| Features: |
| Cannabidiolic acid (CBDA) is the acidic precursor of cannabidiol (CBD) found in Cannabis sativa. - Note that although CBDA shares some pharmacological properties with CBD, its profile can differ due to its carboxylic acid group, which may affect its bioavailability, receptor binding, and overall cellular uptake. Cannabidiolic acid (CBDA) shows promise in modulating several pathways that are relevant to cancer biology—including COX-2 inhibition, PPARγ activation, apoptosis induction, and anti-inflammatory effects. In parallel, CBDA may offer additional benefits such as anti-emetic, anxiolytic, and potential neuroprotective effects. However, the current body of research is largely preclinical. CBDA is often found in raw cannabis plants and does not undergo decarboxylation like its more well-known counterpart cannabidiol (CBD). Unlike the tetrahydrocannabinol (THC) found in cannabis, CBDA is non-psychoactive. This means it does not cause the "high" or altered state of mind commonly associated with cannabis use. CBDA does not directly bind to the primary cannabinoid receptors (CB1 and CB2) in the brain that are responsible for psychoactive effects. Pathways: -CBDA may modulate receptors beyond the classical CB1 and CB2, such as transient receptor potential (TRP) channels (e.g., TRPV1) and possibly the orphan receptor GPR55, thereby influencing cell signaling, calcium homeostasis, and related pathways. -Inhibition of cyclooxygenase enzymes (COX) -Mitochondrial dysfunction and the activation of caspases -Modulation of the PI3K/Akt Pathway -Affect the MAPK family of pathways, including ERK, JNK, and p38 kinases -Modulating matrix metalloproteinases (MMPs) -As an antioxidant (or under some conditions a pro-oxidant) |
| Source: HalifaxProj(inhibit) |
| Type: |
| Cyclooxygenase-2 (COX-2) is an enzyme that plays a critical role in the conversion of arachidonic acid to prostaglandins, which are lipid compounds involved in various physiological processes, including inflammation, pain, and fever. COX-2 is an inducible enzyme, meaning its expression is typically low in normal tissues but can be upregulated in response to inflammatory stimuli, growth factors, and certain oncogenic signals. -Cyclooxygenase-2 (COX-2), the rate-limiting enzyme in prostaglandin biosynthesis, plays a key role in inflammation and circulatory homeostasis. -COX-2 is an inducible enzyme that is upregulated in response to pro-inflammatory signals, including cytokines (e.g., IL-1β, TNF-α) and growth factors. COX-2 is often overexpressed in various tumors, including colorectal, breast, lung, and prostate cancers. The prostaglandins produced by COX-2, particularly prostaglandin E2 (PGE2), have several effects that can facilitate cancer progression: Cell Proliferation: PGE2 can promote the proliferation of cancer cells by activating signaling pathways such as the PI3K/Akt and MAPK pathways. Nonselective NSAIDs, such as aspirin and ibuprofen, inhibit both COX-1 and COX-2. Epidemiological studies have suggested that regular use of NSAIDs may reduce the risk of certain cancers, particularly colorectal cancer. Drugs specifically targeting COX-2, such as celecoxib, have been developed. COX-2 and xanthine oxidase are ROS-producing pro-oxidant enzymes that contribute to inflammation. Elevated COX‑2 levels, often found in inflammatory conditions or certain types of cancers, can contribute to increased production of ROS. |
| 1081- | CBDA, | Down-regulation of cyclooxygenase-2 (COX-2) by cannabidiolic acid in human breast cancer cells |
| - | in-vitro, | BC, | MDA-MB-231 |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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