Neuroinflammation

VCE-003.2 and VCE-004.8 are new cannabinoid derivatives that diminish neuroinflammation

Chronic neuroinflammation has been described in neurodegenerative diseases such as Multiple Sclerosis, Amyothropic Lateral Sclerosis, Huntington’s, Parkinson’s and Alzheimer’s Diseases. Neuroinflammation is defined as a wide spectrum of complex cellular responses at the Central Nervous System that include activation of microglia and astrocytes, elevations in proinflammatory cytokines, infiltration of peripheral leukocytes and secondary degeneration. Activation of the endogenous protective mechanisms against neuroinflammation, neuroprotection, could be the most promising strategy for the development of new therapies against these neurodegenerative disorders.

Cannabinoids have shown to exert neuroprotective actions in animal models by acting at different targets including PPARγ and CB2. PPARγ agonist has been described to have clear therapeutic effect on neurodegenerative diseases (reviewed by Skerrett et al., 2014; and Mandrekar-Colucci et al., 2013). Activation of PPARs can reduce inflammation, confer neuroprotection, and enhance axonal growth and remyelination. On the other hand, neuroprotective effects of CB2 agonists are associated with suppression of microglia via inhibiting the release of neurotoxic factors and by decreasing neuronal cell damage (reviewed by Rom et al., 2013).

VCE-003.2 and VCE-004.8 are two new non-psychotropic cannabinoid derivatives that diminish neuroinflammation in several mice models of neurodegenerative diseases, acting as PPARγ modulators. Additionally, VCE-004.8 is a CB2 agonist. As neuroprotective compounds, VCE-003.2 development is focused on Huntington’s Disease and VCE-004.8 development is focused on Multiple Sclerosis.

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