What is Cesamet (nabilone)?

Cesamet provides proven benefits for the treatment of CINV. Cesamet addresses an unmet medical need by providing an alternative option for the treatment of CINV in patients with an inadequate response to conventional antiemetic treatments.¹

Cesamet has a unique mechanism of action from other antiemetics.^5,6 Nabilone is a synthetic cannabinoid similar to naturally occuring Cannabis sativa L. [Marijuana; delta-9-tetrahydrocannabinol (delata-9-THC)] for oral administration, that exerts its antiemetic effects via agonist action at omnipresent cannabinoid CB1 receptors in neural tissues.¹ Cesamet thereby functions as an omnineuromodulator^7,8 to modulate neuronal signaling in the central nervous system, including important regions that mediate nausea and vomiting.^9-12

Patients who have failed to respond adequately, or experience side effects to conventional antiemetics may benefit from a regimen that includes Cesamet.

Dosing Information¹

• The usual dosage for Cesamet is 1 or 2 mg B.I.D., administered orally
• Start with the lower dose and titrate based on patient response
• Cesamet may be administered 2 or 3 times daily during the entire course of each cycle of chemotherapy and, if needed, for 48 hours after the the last dose of each cycle of chemotherapy

Important Safety Information¹

Cesamet, a synthetic cannabinoid similar to the active ingredient found in naturally occurring Cannabis sativa L. [Marijuana; delta-9-tetrahydrocannabinol (delta-9-THC)], is contraindicated in any patient who has a history of hypersensitivity to any cannabinoid. Patients receiving treatment with Cesamet should be specifically warned not to drive, operate machinery, or engage in any hazardous activity while receiving Cesamet. During controlled clinical trials of Cesamet, virtually all patients experienced at least one adverse reaction. The most commonly encountered events were drowsiness, vertigo, dry mouth, euphoria (feeling “high”), ataxia, headache, and concentration difficulties. Cesamet should not be taken with alcohol, sedatives, hypnotics, or other psychoactive substances because these substances can potentiate the central nervous system (CNS) effects of nabilone. Since Cesamet can elevate supine and standing heart rates and cause postural hypotension, it should be used with caution in the elderly, and in patients with hypertension or heart disease. Cesamet should also be used with caution in patients with current or previous psychiatric disorders, (including manic depressive illness, depression, and schizophrenia) as the symptoms of these disease states may be unmasked by the use of cannabinoids. Cesamet should be used with caution in individuals receiving concomitant therapy with sedatives, hypnotics, or other psychoactive drugs because of the potential for additive or synergistic CNS effects. Cesamet should be used with caution in patients with a history of substance abuse, including alcohol abuse or dependence and marijuana use, since Cesamet contains a similar active compound to marijuana. Cesamet should be used with caution in pregnant patients, nursing mothers, or pediatric patients because it has not been studied in these patient populations.

For complete prescribing details, please see full prescribing information.
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References

1. Cesamet™ [package insert]. Valeant Pharmaceuticals International; 2006.
2. Data on File: Protocols 9, 20 and 28. Valeant Pharmaceuticals International.
3. Lemberger L, Rowe H. Clinical pharmacology of nabilone, a cannabinol derivative. Clin Pharmacol Ther. 1975;18(6):720-726.
4. Einhorn LH, Nagy C, Furnas B, et al. Nabilone: An effective antiemetic in patients receiving cancer chemotherapy. J Clin Pharmacol. 1981;21(suppl):64-69.
5. Tramer MR, Carroll D, Campbell FA, et al. Cannabinoids for control of chemotherapy induced nausea and vomiting: quantitative systematic review. Br Med J. 2001;323:1-8.
6. National Comprehensive Cancer Network. Antiemesis. Clinical practice guidelines in oncology. 2006;1:AE-1-REF-7.
7. Howlett AC, Barth F, Bonner TI, et al. International union of pharmacology. XXVII. Classification of cannabinoid receptors. Pharmacol Rev. 2002;54(2):161-202.
8. Schlicker E, Kathmann M. Modulation of transmitter release via presynaptic cannabinoid receptors. Trends Pharmacol Sci. 2001;22(11):565-572.
9. Croxford JL. Therapeutic potential of cannabinoids in CNS disease. CNS Drugs. 2003;17(3):179-202.
10. Diana MA, Marty A. Endocannabinoid-mediated short-term synaptic plasticity: depolarization-induced suppression of inhibition (DSI) and depolarization-induced suppression of excitation (DSE). Br J Pharmacol. 2004;142(1):9-19. Epub 2004 Apr 20.
11. Dodds LJ. The control of cancer chemotherapy-induced nausea and vomiting. J Clin Hosp Pharm. 1985;10(2):143-166.
12. Hornby PJ. Central neurocircuitry associated with emesis. Am J Med. 2001;111(suppl 8A):106-112.