Mechanism of Action

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Cannabinoids act on multiple systems and it is understood that cannabinoids interact with many neurotransmitter and neuromodulator systems and important to note that cannabinoids have the ability to interact with all kinds of cellular pathways implicated in a range of diseases. GW is particularly well skilled at exploring these therapeutic prospects.

Cannabinoids act as ligands (a small molecule able to dock onto the binding site of a protein) conferring their ability to modulate a receptor’s behavior and consequently their downstream biological pathways. Although the cannabinoids may have similar structures, they display a remarkably wide array of actions. For example it is known that THC and THCV have very different biological effects.

How does CBD work in epilepsy?

As is the case for many other AEDs, the exact MOA by which CBD produces its anticonvulsant effects is unknown. Cannabidiol is a structurally novel anti-convulsant. Cannabidiol does not exert its anti-convulsant effects through CB1 receptors, nor through voltage-gated sodium channels. CBD may exert a cumulative anti-convulsant effect, modulating a number of endogenous systems including, but not limited to neuronal inhibition (synaptic and extrasynaptic GABA channels), modulation of intracellular calcium (TRPV, VDAC, GPR55), and possible anti-inflammatory effects (adenosine). CBD does not directly bind to, nor activate, CB1 and CB2 receptors at concentrations pharmacologically relevant to its anticonvulsant effect. Among the likely mechanisms of action, modulation of intra-cellular calcium via GPR-55, TRPV, and VDAC is under active investigation in our research laboratories. Additional mechanisms under exploration by our researchers include adenosine modulation, glycine and GABAergic modulation, and serotonin agonism.

References

Handbook of Cannabis, ISBN 978-0-19-966268-5, Oxford University Press

The Medicinal Use of Cannabis, 978-0853695172, London: Royal Society of Pharmacists.

Molecular targets of cannabidiol in neurological disorders, Bih and  Whalley, 2015 Neurotherapeutics, doi: 10.1007/s13311-015-0377-3