For US health-care professionals only. Prescribing Information

Patients experiencing delayed CINV may suffer in silence1,2

More than half of patients undergoing emetogenic chemotherapy experience delayed chemotherapy-induced nausea and vomiting (CINV), despite 97% receiving a 5-hydroxytryptamine-3 (serotonin) receptor antagonist (5-HT3 RA) and 78% receiving a corticosteroid.1

Oncologists and nurses commonly underestimate the incidence of delayed CINV1

  • Delayed CINV symptoms occur outside the clinic and often go unreported1-3
  • Patients have ranked nausea and vomiting associated with chemotherapy among the worst possible health states4
  • Despite significant improvements in managing the condition and the availability of a range of antiemetics, there remains a clear unmet need to reduce the incidence of delayed CINV2

Factors that increase CINV risk5,6

Factors that increase CINV risk - younger age Factors that increase CINV risk - female Factors that increase CINV risk - anxiety Factors that increase CINV risk - prior history of nausea and vomiting Factors that increase CINV risk - 1 history of low alcohol intake

a A standard drink is 1.5 ounces (oz) of 80-proof spirits (hard liquor), 12 oz of beer, or 5 oz of wine.

5-HT3, 5-hydroxytryptamine-3 (serotonin); GI, gastrointestinal; NK-1, neurokinin 1.

Blocking both 5-HT3 and NK-1 receptors, rather than inhibiting 5-HT3 receptors alone, has demonstrated superior protection from CINV5,9

Use of combination therapeutics provides greater efficacy and prevention of delayed CINV symptoms5

  • Combination antiemetic therapy is considered more effective than single-agent antiemetic therapy due to the various neuronal pathways targeted by different agents and differentiation in efficacy for distinct phases of CINV5,9
  • As a common pathway has not been identified, a single agent cannot be expected to provide protection from the different phases of CINV5
Brain with the caudate nucleus, vomiting center, chemoreceptor trigger zone and brain stem identified
  • Emetogenic chemotherapy triggers receptors in both the peripheral and central nervous systems5,8,10
  • Following chemotherapy administration, the delayed phase of CINV (25-120 h) is driven by the release of the neurotransmitter substance P8,10
  • Substance P is highly concentrated in the emetic centers of the brain and binds to the NK-1 receptor, stimulating induction of vomiting pathways10,11