Hicks, J. K., Swen, J. J., Thorn, C. F., Sangkuhl, K., Kharasch, E. D., Ellingrod, V. L., ... & Caudle, K. E. (2015). Clinical Pharmacogenetics Implementation Consortium guideline for CYP2C19 and selective serotonin reuptake inhibitors. Clinical Pharmacology & Therapeutics, 98(2), 127–134. https://doi.org/10.1002/cpt.147

Porcelli, S., Drago, A., Fabbri, C., Gibiino, S., Calati, R., & Serretti, A. (2011). Pharmacogenetics of antidepressant response. Journal of Psychiatry & Neuroscience, 36(2), 87–113. https://doi.org/10.1503/jpn.100059

Ohio State University, Columbus

The CYP2C19 gene provides instructions for producing an enzyme that is primarily involved in the metabolism of several medications, including certain SSRIs.

Poor Metabolizers (2/2 or 3/3 genotypes):
These individuals have two nonfunctional alleles, resulting in very little or no CYP2C19 enzyme activity. This leads to slower drug metabolism, higher plasma concentrations, and greater risk of side effects, such as sedation, nausea, or emotional blunting. Poor metabolizers may experience exaggerated side effects or toxicity at standard doses due to an impairment in drug clearance.

Intermediate Metabolizers (1/2): Reduced enzyme function. Individuals may still metabolize drugs but at a slower rate than normal.

Ultrarapid Metabolizers (17/17): Increased enzyme activity leads to faster clearance of SSRIs which can reduce effectiveness. Ultrarapid metabolizers may receive less of a therapeutic benefit unless the dose is increased.

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