About Medication Match

The science behind the tool, and every gene we analyse.

What it does

Medication Match parses your raw DNA genotype file and cross-references specific pharmacogenomically relevant SNPs (single nucleotide polymorphisms) against a curated database of published gene–drug associations. It then generates a plain-English summary of how your genetics might influence how certain medications are processed and responded to in your body.

You choose which medication categories to analyse. Results are grouped by category and colour-coded by their potential clinical significance.

Supported file formats

Provider File format How to download
AncestryDNA .txt or .zip  ·  5 columns: rsid, chromosome, position, allele1, allele2 DNA → Settings → Download Raw DNA Data
23andMe .txt or .zip  ·  4 columns: rsid, chromosome, position, genotype Account → 23andMe Data → Browse Raw Data → Download
Genes We Analyse
Filter by category:
Your Drug Processor
CYP2D6
ADHD Non-Stimulants Anti-Nausea Tamoxifen Opioids SSRIs TCAs
This gene tells your liver how fast to break down certain medications — including atomoxetine for ADHD, several antidepressants (paroxetine, fluoxetine), and all tricyclic antidepressants. Slow processors accumulate the drug; fast processors clear it before it can work. IMPORTANT: consumer DNA chips cannot detect gene duplications or large deletions in CYP2D6 — a clinical test is needed for a complete picture.
Molecular & clinical detail
CYP2D6 is a hepatic cytochrome P450 enzyme responsible for oxidative metabolism of ~25% of clinical drugs. Highly polymorphic (>100 alleles), subject to copy number variation. Poor metabolisers (PMs) carrying two loss-of-function alleles exhibit up to 10-fold higher AUC for substrates such as atomoxetine, paroxetine, fluoxetine, and TCAs. Ultrarapid metabolisers (UMs) carrying gene duplications show sub-therapeutic exposures. CRITICAL LIMITATION: copy number variants (gene deletion *5, duplication *2×N) cannot be detected from SNP arrays.
Another Drug Processor
CYP2C19
ADHD Non-Stimulants Antifungals Antiplatelet PPIs SSRIs TCAs
This liver enzyme processes several important medication groups differently: for SSRIs and TCAs, slow processors accumulate the drug (more side effects); for clopidogrel (blood thinner), slow processors CANNOT properly activate the drug (reduced protection against clots); for proton pump inhibitors, slow processors get stronger acid suppression. AncestryDNA chips cover CYP2C19 very well.
Molecular & clinical detail
CYP2C19 is a cytochrome P450 enzyme metabolising ~10% of clinical drugs. The *2 allele (681G>A) creates a non-functional splice variant; the *3 allele introduces a premature stop codon; the *17 allele (-806C>T) increases promoter transcription (ultrarapid). Key drug-class-specific impacts: (1) SSRIs/TCAs — PM has elevated plasma levels (substrate accumulation); (2) clopidogrel — PM cannot convert the prodrug to active thiol metabolite (CPIC: use alternative antiplatelet); (3) PPIs — UM shows reduced efficacy; PM shows enhanced acid suppression with accumulation risk. CPIC provides class-specific dosing recommendations.
Your Warfarin Processor (CYP2C9)
CYP2C9
Anticoagulants Antiepileptics
This liver enzyme breaks down warfarin — the most common blood thinner. If your version is slow, warfarin builds up and thins your blood too much (bleeding risk). Poor metabolisers can need 30-50% lower doses than average. This gene, together with VKORC1 and CYP4F2, explains about half of all variation in warfarin dose requirements between people.
Molecular & clinical detail
CYP2C9 catalyses the hydroxylation of S-warfarin (the more potent enantiomer) to inactive 7-hydroxy-warfarin. The *2 allele (rs1799853, Arg144Cys) reduces activity to ~12% of wild-type; the *3 allele (rs1057910, Ile359Leu) reduces activity to ~5%. CPIC/IWPC guidelines recommend dose reductions for *1/*2, *1/*3 (intermediate metabolisers) and dramatic reductions or alternative anticoagulants for *2/*2, *2/*3, *3/*3 (poor metabolisers). Bleeding risk is substantially elevated in PMs at standard doses.
Your Warfarin Sensitivity Gene
VKORC1
Anticoagulants
This gene makes the protein that warfarin directly blocks to thin your blood. Variations change how sensitive you are — people with the 'A' version of this gene have fewer of these proteins and need much lower warfarin doses. VKORC1 is the single biggest genetic predictor of warfarin dose requirements.
Molecular & clinical detail
VKORC1 encodes vitamin K epoxide reductase complex subunit 1 — the direct pharmacological target of warfarin. The -1639G>A promoter variant (rs9923231) reduces VKORC1 mRNA expression: A/A carriers have ~3-fold lower enzyme levels than G/G carriers. VKORC1 accounts for ~25% of inter-individual warfarin dose variance. The IWPC algorithm uses VKORC1 genotype as a primary dosing variable. A/A carriers typically require 3-4 mg/day vs 5-7 mg/day for G/G carriers.
Your Vitamin K Controller (CYP4F2)
CYP4F2
Anticoagulants
This enzyme breaks down vitamin K in the liver. If your version is less active, more vitamin K remains available, which partially counteracts warfarin's blood-thinning effect — meaning you may need a somewhat higher warfarin dose. The effect is smaller than VKORC1 or CYP2C9, but adds up when combined with those genes.
Molecular & clinical detail
CYP4F2 is the primary hepatic enzyme for oxidation of vitamin K1 and MK-4 to their inactive metabolites. The Val433Met variant (rs2108622, T allele) reduces CYP4F2 activity, elevating hepatic vitamin K concentrations that partially offset warfarin's inhibition of VKORC1. T allele carriers require ~0.9-1.0 mg/day higher warfarin doses on average. CYP4F2 is included in the IWPC pharmacogenomics-guided warfarin dosing algorithm alongside CYP2C9 and VKORC1.
Your Chemo Safety Gene (DPYD)
DPYD
5-FU / Capecitabine
CRITICAL SAFETY GENE. This gene produces an enzyme that breaks down fluoropyrimidine chemotherapy drugs (5-FU and capecitabine). If you carry a non-functional variant, you cannot safely clear these drugs — they accumulate to life-threatening levels even at standard doses, causing fatal gut damage, immune suppression, and nerve damage. DPYD testing is now required before treatment in many countries. A variant detected here must be discussed with your oncologist before any fluoropyrimidine chemotherapy is given.
Molecular & clinical detail
DPYD encodes dihydropyrimidine dehydrogenase (DPD), responsible for >80% of fluorouracil catabolism. Four CPIC-annotated variants together predict ~50% of severe/fatal toxicity cases. The *2A splice-site variant (rs3918290, IVS14+1G>A) and *13 (rs55886062, Ile560Ser) completely abolish enzyme function; c.2846A>T (rs67376798, Asp949Val) and HapB3 (rs75017182 proxy) substantially reduce activity. In homozygous or compound heterozygous poor metabolisers, standard 5-FU doses can be lethal. CPIC mandates 50% dose reduction for activity score <1.5, and complete avoidance at AS=0. EMA and Health Canada mandate DPYD testing before all fluoropyrimidine prescribing.
Your Immune Drug Safety Gene (TPMT)
TPMT
Thiopurines
This gene produces an enzyme that deactivates thiopurine medications (azathioprine, mercaptopurine) used to suppress the immune system. If your version runs slowly, toxic byproducts build up in blood-forming cells, causing potentially life-threatening bone marrow failure. Standard dosing is contraindicated in poor metabolisers — the dose must be dramatically reduced or avoided entirely. Many hospitals test for TPMT before prescribing these drugs.
Molecular & clinical detail
TPMT (thiopurine S-methyltransferase) catalyses S-methylation of thiopurine drugs to inactive metabolites, competing with the pathway producing cytotoxic 6-thioguanine nucleotides (6-TGN). The three common variant alleles (*2 rs1800462, *3B rs1800460, *3C rs1142345) account for ~95% of reduced-activity phenotypes. Poor metabolisers accumulate high 6-TGN concentrations causing severe myelosuppression. CPIC guideline: reduce to 10% of standard dose for PMs, 30-70% reduction for IMs. Note: *3A (compound heterozygote for *3B and *3C, common in Europeans) is the most common deficient haplotype.
Another Immune Drug Safety Gene (NUDT15)
NUDT15
Thiopurines
Like TPMT, this gene helps prevent toxic buildup from thiopurine medications. It is especially important in people of East and Southeast Asian descent, where NUDT15 variants are more common. Even one copy of the non-functional variant can cause significant toxicity. Both TPMT and NUDT15 must be checked together before prescribing thiopurines.
Molecular & clinical detail
NUDT15 (nudix hydrolase 15) dephosphorylates 6-thioguanine triphosphate (6-TGTP), reducing its incorporation into DNA. The *3 allele (rs116855232, Arg139Cys) is a loss-of-function variant with allele frequency ~3-9% in East Asian populations vs <0.5% in Europeans. NUDT15 *3 carriers are at high risk of severe thiopurine-induced myelosuppression. CPIC guidelines recommend treating NUDT15 PM patients identically to TPMT PM patients — dose at 10% of standard or consider alternative therapy.
Your Statin Transporter
SLCO1B1
Statins
This gene makes a transporter protein that carries statin drugs from the blood into liver cells, where they lower cholesterol. If your transporter is less efficient, statins (especially simvastatin) build up in the bloodstream at higher levels than intended. The main risk is muscle damage — from mild aches to, rarely, serious breakdown of muscle tissue (rhabdomyolysis). The CC variant has roughly 18 times the muscle damage risk of the normal TT version.
Molecular & clinical detail
SLCO1B1 encodes OATP1B1, the primary hepatic uptake transporter for most statins. The Val174Ala variant (rs4149056, *5 allele, C allele) reduces transporter activity, increasing statin plasma AUC. For simvastatin, CC genotype confers ~18× increased myopathy risk; CT ~4× vs TT reference. CPIC guideline recommends simvastatin ≤20 mg/day for CT and alternative statin consideration for CC. Atorvastatin, rosuvastatin, and pravastatin are less affected; pravastatin and fluvastatin show the smallest SLCO1B1 interaction.
Your Dopamine Recycler
COMT
ADHD Stimulants Opioids
Dopamine is the brain chemical most linked to focus, motivation, and reward. This gene controls how quickly your brain clears it away. Fast recyclers may have lower baseline focus and benefit more from stimulants. Slow recyclers have a higher dopamine baseline and can be more sensitive to stimulant side effects at higher doses.
Molecular & clinical detail
Catechol-O-methyltransferase (COMT) catalyses O-methylation of catecholamines in the prefrontal cortex. The Val158Met polymorphism (rs4680) alters enzyme thermostability: Val/Val has ~3-4× higher enzymatic activity than Met/Met. The PFC operates on an inverted-U dopamine dose-response curve — both insufficient and excessive dopamine impair executive function.
Your Ritalin Target (DAT1)
SLC6A3
ADHD Stimulants
This gene builds the 'docking stations' (dopamine transporters) that Ritalin attaches to. More docking stations can mean Ritalin has to work harder; fewer means it may be especially effective.
Molecular & clinical detail
SLC6A3 encodes the dopamine transporter (DAT), the primary synaptic reuptake mechanism for dopamine and the principal target of methylphenidate. The 3' VNTR polymorphism influences DAT mRNA stability and striatal transporter density. The 10R allele is associated with higher DAT expression.
Your Focus Receptor
ADRA2A
ADHD Non-Stimulants ADHD Stimulants
This gene makes receptors that respond to adrenaline-like signals in the brain's decision-making area — the same signals that non-stimulant medications like Intuniv (guanfacine) and Kapvay (clonidine) target. More receptors generally means a better response to these medications.
Molecular & clinical detail
ADRA2A encodes the alpha-2A adrenergic receptor, highly expressed on PFC pyramidal neurons. NE stimulation of ADRA2A strengthens PFC network connectivity. The 1291C>G promoter variant (rs1800544) modulates receptor expression.
Your Dopamine Sensor
DRD4
ADHD Stimulants
This gene makes a dopamine receptor in the brain's decision-making centre. Variations are linked to impulsivity and can influence how well stimulants work.
Molecular & clinical detail
DRD4 encodes the dopamine D4 receptor. The -521C>T promoter variant (rs1800955) influences transcriptional activity and receptor density in the PFC.
Your Serotonin–Dopamine Bridge
HTR1B
ADHD Stimulants
This receptor controls how much dopamine is released in key brain areas via the serotonin system — subtly affecting stimulant medication response.
Molecular & clinical detail
HTR1B encodes the serotonin 1B receptor, a Gi/o-coupled autoreceptor on dopaminergic terminals. Activation inhibits dopamine release. The G861C variant (rs6296) is associated with altered receptor function.
Your Brain's Chemical Janitor
MAOA
ADHD Non-Stimulants ADHD Stimulants
This gene produces an enzyme that breaks down dopamine, serotonin, and norepinephrine. A slow version means these chemicals linger longer — making you more sensitive to stimulants. X-linked: males carry one copy.
Molecular & clinical detail
MAOA encodes monoamine oxidase A, a mitochondrial enzyme catabolising monoamine neurotransmitters. The promoter uVNTR produces low-activity (3R) and high-activity (4R) alleles. MAOA is X-linked — males are hemizygous.
Your Mood Resilience Gene
SLC6A4
ADHD Non-Stimulants ADHD Stimulants
This gene controls how efficiently your brain recycles serotonin. Variations here affect whether stimulant medications might trigger anxiety or mood swings.
Molecular & clinical detail
SLC6A4 encodes the serotonin transporter (SERT). The 5-HTTLPR polymorphism creates short (S) and long (L) alleles; rs25531 distinguishes high-expression L_A from low-expression L_G. S and L_G carriers show reduced SERT expression and higher trait anxiety.
Your Opioid Receptor
OPRM1
Opioids
This gene makes the main receptor that opioid pain medications (like codeine, tramadol, and morphine) bind to. A common variant (A118G) changes how sensitive that receptor is — people with the G allele may feel less pain relief from opioids at standard doses and sometimes require higher amounts for the same effect. This does not affect the liver processing of opioids (that's CYP2D6's job) — it affects how the drug works once it reaches the brain.
Molecular & clinical detail
OPRM1 encodes the mu-opioid receptor (MOR), the primary target of opioid analgesics. The A118G variant (rs1799971, Asn40Asp) substitutes an asparagine for aspartate at position 40 of the extracellular domain, disrupting an N-glycosylation site. The G allele is associated with reduced receptor expression (~3-fold lower in some studies) and reduced endorphin binding affinity. Clinical meta-analyses show G allele carriers require ~15-20% higher opioid doses for equivalent analgesia. CPIC evidence level B — included as a modifier in opioid dosing guidelines.
Your Tacrolimus Processor (CYP3A5)
CYP3A5
Tacrolimus
This enzyme helps process tacrolimus — the main anti-rejection medication used after organ transplants. If your version of this gene is active, you break down tacrolimus much faster than average and will need a higher starting dose to reach therapeutic blood levels. Most people of European descent have an inactive version and require standard doses. Active expressors (more common in African ancestry) who receive standard doses may have sub-therapeutic levels, putting their transplanted organ at risk.
Molecular & clinical detail
CYP3A5 is a cytochrome P450 enzyme expressed in intestine and liver. The *3 allele (rs776746, 6986A>G) creates a cryptic splice site producing a non-functional truncated protein. *3/*3 homozygotes are CYP3A5 non-expressors (~80-85% of Europeans, ~30% of Africans). *1 allele carriers are expressors — CYP3A5 contributes substantially to tacrolimus CL/F. CPIC guideline (Birdwell et al. 2015) recommends 1.5-2× standard starting dose for *1/*1 expressors. Blood level monitoring adjusts maintenance dosing regardless, but genotype-guided initiation accelerates time-to-target.
Your Drug Hypersensitivity Gene (HLA-B)
HLA-B
Antiepileptics
This gene is part of your immune system's identity tag system. Certain variants are strongly associated with severe, life-threatening skin reactions (Stevens-Johnson syndrome / toxic epidermal necrolysis) when taking carbamazepine or oxcarbazepine. The HLA-B*15:02 variant is most common and dangerous in people of Southeast Asian, East Asian, and South Asian descent. IMPORTANT: Consumer DNA chip results for HLA genes are approximations only — clinical HLA typing is required for definitive results. If you are of Asian descent and plan to start carbamazepine, always request formal clinical HLA testing first.
Molecular & clinical detail
HLA-B is a highly polymorphic MHC class I gene. HLA-B*15:02 is strongly associated with carbamazepine-induced SJS/TEN (OR >1000 in Han Chinese). Mechanism: the variant presents carbamazepine or its reactive metabolites to cytotoxic T cells, triggering immune-mediated keratinocyte apoptosis. FDA (2007) and CPIC mandate HLA-B*15:02 testing before carbamazepine in at-risk populations. Tag SNPs on consumer arrays (rs3909184, rs2844682) have moderate sensitivity for *15:02 but are NOT equivalent to formal HLA typing — false negatives occur. HLA-B*58:01 is associated with allopurinol SJS/TEN in Asian populations (not covered here).
Your Drug Hypersensitivity Gene (HLA-A)
HLA-A
Antiepileptics
Like HLA-B, this gene is part of your immune identity system. A variant called HLA-A*31:01 increases the risk of immune reactions to carbamazepine — including a severe drug reaction called DRESS syndrome and skin reactions. This variant is more relevant in European and Japanese populations than HLA-B*15:02. Again, consumer chip results for HLA genes are approximations and not a substitute for formal clinical HLA typing.
Molecular & clinical detail
HLA-A*31:01 is associated with carbamazepine hypersensitivity across multiple ancestry groups, including DRESS (drug reaction with eosinophilia and systemic symptoms), SJS/TEN, and maculopapular exanthema (MPE). Unlike HLA-B*15:02, *31:01 is clinically relevant in Europeans (~5-8% carrier frequency). CPIC recommends alternative anticonvulsants (oxcarbazepine with caution, or non-aromatic agents) for HLA-A*31:01 carriers. Tag SNP rs1061235 is a proxy marker with limited sensitivity — clinical sequencing-based HLA typing is definitive.
Your Irinotecan Safety Gene (UGT1A1)
UGT1A1
Irinotecan
This gene produces an enzyme that detoxifies SN-38, the active and toxic byproduct of irinotecan chemotherapy. If your version is slower than average, SN-38 builds up in your body, causing severe diarrhea and dangerous drops in white blood cell counts (neutropenia). The UGT1A1*28 variant — a TA repeat in the gene's promoter — is the main variant checked before irinotecan treatment. IMPORTANT: This variant is a repeat sequence that consumer DNA chips may not reliably capture — coverage varies by chip version. If rs8175347 is absent from your data, it does not mean you have normal function.
Molecular & clinical detail
UGT1A1 (UDP-glucuronosyltransferase 1A1) glucuronidates SN-38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of irinotecan, to inactive SN-38G. The *28 allele carries 7 TA repeats in the promoter TATAAA box (vs. 6 in *1), reducing UGT1A1 expression ~70%. Homozygous *28/*28 patients show ~2.3-fold elevated SN-38 AUC. CPIC guideline (Gammal et al. 2016): consider dose reduction for *28/*28; consider reduction for *1/*28 at high-intensity regimens. FDA labelling includes UGT1A1 pharmacogenomics information. rs8175347 is a tag proxy for the TA repeat — direct repeat genotyping via fragment analysis is definitive.
No genes found for this medication category.
Data Sources & Guidelines

The variant interpretations and dosing guidance in this tool are drawn from peer-reviewed pharmacogenomics guidelines and published literature. Key sources by medication category:

Category Source / Guideline
ADHD — All PharmGKB gene–drug relationship annotations (pharmgkb.org). Zhu et al. (2008) Pharmacogenet Genomics 18(5):379–387 — ADRA2A rs1800544 and methylphenidate response. Kereszturi et al. (2008) Neurochem Int 53(5):169–174 — COMT Val158Met and methylphenidate efficacy. Froehlich et al. (2011) Arch Pediatr Adolesc Med 165(5):406–413 — DAT1 3′-VNTR and stimulant response. Babusyte et al. (2012) ADHD Atten Def Hyp Disord — HTR1B pharmacology.
CYP2D6
(Atomoxetine, SSRIs, TCAs)		 CPIC Guideline for CYP2D6 and Atomoxetine — Strawn et al. (2019) Clin Pharmacol Ther 106(1):94–102. CPIC Guideline for TCAs — Hicks et al. (2017) Clin Pharmacol Ther 102(1):37–44. CPIC Guideline for SSRIs (CYP2D6/CYP2C19) — Hicks et al. (2015) Clin Pharmacol Ther 98(5):501–509.
CYP2C19
(SSRIs, TCAs, clopidogrel, PPIs)		 CPIC Guideline for clopidogrel and CYP2C19 — Scott et al. (2013) Clin Pharmacol Ther 94(3):317–323; updated Gong et al. (2017). CPIC Guideline for PPIs and CYP2C19 — Lima et al. (2021) Clin Pharmacol Ther 109(6):1417–1423. FDA black-box warning on clopidogrel (2010) regarding CYP2C19 poor metaboliser status.
Warfarin
(CYP2C9, VKORC1, CYP4F2)		 CPIC Guideline for warfarin — Johnson et al. (2017) Clin Pharmacol Ther 102(3):397–404. IWPC dosing algorithm — International Warfarin Pharmacogenomics Consortium (2009) N Engl J Med 360(8):753–764. Takeuchi et al. (2009) Nat Genet 41(6):663–665 — CYP4F2 V433M and warfarin dose.
DPYD
(5-FU, capecitabine)		 CPIC Guideline for DPYD and fluoropyrimidines — Amstutz et al. (2018) Clin Pharmacol Ther 103(2):210–216. EMA (2020) — Mandatory DPYD testing label update for all fluoropyrimidine-containing products. Health Canada (2016) — DPYD testing recommendation for capecitabine. Henricks et al. (2018) Lancet Oncol 19(11):1459–1467 — prospective validation of DPYD-guided dosing.
TPMT / NUDT15
(Thiopurines)		 CPIC Guideline for thiopurines and TPMT/NUDT15 — Relling et al. (2019) Clin Pharmacol Ther 105(5):1095–1105. Yang et al. (2015) Nat Genet 47(9):1027–1031 — NUDT15 R139C and thiopurine toxicity in Asian populations.
SLCO1B1
(Statins)		 CPIC Guideline for statins and SLCO1B1 — Ramsey et al. (2014) Clin Pharmacol Ther 96(4):423–428; updated Cooper-DeHoff et al. (2022). SEARCH Collaborative Group (2008) N Engl J Med 359(8):789–799 — SLCO1B1 rs4149056 and simvastatin myopathy.
Limitations

Our Goal

Medication Match was built with a single purpose: to help people develop a deeper, more informed understanding of their own bodies, their health, and the medications that affect them. We believe that everyone deserves access to the science that shapes their treatment. Pharmacogenomics has the potential to transform how medications are prescribed, and we want to make that knowledge accessible, readable, and meaningful to anyone who is curious about it.

That said, I want to be direct about what this tool is, and what it is not. Medication Match is for educational and informational purposes only. It is not a medical device. It is not a clinical diagnostic test. It is not a replacement for a conversation with your doctor, pharmacist, or a certified pharmacogenomics specialist. Nothing on this site constitutes medical advice, a clinical diagnosis, or a recommendation to start, stop, or adjust any medication.

Consumer DNA files — such as those from AncestryDNA — were designed for ancestry purposes. They cover a limited subset of the variants that matter pharmacogenomically, and they cannot detect all structural changes in genes like CYP2D6. A negative result on this site does not mean you have no relevant genetic variants. A positive finding does not mean you will definitely experience the described effects. Genetics is one piece of a much larger picture that includes your age, other medications, organ function, diet, and clinical history.

For the critical-safety categories — particularly DPYD (fluoropyrimidine chemotherapy) and TPMT/NUDT15 (thiopurine immunosuppressants) — the stakes are highest. If you are about to receive or are currently receiving one of these medications, please do not rely on this tool as your primary safety check. Seek a formal clinical pharmacogenomics panel through your healthcare provider or institution.

By using Medication Match, you acknowledge that you are doing so for educational purposes, and that you will consult a qualified healthcare provider before making any decisions about your medications. We are not liable for decisions made based on the output of this tool.

Our hope is simple: that by understanding a little more about how your genes interact with medications, you become a more informed participant in your own healthcare. We want people to ask better questions, and have richer conversations with their doctor. The dose or medication that works for someone else may not be right for you, and that is biology, not failure.

Medication Match was created by Victor Janse van Rensburg.

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