Cannabidiol
Cannabidiol
Definition
A phytocannabinoid derived from Cannabis species, which is devoid of psychoactive activity, with analgesic, anti-inflammatory, antineoplastic and chemopreventive activities. Upon administration, cannabidiol (CBD) exerts its anti-proliferative, anti-angiogenic and pro-apoptotic activity through various mechanisms, which likely do not involve signaling by cannabinoid receptor 1 (CB1), CB2, or vanilloid receptor 1. CBD stimulates endoplasmic reticulum (ER) stress and inhibits AKT/mTOR signaling, thereby activating autophagy and promoting apoptosis. In addition, CBD enhances the generation of reactive oxygen species (ROS), which further enhances apoptosis. This agent also upregulates the expression of intercellular adhesion molecule 1 (ICAM-1) and tissue inhibitor of matrix metalloproteinases-1 (TIMP1) and decreases the expression of inhibitor of DNA binding 1 (ID-1). This inhibits cancer cell invasiveness and metastasis. CBD may also activate the transient receptor potential vanilloid type 2 (TRPV2), which may increase the uptake of various cytotoxic agents in cancer cells. The analgesic effect of CBD is mediated through the binding of this agent to and activation of CB1.
Also known as 1,3-Benzenediol, 2-(3-methyl-6-(1-methylethenyl)-2-cyclohexen-1-yl)-5-pentyl-, (1R-trans)-, CANNABIDIOL, CBD, CBD Oil, Epidiolex, GWP42003-P — per NCIT
Also identified as
- ATC N03AX24 per RXNORM
- NCIT NCIT:C118452 per NCIT
- SCTID 771981005 per RXNORM
- SCTID 96223000 per RXNORM
- UNII 19GBJ60SN5 per RXNORM
Indications
| Disease | Relation | Source |
|---|---|---|
| Lennox-Gastaut syndrome | may treat | MEDRT · Public domain (U.S. Government work) |
Organ Effects
| Organ | Side effect / interaction | Source |
|---|---|---|
| Brain | may treat a disease of this organ | DERIVED · CC BY 4.0 |
| Central nervous system | may treat a disease of this organ | DERIVED · CC BY 4.0 |
| Nervous system | may treat a disease of this organ | DERIVED · CC BY 4.0 |
3 entries above are marked DERIVED: Atlas Médico inferred them by combining two sourced claims, and no source asserts these links directly. Treat them as a navigation aid, not as a clinical statement.