Ritalin

Raw research findings for this medication. Mostly single studies, not curated or confirmed robust.

About Ritalin

What it is

Methylphenidate is a central nervous system stimulant that blocks the reuptake of dopamine and noradrenaline, so more of both stay available in the parts of the brain involved in attention and impulse control. It is the most widely used medicine for ADHD in children and adults, and is also used for narcolepsy. It is sold as Ritalin, Concerta, Medikinet and other names.

How genes come into it

Methylphenidate is broken down mainly by the liver esterase CES1, not by CYP enzymes, and a CES1 variant (G143E, rs71647871) markedly raises its levels. Most of the over 150 studies on it looked for genes that predict response in ADHD: the noradrenaline transporter SLC6A2, ADGRL3 (latrophilin 3), ADRA2A, COMT and the dopamine transporter SLC6A3. The results are mixed, and there is no CPIC or DPWG guideline.

What research found

Every published finding on gene variants and Ritalin. Upload your DNA file to see which of these rows apply to you.

Rated evidence (50 rated variants)

PharmGKB weighs all studies of a variant and rates how strong the evidence is, from 1A (strongest) to 4.

SLC6A2 rs28386840: Level 3. Efficacy: Attention Deficit Disorder with Hyperactivity. 7.

ADGRL3 rs6551665: Level 3. Efficacy: Attention Deficit Disorder with Hyperactivity. 7.

CES1 rs71647871: Level 3. Metabolism/PK. 2.

PYROXD2 rs1061115: Level 3. Efficacy: Attention Deficit Disorder with Hyperactivity. 1.

Metabolism (2 findings)

Studies of how quickly the body processes this medication.

CES1 rs71647871: Allele T is associated with decreased metabolism of methylphenidate in healthy individuals as compared to allele C.

CYP2D6 CYP2D6 poor metabolizer: CYP2D6 poor metabolizer is not associated with increased concentrations of methylphenidate or ritalinic acid as compared to CYP2D6 normal metabolizer.

Response (159 findings)

Studies of how well it worked in people carrying a variant.

ADGRL3 rs1355368: Genotypes AG + GG are associated with increased response to methylphenidate in children Attention Deficit Disorder with Hyperactivity as compared to genotype AA.

ADGRL3 rs1868790: Genotype AA is associated with decreased response to methylphenidate in children with Attention Deficit Disorder with Hyperactivity as compared to genotypes AT + TT.

ADGRL3 rs6813183: Genotypes CC + CG are associated with increased response to methylphenidate in children Attention Deficit Disorder with Hyperactivity as compared to genotype GG.

ADGRL3 rs734644: Genotypes CC + CT are associated with increased response to methylphenidate in children Attention Deficit Disorder with Hyperactivity as compared to genotype TT.

Dosing (17 findings)

Studies of how much of the drug people needed or tolerated.

CES1 rs114119971: Genotype CG is associated with decreased dose of methylphenidate in children with Attention Deficit Disorder with Hyperactivity as compared to genotype GG.

CES1 rs71647871: Genotype CT is associated with decreased dose of methylphenidate in children with Attention Deficit Disorder with Hyperactivity as compared to genotype CC.

rs9627183: Allele G is associated with increased response to methylphenidate in children with Attention Deficit Disorder with Hyperactivity as compared to allele A.

CES1 rs12443580: Genotype TT is not associated with dose of methylphenidate in children with Attention Deficit Disorder with Hyperactivity as compared to genotypes CC + CT.

Study findings and evidence levels: PharmGKB (CC BY-SA 4.0). Guidelines: CPIC and DPWG, as bundled in PharmCAT. Most studies were done mainly in people of European ancestry.

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Not a prescribing recommendation. This page is educational information about pharmacogenomic research and clinical guidelines - it is not medical or dosing advice, and not a prediction of how any medication will work for you. Never start, stop, or change a medication or dose based on it; talk to your doctor or pharmacist, who can order clinical-grade testing if appropriate.

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Content updated September 2026.

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