The quinol VCE-004.8 is a second-generation of semi-synthetic cannabinoid derived of natural non-psychotropic cannabidiol. VCE-004.8 behaves as a dual agonist of PPARγ and CB2 receptors. VCE-004.8 is currently developed under Collaborative Research Agreement with Emerald Health Pharmaceuticals Inc, a Canadian company focused on developing pharmaceutical candidates from cannabinoid derivatives. VCE-004.8 is currently under two development pathways:

Neuroinflammation – Multiple Sclerosis

As a neuroprotective compound, VCE-004.8 development is focused on the treatment of Multiple Sclerosis (MS). MS is a chronic, autoimmune disease, often disabling, that affects 2.5 million people worldwide. This disease leads to focal inflammatory demyelinated lesions and neurodegeneration. The current therapies for MS are unable to stop or cure the disease but basically trying to alleviate the symptoms and reduce the frequency of outbreaks. VCE-004.8 has a neuroprotective effect on different neurons cells and improves the clinical score in EAE and TMEV-DD mice models of MS, prevents microgliosis and demyelinization, and reduces the expression of pro-inflammatory markers. The effects of VCE-004.8 are made through PPARγ and CB2 agonism. PPARγ and CB2 have been specifically proposed as therapeutic targets of MS (Drew et al., 2008; Pryce et al., 2015).

Fibrotic diseases - Scleroderma

Scleroderma or Systemic Sclerosis (SSc) is a rare diseases associated with early and transient inflammation and vascular injury, followed by fibrosis affecting the skin and multiple internal organs. Currently, there is no cure for this disease, which affects 1-5/10.000 people. Both PPARγ and CB2 receptors represent attractive targets for the treatment of Scleroderma because of its potential role in modulating inflammatory and fibrotic responses (Reviewed by Dantas et al., 2015; Akhmetshina et al., 2009). VCE-004.8 inhibited TGFβ–mediated myofibroblast differentiation and impaired wound-healing activity. The anti-fibrotic efficacy in vivo was investigated in a murine model of dermal fibrosis induced by bleomycin. Through PPARγ and CB2 activation, VCE-004.8 reduced dermal thickness, blood vessels collagen accumulation and prevented mast cell degranulation and macrophage infiltration in the skin of experimental mice. These results also indicate the potential of VCE-004.8 in the treatment of other fibrotic diseases.

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