Question:medium
All are true about Aprepitant except?
All are true about Aprepitant except?
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Antiemetics block substance P; is aprepitant really an agonist?
Updated On: Jun 24, 2026
- Agonist at NK1
- Crosses blood brain barrier
- Ameliorates nausea and vomiting of chemotherapy
- Metabolized by CYP3A4
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The Correct Option is A
Solution and Explanation
Aprepitant is the prototype small-molecule blocker of the substance P pathway used to control vomiting from cancer chemotherapy. The trick in this except-style question is that one statement reverses its actual pharmacology.
The vomiting reflex is partly driven by substance P binding to neurokinin-1 receptors in the central emetic centres. Aprepitant works by occupying those receptors and preventing substance P from acting, so it is an antagonist, not an agonist. The statement that it is an NK1 agonist is therefore incorrect and is the answer to the question.
The other three statements describe it accurately. Its lipophilic structure allows central nervous system penetration, which it needs because the target receptors are in the brainstem. It is particularly valued for controlling the delayed phase of chemotherapy-induced nausea and vomiting, usually as part of a triple regimen with a 5-HT3 antagonist and a corticosteroid. Pharmacokinetically it is handled by CYP3A4 and modulates the same enzyme, which explains its interaction potential with drugs like dexamethasone and certain chemotherapeutic agents.
\[\boxed{\text{Agonist at NK1 (false statement)}}\]
The vomiting reflex is partly driven by substance P binding to neurokinin-1 receptors in the central emetic centres. Aprepitant works by occupying those receptors and preventing substance P from acting, so it is an antagonist, not an agonist. The statement that it is an NK1 agonist is therefore incorrect and is the answer to the question.
The other three statements describe it accurately. Its lipophilic structure allows central nervous system penetration, which it needs because the target receptors are in the brainstem. It is particularly valued for controlling the delayed phase of chemotherapy-induced nausea and vomiting, usually as part of a triple regimen with a 5-HT3 antagonist and a corticosteroid. Pharmacokinetically it is handled by CYP3A4 and modulates the same enzyme, which explains its interaction potential with drugs like dexamethasone and certain chemotherapeutic agents.
\[\boxed{\text{Agonist at NK1 (false statement)}}\]
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