CP-x Synthetic Cannabinoids Research Dashboard
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CannaKeys has 85 studies associated with CP-x Synthetic Cannabinoids.
Here is a small sampling of CP-x Synthetic Cannabinoids studies by title:
- Synthetic cannabinoid CP-55,940 induces apoptosis in a human skeletal muscle model via regulation of CB1 receptors and L-type Ca2+ channels
- Age-dependent hormesis-like effects of the synthetic cannabinoid CP55940 in C57BL/6 mice
- Cannabinoid-profiled agents improve cell survival via reduction of oxidative stress and inflammation, and Nrf2 activation in a toxic model combining hyperglycemia+Aβ 1-42 peptide in rat hippocampal neurons
- Comparing the effects of endogenous and synthetic cannabinoid receptor agonists on survival of gastric cancer cells.
- Biased Type 1 Cannabinoid Receptor Signaling Influences Neuronal Viability in a Cell Culture Model of Huntington Disease.
Components of the CP-x Synthetic Cannabinoids Research Dashboard
- Top medical conditions associated with CP-x Synthetic Cannabinoids
- Proven effects in clinical trials for CP-x Synthetic Cannabinoids
- Receptors associated with CP-x Synthetic Cannabinoids
- Individual study details for CP-x Synthetic Cannabinoids
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Overview - CP-x Synthetic Cannabinoids
Description of CP-x Synthetic Cannabinoids
The CP- class of synthetic cannabinoids are named after the company Carl Pfizer where they were first synthesized. CP-55,940 was discovered in 1974 and is one of the most studied member of this class. It binds to the same classical endocannabinoid receptor sites i.e., CB1 and CB2 as THC albeit with stronger efficacies (see receptor binding).
Here we focus on CP-55,940
Other members of the CP-x class include: • CP-47,497 • CP-50,556-1 (aka Levonantradol) • CP-55,244 • CP-945,598 (aka Otenabant) • Plus others
Other Names:
CP Family of Synthetic CannabinoidsCP-55,940 syn.: CP55,940; CP-55940 plus numerous supplier-based synonyms.
IUPAC Name: 2-[(1R,2R,5R)-5-hydroxy-2-(3-hydroxypropyl)cyclohexyl]-5-(2-methyloctan-2-yl)phenol
Molecular Formula: C24H40O3
Source–PubChem
CP-x Synthetic Cannabinoids Properties and Effects
CP-55,940 may induce:
- Apoptosis in human embryonic rhabdomyosarcoma cell line (Ken-Ichi Tomiyama et al., 2020)
- Enhancement of cell viability and stimulation of mitochondrial membrane potential (Z. Elmazoglu et. al., 2020)
- Apoptotic mechanisms in gastric cancer cell lines (A. Ortega et al., 2016)
- Reduce CB1 protein levels and cell viability in Huntington's disease cell line (R. Laprairie et al., 2016)
- Reversal of urinary frequency in overactive bladder syndrome (E. Bakali 2016)
- Apoptosis in glioblastoma cell lines i.e., C6 and U373 (A. Ortega et al., 2015)
- Analgesic in sickle cell disease (Divyanshoo R. Kohli et al., 2010; David Cain et al., 2013)
- Reduction of SKF (dopamine D1 receptor agonist)-induced oral dyskinesia (Morten V Madsen et al., 2011)
- Antagonistic modulation of GPR55 with potential relevance to obesity (A. Kapur et al., 2009)
- Potent anti-inflammatory effect via a non-CB1/CB2 with potential relevance to rheumatoid arthritis (E. Selvi et al., 2008)
- Restoration of the integrity of human brain microvascular endothelial cells and the BBB following insults by HIV-1 Gp120 (Tzong-Shi Lu et al., 2008
- Reduction of radiation-induced emesis (N. Darmani et al., 2007)
- Co-administration of delta-9-THC with CP 55,940 prevented MDMA-induced hyperthermia instead causing a powerful hypothermia (K. Morley et al., 2004).
CP-x Synthetic Cannabinoids Receptor Binding
Endocannabinoid System (ECS) and CP-55,940:
- Agonist at CB1 with a mean Ki at ~0.6nM, which is ~40 times more potent than THC at the same receptor site (Gurney et al., 2014)
- Agonist at CB2 with a mean Ki at ~0.7nM, which is ~50 times more potent than THC at the same receptor site (Gurney et al., 2014)
Endocannabinoidome (eCBome) and CP-55,940:
- PPAR-Gamma with anti-inflammatory responses (S. O'Sullivan 2010)
- GPR55 antagonist/partial agonist (A. Kapur et al., 2009)
- 5-HT2A serotonin receptor sites (J. Franklin et al., 2013)
Ki legend:
- Full/strong agonist Ki ~1-9nM
- Moderate agonist Ki ~10-99nM
- Weak agonist Ki ~100-999nM
- Very weak agonist Ki ~1,000-up nM
(The reader is reminded that a smaller Ki is associated with the strongest effects.)
Disclaimers: Information on this site is provided for informational purposes only and is not meant to substitute for the advice provided by your own physician or other medical professional. You should not use the information contained herein for diagnosing a health problem or disease. If using a product, you should read carefully all product packaging. If you have or suspect that you have a medical problem, promptly contact your health care provider.
Information on this site is based on scientific studies (human, animal, or in vitro), clinical experience, or traditional usage as cited in each article. The results reported may not necessarily occur in all individuals. For many of the conditions discussed, treatment with prescription or over-the-counter medication is also available. Consult your physician, nutritionally oriented health care practitioner, and/or pharmacist for any health problem and before using any supplements or before making any changes in prescribed medications.
