Pearls

Understanding the brexpiprazole therapeutic window: Why more isn’t always better

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References

Dosage windows could be difficult to understand pharmacologically, but for a partial agonist the presumed mechanism could be more evident. Clinicians should be aware that more is not always better, meaning that with partial agonist drugs a higher dosage might not lead to greater patient response. With brexpiprazole, a dopamine D2 partial agonist FDA-approved for schizophrenia and an adjunct for major depressive disorder (MDD),1 moderation is best because of the drug’s known dosage window of efficacy in the treatment of MDD. It is important to note that studies examine populations and not individuals. Specific patients could have genetic variations or be taking agents that may alter metabolism of brexpiprazole, and therefore may benefit from lower or higher doses.

Recommended dosage

Two placebo-controlled studies2,3 examined brexpiprazole dosages of 1, 2, and 3 mg/d. The recommended dosage of 2 mg/d for MDD was determined by changes in Montgomery-Åsburg Depression Rating Scale scores (Figure).4 Lower dosages of 1 mg/d did not reach statistical significance, and 3 mg/d were less effective than the intermediate dosage of 2 mg/d. This result suggests a window of efficacy for brexpiprazole for MDD. This therapeutic window likely applies to most patients; however, patient-specific variables could alter the optimum dosage.

Dosage window

Brexpiprazole has high affinity for dopamine D2, D3, serotonin 5-HT1A, 5-HT2A, norepinephrine α1B, and α2 Creceptors. At relatively low drug concentrations, brexpiprazole achieves high receptor occupancy. At receptors for which brexpiprazole is a partial agonist (5-HT1A, D2, D3) the drug blocks the receptor and stimulates it at a fraction of the endogenous neurotransmitter. With a very high affinity agent, the endogenous neuro­transmitter could be completely excluded from interacting with these receptors if brexpiprazole occupancy is high. At lower dosages, the drug occupies only a fraction of the receptors, allowing the endogenous neuro­transmitters to continue interacting with their receptors, thereby magnifying the signal of that receptor above baseline.

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