The same pharmacogenomics that sits on our condition pages, read from the other end. People rarely arrive asking about SLCO1B1 — they arrive having been prescribed a statin. Each page below collects what published guidelines say about one drug, names the genes involved, and links to the variants your own file would contain.
Supplements — kept apart, with the evidence stated on each →
None of this is dosing guidance. Where a clinical guideline exists it is written for prescribers, and the pages say so. Nothing here is a reason to start, stop or change a medication.
Several hundred medicines lengthen the heart's recovery time as a side effect. Most people absorb it without consequence — and the reason some do not is partly written in common variants that do nothing on their own.
NOS1AP
See what the research says → DependenceThe one place on this site where genetics points at a choice between two treatments rather than at a dose — and even here the honest reading is narrower than the headline suggests.
CYP2A6
See what the research says → Antidiabetic (first-line)The first-line drug for type 2 diabetes, used by over 100 million people worldwide, and one whose exact mechanism is still not fully settled. Two variants here move how well it works, not whether someone should take it.
ATM · SLC2A2
See what the research says → DiabetesAmong the oldest diabetes drugs still in wide use, and a clean example of a real pharmacogenomic effect that guidelines deliberately decline to act on — which is more useful to know than one they do act on.
CYP2C9
See what the research says → PalatabilityThe one entry here that is not about how a drug is handled once it is inside you. It is about whether it gets inside you at all — a medicine that tastes unbearably bitter to one child and merely unpleasant to another is a real adherence problem with a genetic explanation.
TAS2R38
See what the research says → IBD therapyA first-line inflammatory bowel disease drug with an allergy-like reaction — fever and worsening diarrhea after starting it — that a 2022 Japanese GWAS linked to one variant. A rare, large-effect finding, not a dosing rule.
OTUD7A (nearest gene by distance — not gene-reported by the study itself)
See what the research says → ImmunosuppressantAzathioprine and mercaptopurine, used in inflammatory bowel disease and leukaemia. Two genes decide how much a person can tolerate, and testing before the first dose is standard practice in many hospitals.
TPMT · NUDT15
See what the research says → AnalgesicProdrugs, which is what makes them different from the other opioids: the enzyme does not clear them, it switches them on. Too little and there is no pain relief; too much and there is far more drug than intended.
CYP2D6
See what the research says → AnalgesicOne of the most studied genes in all of pharmacogenomics sits here — and the guideline that reviewed it concluded that no dosing recommendation can be made. That conclusion is the finding.
OPRM1 · OPRM1 (upstream locus)
See what the research says → AntiretroviralThe only entry here where the consequence is entirely cosmetic and entirely consequential: visible jaundice that harms nobody, and makes people stop taking a drug that was working.
UGT1A1
See what the research says → AntiretroviralA standard dose can put several times the intended amount of drug into somebody who clears it slowly, and what follows — vivid dreams, dizziness, trouble concentrating — is the commonest reason people stop.
CYP2B6
See what the research says → AnticoagulantThe coumarins much of Europe uses where warfarin is used elsewhere. Same mechanism, same genes, one level of evidence below — because the studies are smaller, not because the biology differs.
CYP2C9
See what the research says → AnticoagulantAn anticoagulant with a narrow therapeutic index, whose effective dose differs several-fold between people. More of that variation is explained by genotype than for almost any other drug in common use.
VKORC1 · CYP2C9 · CYP4F2
See what the research says → ContraceptiveA case where two risks multiply rather than add. Estrogen raises clot risk on its own; in someone who also carries a thrombophilia variant the two compound.
F5
See what the research says → Alzheimer disease therapyHere genotype is used before treatment rather than to explain a reaction afterwards: APOE status predicts how likely a person is to develop brain swelling or small bleeds on these drugs.
APOE
See what the research says →Showing 15 of 55 · page 3 of 3
The same pharmacogenomics already published on our condition pages, read from the drug side instead: what published guidelines say about one medicine, which genes are involved, and the variants your own file would contain.
No. Where a clinical guideline exists it is written for prescribers, and nothing here is a reason to start, stop or change a medication — that belongs with the clinician or pharmacist managing treatment.
Because almost nothing sold as a supplement has a prescribing guideline behind it the way a drug does, and listing the two together would lend the second the authority of the first.
By gene symbol as a whole word, gathered from the pgx_notes already published on the condition pages that discuss each drug — not a second, separate copy of that information.