's just say a broad range is covered and you would do yourself some good to see how you interpret them. Worst case scenario you spent some time and helped medical research only to realize you get confused by certain scents. The test only took me thirty minutes.
https://en.wikipedia.org/wiki/HU-345
I'm curious if anyone else thinks it is perhaps unwise to experiment with such high ratios of CBN in vaporization devices until we know exactly what happens when we do that. Currently only one of the possible byproducts has a chemical name, and we know almost nothing about how it effects humans. I see people making their own mixes with large amounts of CBN, just like the industry is. For edibles and tinctures, fine, since you aren't heating it again to further degrade it.
What concerns me is starting off with an amount of CBN that is many times above what is naturally possible in the plant were it sun dried like people did decades ago (or perhaps in some cultures still) and then heating it again. I feel like products whether professional or homemade should start off mimicking what the plant would produce unless they know it is safe otherwise to go outside those bounds.
For reference CBD degrades to CBE. If you are smoking a type 3/2 a tiny portion will degrade every time. I've experimented some with it, as GVB BioPharma produced a Crystal Resistant Distillate high in CBE and other minors which I've used on rare occasions. I haven't noticed any weird effect from that so far. When I first tried it, I definitely noticed it felt different, and more "whole" than any commercial cartridge I had ever purchased. Obviously I haven't used grams and grams of it, so I can't state for certain it's safe or not, just that I don't notice side effects.
CBC degrades into CBL, some naturally before you've even smoked/vaped it. Again, CBL is a known cannabinoid that was first isolated in the 1960's and you can buy in pure form today if you want to experiment with it. It is suspected to have health benefits, but like many of the relatively unknown minors, nobody seems to be researching it yet.
Now when it comes to CBN, itself already being a degradation of THC, I just don't want to jump to the assumption before we have any actual evidence that whatever it turns into is a useful or positive drug. Wikipedia lists HU-345 as a "non-classical cannabinoid", whatever that means. If any of you have used these products feel free to share your experiences with them. Do you think going above like 2-5% CBN in a vaporizer adds any benefit to the user? How is it different? Have you also tried products that were closer to natural ratios of CBN to THC?
https://www.frontiersin.org/journals/chemistry/articles/10.3389/fchem.2022.1038729/full