Cannabidiol Compound, EHP-101, Seen to Prevent Nerve Cell Damage in MS Mouse Model

Cannabidiol Compound, EHP-101, Seen to Prevent Nerve Cell Damage in MS Mouse Model
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An investigational cannabidiol-derived compound called EHP-101 may help to boost remyelination, prevent nerve cell damage and lower the reactivity of microglia cells — immune cells of the brain and spinal cord — a  study in mouse models of multiple sclerosis (MS) reports.

EHP-101, being developed by Emerald Health Pharmaceuticals, was also reported to be of benefit in a model of scleroderma.

Emerald plans to start a Phase 1 clinical trial of the oral, cannabidiol (CDB)-derived potential treatment later this year.

These findings were presented at the recent 28th Annual Symposium of the International Cannabinoid Research Society (ICRS), held in Leiden, The Netherlands.

CBD is one of the more than 100 pharmacologically active compounds (cannabinoids) found in the cannabis plant.

Researchers investigated the effects of EHP-101 (previously known as VCE-004.8) in two mouse models of MS, the experimental autoimmune encephalomyelitis (EAE) and the Theiler’s virus-induced encephalopathy (TMEV) models.

In the TMEV model, treatment with EHP-101 — which is based on a new, synthetic cannabidiol — prevented such MS hallmark alterations as demyelination (the loss of the protective layer of nerve fibers, or axons, called myelin) and nerve cell damage. Its use also suggested an increase in remyelination.

In the widely used EAE mouse model, EHP-101 demonstrated marked dose-dependent benefits. In the spinal cord, it reduced the expression of diverse genes involved in MS, including inflammatory molecules and proteins implicated in cellular adhesion to other cells or the extracellular matrix — which provides structural and biochemical support to cells.

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Data also revealed lesser microgliosis, which is a nonspecific and intense reaction by microglia — a cell of the central nervous system — in response to damage. These effects were mediated through activation of the hypoxia inducible factor (HIF)-dependent neuroprotective pathway, known to play a role in immunological responses and the formation of blood vessels.

The MS-related study, “Effect of Oral VCE-004.8, A Cannabidiol Quinol Derivative On Experimental Autoimmune Encephalomyelitis,” was presented by Carmen Navarrete, PhD.

Results of these preclinical EHP-101 studies in MS mice were also published in the Journal of Neuroinflammation in March.

“The development of novel treatments aimed at axonal repair and remyelination remains a key objective in the treatment of MS,” Jim DeMesa, MD, CEO at Emerald, said in a press release. “Our scientists have demonstrated EHP-101’s potential to address this significant unmet medical need and possibly transform the treatment of MS, in addition to its potential as a disease-modifying treatment for scleroderma.”

Emerald’s study in scleroderma, Oral EHP-101 Alleviates Skin and Lung Fibrosis in Bleomycin Model of Scleroderma,“presented by Adela Garcia, expanded on previous research in showing that EHP-101 worked to prevent skin and lung fibrosis (scarring) in mice, with efficacy comparable to another synthetic cannabinoid derivative called ajulemic acid.

However, unlike ajulemic acid, EHP-101 was seen by researchers to lessened vascular damage. EHP-101 was also reported to decrease skin thickness and inhibit the infiltration of inflammatory cells, and further reduced the expression of genes and biomarkers associated with inflammation and fibrosis.

The scientists believe these results suggest that EHP-101 is a potential new way to manage and treat scleroderma and other fibrotic diseases.

According to Emerald,  EHP-101’s potential benefits are superior to other CBD products in development because of its greater  agonist activity via the cannabinoid receptors CB2 and PPAR-gamma. Prior research showed that these receptors help prevent inflammation and demyelination in the central nervous system, and the proliferation of fibers in the periphery.

José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has studied Biochemistry also at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario, in London, Ontario. His work ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has studied Biochemistry also at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario, in London, Ontario. His work ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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