ABSTRACT
In the last two decades, there have been considerable advances in our understanding of emetic circuits and the mechanisms by which chemotherapeutics produce emesis. Cancer chemotherapy is often accompanied by severe nausea and vomiting, which can lead to refusal or delay of treatment by patients. A number of different classes of antiemetics have been employed clinically to control chemotherapy-induced emesis. These include: dopamine D2 antagonists (butyrophenones, phenothiazines), cannabinoids, corticosteroids, substituted benzamides, serotonin 5-HT3-and tachykinin NK1-antagonists. Of these, serotonin 5-HT3 antagonists appear to be most effective for the prevention of the acute phase of chemotherapy-induced emesis. Recent clinical trials suggest that NK1 antagonists have broadspectrum antiemetic properties controlling both the acute and delayed phases of emesis in cancer patients.
