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      A review of nabilone in the treatment of chemotherapy-induced nausea and vomiting

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          Abstract

          Chemotherapy-induced nausea and vomiting (CINV) in cancer patients places a significant burden on patients’ function and quality of life, their families and caregivers, and healthcare providers. Despite the advances in preventing CINV, a substantial proportion of patients experience persistent nausea and vomiting. Nabilone, a cannabinoid, recently received Food and Drug Administration approval for the treatment of the nausea and vomiting in patients receiving cancer chemotherapy who fail to achieve adequate relief from conventional treatments. The cannabinoids exert antiemetic effects via agonism of cannabinoid receptors (CB1 and CB2). Clinical trials have demonstrated the benefits of nabilone in cancer chemotherapy patients. Use of the agent is optimized with judicious dosing and selection of patients.

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          The molecular logic of endocannabinoid signalling.

          Daniele Piomelli (2003)
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            Role of endogenous cannabinoids in synaptic signaling.

            Tamás Freund, István Katona, Daniele Piomelli (2003)
            Research of cannabinoid actions was boosted in the 1990s by remarkable discoveries including identification of endogenous compounds with cannabimimetic activity (endocannabinoids) and the cloning of their molecular targets, the CB1 and CB2 receptors. Although the existence of an endogenous cannabinoid signaling system has been established for a decade, its physiological roles have just begun to unfold. In addition, the behavioral effects of exogenous cannabinoids such as delta-9-tetrahydrocannabinol, the major active compound of hashish and marijuana, await explanation at the cellular and network levels. Recent physiological, pharmacological, and high-resolution anatomical studies provided evidence that the major physiological effect of cannabinoids is the regulation of neurotransmitter release via activation of presynaptic CB1 receptors located on distinct types of axon terminals throughout the brain. Subsequent discoveries shed light on the functional consequences of this localization by demonstrating the involvement of endocannabinoids in retrograde signaling at GABAergic and glutamatergic synapses. In this review, we aim to synthesize recent progress in our understanding of the physiological roles of endocannabinoids in the brain. First, the synthetic pathways of endocannabinoids are discussed, along with the putative mechanisms of their release, uptake, and degradation. The fine-grain anatomical distribution of the neuronal cannabinoid receptor CB1 is described in most brain areas, emphasizing its general presynaptic localization and role in controlling neurotransmitter release. Finally, the possible functions of endocannabinoids as retrograde synaptic signal molecules are discussed in relation to synaptic plasticity and network activity patterns.
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              International Union of Pharmacology. XXVII. Classification of cannabinoid receptors.

              A Howlett (2002)
              Two types of cannabinoid receptor have been discovered so far, CB(1) (2.1: CBD:1:CB1:), cloned in 1990, and CB(2) (2.1:CBD:2:CB2:), cloned in 1993. Distinction between these receptors is based on differences in their predicted amino acid sequence, signaling mechanisms, tissue distribution, and sensitivity to certain potent agonists and antagonists that show marked selectivity for one or the other receptor type. Cannabinoid receptors CB(1) and CB(2) exhibit 48% amino acid sequence identity. Both receptor types are coupled through G proteins to adenylyl cyclase and mitogen-activated protein kinase. CB(1) receptors are also coupled through G proteins to several types of calcium and potassium channels. These receptors exist primarily on central and peripheral neurons, one of their functions being to inhibit neurotransmitter release. Indeed, endogenous CB(1) agonists probably serve as retrograde synaptic messengers. CB(2) receptors are present mainly on immune cells. Such cells also express CB(1) receptors, albeit to a lesser extent, with both receptor types exerting a broad spectrum of immune effects that includes modulation of cytokine release. Of several endogenous agonists for cannabinoid receptors identified thus far, the most notable are arachidonoylethanolamide, 2-arachidonoylglycerol, and 2-arachidonylglyceryl ether. It is unclear whether these eicosanoid molecules are the only, or primary, endogenous agonists. Hence, we consider it premature to rename cannabinoid receptors after an endogenous agonist as is recommended by the International Union of Pharmacology Committee on Receptor Nomenclature and Drug Classification. Although pharmacological evidence for the existence of additional types of cannabinoid receptor is emerging, other kinds of supporting evidence are still lacking.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Ther Clin Risk Manag
                Journal ID (publisher-id): Therapeutics and Clinical Risk Management
                Title: Therapeutics and Clinical Risk Management
                Publisher: Dove Medical Press
                ISSN (Print): 1176-6336
                ISSN (Electronic): 1178-203X
                Publication date (Print): February 2008
                Publication date (Electronic): February 2008
                Volume: 4
                Issue: 1
                Pages: 99-107
                Affiliations
                [1 ]Pain Center, McGill University Health Center Montréal, Quebec, Canada
                [2 ]Pain and Symptom Clinic, CancerCare Manitoba, Winnipeg Manitoba, Canada
                [3 ]University of Toronto Toronto, Ontario, Canada
                Author notes
                Correspondence: Mark Ware E19.145 Montreal General Hospital, 1650 Cedar Avenue, Montreal, Quebec, Canada H3G 1A4 Tel +1 514 934 8242 Fax +1 514 934 8096 Email mark.ware@ 123456muhc.mcgill.ca
                Article
                DOI: 10.2147/TCRM.S1132
                PMC ID: 2503671
                PubMed ID: 18728826
                SO-VID: 30ec7e35-a297-486b-8716-398fc40aad7f
                Copyright © © 2008 Dove Medical Press Limited. All rights reserved
                History
                Categories
                Subject: Review

                ScienceOpen disciplines: Medicine
                Keywords: nabilone,pain,chemotherapy-induced nausea/vomiting
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: nabilone, pain, chemotherapy-induced nausea/vomiting

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