Marijuana mouth spray for cancer patients tough to abuse – NBC

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“The medical marijuana drug Sativex, which could be approved in the United States in the coming years as a treatment for pain relief, has little potential for abuse, experts say.

The British pharmaceutical company GW Pharmaceuticals is currently testing the drug, which is delivered as a mouth spray and called Sativex, in clinical trials. The company plans to seek U.S. Food and Drug Administration approval for the drug as a treatment for cancer pain when the trials are completed, likely sometime in 2014, a spokesperson for GW Pharmaceuticals told MyHealthNewsDaily.

The active ingredients in Sativex, known as cannabinoids, are derived from the cannabis plant. It is the first marijuana-based drug to be made by extracting the compounds from the plant, rather than synthesizing them. Two other drugs, Marinol and Cesamet, based on synthetic cannabinoids, were approved by the FDA in the 1980s.”

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The Cannabinoid CB2 Receptor as a Target for Inflammation-Dependent Neurodegeneration

“THE CANNABINOID CB2 RECEPTOR AS A BIORATIONAL TARGET FOR THE TREATMENT OF NEURODEGENERATION. The presence of CB2 receptors in microglia in the human Alzheimer’s diseased brain suggests that CB2 may provide a novel target for a range of neuropathologies.

 The first approved cannabinoid drugs were analogues of Δ9-tetrahydrocannabinol (Δ9-THC). Dronabinol is a natural isomer of THC that is found in the cannabis plant, and Marinol contains synthetic dronabinol. Marinol, and another analogue nabilone (Cesamet ) are used to prevent nausea and vomiting after treatment with anti-cancer medicines. More recently, GW-100 (Sativex) which combines nearly equal amounts of Δ9-THC and cannabidiol in a whole plant extract from cultivated cannabis, has been approved in Canada…

We conclude that the administration of CB2 agonists and antagonists may differentially alter microglia-dependent neuroinflammation. CB2 specific compounds have considerable therapeutic appeal over CB1 compounds, as the exclusive expression of CB2 on immune cells within the brain provides a highly specialised target, without the psychoactivity that plagues CB1 directed therapies.

In addition, CB2 activation appears to prevent or decrease microglial activation.

In a rodent model of Alzheimer’s disease microglial activation was completely prevented by administration of a selective CB2 agonist.”

http://www.ncbi.nlm.nih.gov/pubmed/18615177