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.
Another way to hold transthyretin together: a newer pill, taken twice a day, for the heart form of ATTR, hereditary or not.
TTR
See what the research says → TTR stabiliserTransthyretin normally travels as four pieces held together. When they come apart, they clump into amyloid in the heart. Tafamidis holds the pieces together, and it works whether the problem came from your genes or from age.
TTR
See what the research says → TTR silencerInstead of holding transthyretin together, vutrisiran turns down how much of it the liver makes. For the heart, genotype does not matter; for the nerves, it does.
TTR
See what the research says → Triglyceride-loweringPrescribed for high triglycerides, and known to shift particle size across the whole lipid panel, not just lower one number. How much it shifts differs between people.
AHCYL2
See what the research says → Cholesterol-loweringAmong the most prescribed drugs in the world. Muscle symptoms are the leading reason people stop taking them, and stopping means losing the cardiovascular protection they were prescribed for.
SLCO1B1 · ABCG2 · CYP2C9 · CLMN · CETP
See what the research says → TricyclicTwo enzymes act on one prescription, and one of them turns the first drug into the second — which is why two of these are prescribed in their own right. The guideline sets a dose; it does not say which antidepressant will work, and no genotype currently does.
CYP2D6
See what the research says → AntiseizureAn ordinary dosing question, and it sits on the same page as valproate — which is the useful comparison. One level of evidence apart, and a world apart in what it asks a prescriber to do.
CYP2C19
See what the research says → AntiseizureThe strongest kind of finding on this site: not a smaller dose but a drug that must not be given at all. Two mechanisms, seven genes, and neither is visible to a consumer test.
POLG
See what the research says → Wake-promotingIt works by taking the brake off the brain’s own histamine rather than by stimulating it from outside — and a slow CYP2D6 means the same dose delivers considerably more of it.
CYP2D6
See what the research says → CFTR modulatorYour cells have tiny doors that let salt and water out. The CFTR gene is the blueprint for them, and cystic fibrosis is what happens when the blueprint has a typo. Trikafta puts the door back in place and opens it, but whether it works depends on which typo you carry.
CFTR
See what the research says → CFTR modulatorNot a drug for cystic fibrosis — a drug for particular CFTR variants. Two people with the same diagnosis get opposite answers depending on which change they carry, which is the whole argument of this site in one prescription.
CFTR
See what the research says → CFTR modulatorThe same idea as Trikafta, rebuilt: two medicines set the CFTR door in place and one opens it, now in a single dose a day. Who can take it still depends on which CFTR typo you carry.
CFTR
See what the research says → ImmunosuppressantThe standard starting dose was calibrated on people whose CYP3A5 does not work, because in Europe that is most people. The ones whose enzyme is intact get too little — in the first days after a transplant, when too little means rejection.
CYP3A5
See what the research says → AntibioticMonitoring the blood level is the standard safeguard for this class, and for a person carrying one mitochondrial change it does not work — the hearing can go after a single ordinary dose at a normal level.
MT-RNR1
See what the research says → VariousUnrelated drugs with one thing in common: they oxidise. In a G6PD-deficient person that is enough to break red cells at an ordinary dose, and in most cases there is something else to prescribe.
G6PD
See what the research says → AntimalarialThe only drugs that clear the dormant liver stage of malaria, and they cause haemolysis in G6PD deficiency — which is common precisely where malaria is. Testing before prescribing is genuinely routine here, which is rare.
G6PD
See what the research says → Uric acid loweringIt breaks uric acid down and makes hydrogen peroxide doing it. For almost everyone that is nothing. For someone whose red cells cannot handle oxidative stress it is the one contraindication on this site printed in a box on the label.
G6PD
See what the research says → AnaestheticThe trigger for malignant hyperthermia. What makes this the clearest case in pharmacogenomics is that the alternative is easy: an anaesthetic without any of these agents is routine, provided somebody knows beforehand.
RYR1 · CACNA1S
See what the research says → AntiretroviralThe example everyone reaches for when they want to show that pharmacogenomics changed practice — and it did. Test before the first dose, do not prescribe if positive, and a reaction people used to fear became rare.
HLA-B
See what the research says → Acid suppressionThe rare case where losing an enzyme helps. A poor metaboliser clears these more slowly, gets more drug for longer, and often ends up better treated than everybody else.
CYP2C19
See what the research says →Showing 20 of 55 · page 1 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.