InstalabPGx Comprehensive
Should you take a PGx Comprehensive test?
This test is most useful if any of these apply to you.
49 biomarkers included
- ABCB1 GenotypeA drug pump at the gut wall and blood-brain barrier, affecting absorption and brain exposure.Why it mattersVariants may shift antidepressant and opioid exposure, but the link is still exploratory.
- ABCG2 GenotypeA drug transporter with formal statin guidance, especially for rosuvastatin dose limits when function is low.Why it mattersReduced function raises rosuvastatin levels and can cap the dose.
- ACE GenotypeThe insertion/deletion variant in the enzyme targeted by a major class of blood pressure drugs.Why it mattersUse it as blood-pressure context; medication choice still depends on measured response.
- ANKK1 GenotypeCarries the Taq1A variant, inherited near DRD2 and used as a proxy for dopamine receptor availability.Why it mattersRead with DRD2 as dopamine context, not as an established prescribing marker.
- APOE GenotypeAffects Alzheimer's risk, cholesterol handling and safety risk for newer amyloid antibody drugs.Why it mattersTwo e4 copies raise Alzheimer's risk and brain-swelling risk on amyloid antibody therapy.
- ATM GenotypeCoordinates the cell response to DNA damage, shaping how normal tissue may tolerate radiation and chemotherapy.Why it mattersA notable variant belongs in formal genetics review, not a dosing change.
- BCHE GenotypeBreaks down succinylcholine and mivacurium, short-acting muscle relaxants used to place a breathing tube.Why it mattersA deficiency variant means paralysis after anesthesia can last hours instead of minutes.
- CACNA1S GenotypeSecond malignant hyperthermia gene, covering susceptible families whose risk is not explained by RYR1.Why it mattersCatches inherited anesthesia risk in people whose RYR1 result comes back clean.
- CES1 GenotypeThe liver enzyme that switches on dabigatran and clears methylphenidate.Why it mattersVariant carriers had lower dabigatran levels and less bleeding in trial data, with no dosing guidance yet.
- COMT Genotype (Val158Met)Sets dopamine-clearing speed, a proposed explanation for differences in antipsychotic and pain response.Why it mattersOne input to a dopamine-response hypothesis, not a reason by itself to choose a drug.
- CYP2B6 GenotypeClears efavirenz, methadone, bupropion and ketamine, with formal dosing guidance for efavirenz and for sertraline.Why it mattersPoor metabolizers accumulate efavirenz and more often get nervous system side effects from it.
- CYP2C18 GenotypeSits inside the CYP2C gene cluster, where its variants help pin down haplotypes affecting CYP2C19 and CYP2C9 activity.Why it mattersAdds cluster-level context that sharpens an otherwise ambiguous CYP2C19 or CYP2C9 call.
- CYP2C19 GenotypeActivates clopidogrel and clears several antidepressants and acid-reflux drugs, making it one of the most often actionable genes here.Why it mattersPoor metabolizers may not convert enough clopidogrel into its active form after a stent.
- CYP2C8 GenotypeClears some diabetes drugs, montelukast and paclitaxel chemotherapy, covering a route no other enzyme here tracks.Why it mattersReduced activity raises exposure to a drug set no other gene in this panel tracks.
- CYP2C9 GenotypeClears warfarin, several anti-inflammatory drugs and some diabetes drugs, and pairs with VKORC1 for warfarin dosing.Why it mattersReduced activity means a lower warfarin dose and more early bleeding risk at standard dosing.
- CYP2D6 GenotypeClears many antidepressants, antipsychotics, tamoxifen, codeine and tramadol, with poor and ultrarapid results both changing prescribing.Why it mattersPoor or ultrarapid results change both exposure and whether codeine or tramadol will work.
- CYP3A4 GenotypeBreaks down a large share of prescription drugs, including many statins and immune-suppressing medicines.Why it mattersA reduced-function variant can shift exposure across an unusually wide range of common drugs.
- CYP3A5 GenotypeGuides tacrolimus dosing after organ transplant, where expressers need more drug to reach target levels.Why it mattersAn expresser result predicts underdosing on a standard tacrolimus starting dose.
- CYP4F2 GenotypeRecycles vitamin K, which nudges warfarin requirements beyond CYP2C9 and VKORC1.Why it mattersCarriers tend to need a slightly higher warfarin dose.
- DPYD GenotypeBreaks down fluorouracil and capecitabine chemotherapy. Reduced activity leaves those drugs circulating far longer than intended.Why it mattersA reduced-function result before treatment is a clear signal to lower or avoid these chemotherapy doses.
- DRD2 GenotypeThe dopamine receptor every antipsychotic binds, included for possible response and prolactin-related side-effect context.Why it mattersAdds dopamine-pathway context on antipsychotic response; measured effects are small, so it stays context rather than instruction.
- ERCC1 GenotypeA DNA repair gene studied for response to platinum chemotherapy.Why it mattersExplored as a platinum chemotherapy response marker, with results varying across large trials.
- F2 GenotypeThe prothrombin G20210A variant, another inherited clotting risk factor that matters most around estrogen exposure and prior clots.Why it mattersProthrombin carriers had about fivefold early clot risk during oral contraceptive use in United Kingdom Biobank.
- Factor V LeidenThe most common inherited clotting variant. It asks how readily your blood forms a clot, not how you clear drugs.Why it mattersCarriers had close to sixfold early clot risk during oral contraceptive use in United Kingdom Biobank.
- G6PD GenotypeReads the gene for glucose-6-phosphate dehydrogenase, the enzyme that helps red blood cells survive certain medicines.Why it mattersDeficiency means rasburicase, dapsone and some malaria drugs can break red blood cells apart.
- GGCX GenotypeCovers another vitamin K clotting step that contributes a smaller share of stable warfarin dose variation.Why it mattersHelps explain warfarin dose needs the two main warfarin genes leave unexplained.
- GRIK4 GenotypeA glutamate receptor gene, giving the panel one look beyond serotonin and dopamine signaling.Why it mattersFlags variation in a glutamate pathway tied to antidepressant response in early cohorts. Exploratory.
- GSTP1 GenotypeHelps clear chemotherapy byproducts, one route used to study side-effect differences.Why it mattersLinked to specific chemotherapy side effects in cohorts, without dosing guidance.
- HLA-A GenotypeAdds a second immune signal for carbamazepine hypersensitivity, covering reactions HLA-B variants don't explain.Why it mattersBroadens the warning for anticonvulsant skin reactions beyond the single best-known allele.
- HLA-B GenotypeFlags immune variants tied to severe reactions to abacavir, carbamazepine, allopurinol and several other drugs.Why it mattersA risk variant here usually means avoiding the matching drug, not adjusting the dose.
- HTR1A GenotypeAnother serotonin receptor in the panel's map of how serotonin signaling may shape treatment response.Why it mattersLinked to antidepressant response in some cohorts, with inconsistent replication. Treat as exploratory.
- HTR2A GenotypeA serotonin receptor that antidepressants act on, included to capture target sensitivity rather than drug levels.Why it mattersAdds target-side context on antidepressant tolerability that current prescribing guidance does not yet use.
- HTR2C GenotypeA serotonin receptor with one of the more reproducible target-side signals in psychiatry: antipsychotic weight gain.Why it mattersMay flag higher antipsychotic weight-gain risk, useful as context rather than a prescribing rule.
- IFNL4 GenotypeReads the interferon-lambda variant that shapes how the immune system handles hepatitis C infection and older interferon treatment.Why it mattersIdentifies the genotype most likely to clear hepatitis C on its own or with interferon-based therapy.
- ITPA GenotypeAffects how thiopurine and ribavirin byproducts build up, adding a third layer to drug tolerance.Why it mattersLinked to thiopurine side effects and protection from ribavirin-related anemia. Guidance is still emerging.
- KIF6 GenotypeA cardiovascular variant studied for coronary risk and for who gains most from statin therapy.Why it mattersAdds inherited cardiovascular context; statin decisions still rest on lipids and overall risk.
- MT-RNR1 GenotypeFlags inherited variants that make the inner ear vulnerable to aminoglycoside antibiotics such as gentamicin.Why it mattersCarriers can lose hearing permanently after even one standard dose of that antibiotic class.
- MTHFR GenotypeReads the folate-processing enzyme behind some homocysteine elevations, interpreted alongside a homocysteine blood level.Why it mattersReduced activity points toward measuring homocysteine, not changing medication by itself.
- NAT2 GenotypeSets how quickly your liver clears isoniazid, hydralazine and sulfa drugs.Why it mattersSlow clearance raises the risk of isoniazid liver injury and lupus-like drug reactions.
- NQO1 GenotypeProcesses some chemotherapy-related compounds and is studied for treatment response and toxicity.Why it mattersExploratory for chemotherapy response and side effects, with no prescribing guideline attached.
- NUDT15 GenotypeCovers the second thiopurine toxicity pathway, with risk variants more common in East Asian and Hispanic ancestry.Why it mattersCatches thiopurine intolerance risk that TPMT alone can miss.
- OPRM1 GenotypeThe opioid receptor gene, included for target-side context on opioid dose needs and pain response.Why it mattersSome studies link A118G to higher opioid needs, but no guideline uses it.
- RYR1 GenotypeMain gene behind malignant hyperthermia, a life-threatening reaction to inhaled anesthetics and succinylcholine.Why it mattersA risk variant changes the anesthetic plan and needs to be known before any surgery.
- SLCO1B1 Genotype (Val174Ala)Shows how well the liver takes up statins from blood, which affects muscle exposure.Why it mattersReduced function helps explain or predict statin muscle symptoms and points toward a different statin.
- TPMT GenotypeClears thiopurine drugs used in inflammatory bowel disease, autoimmune disease and leukemia.Why it mattersLow activity means a standard thiopurine dose can crash your white blood cell count.
- UGT1A1 GenotypeHelps clear irinotecan chemotherapy and atazanavir, and explains lifelong mild jaundice in Gilbert syndrome.Why it mattersReduced activity raises the chance of severe diarrhea and low white counts on irinotecan.
- UGT1A4 GenotypeHelps clear lamotrigine and several antipsychotics outside the main CYP enzyme family.Why it mattersVariants can shift lamotrigine levels, one explanation for dose needs CYP genes miss.
- VKORC1 GenotypeMeasures warfarin sensitivity at the drug target, separate from how fast you clear the drug.Why it mattersThe sensitive genotype reaches the same blood-thinning effect on a smaller dose.
- XRCC1 GenotypeAnother DNA repair pathway relevant to how chemotherapy damage is handled.Why it mattersLinked to differences in platinum chemotherapy tolerance across cohorts, without consistent replication.
About PGx Comprehensive
Most prescribing is educated guessing. A standard dose goes out, and if it doesn't work or it makes you sick, the plan changes. Part of that variation is already written in your DNA, and unlike almost every other test you'll ever take, you only have to measure it once.
This panel checks 49 genes that shape how drugs move through you and what they do when they arrive. Some carry formal prescribing rules and warnings printed on drug labels. Others are research markers that shouldn't change what you take yet. The work is telling those two apart.
What This Panel Reveals
Most genes here answer one of two questions: how much drug ends up in your bloodstream, or what happens when it gets there. The first question is the one genetics answers best. Many of these genes have names starting with CYP. CYP means cytochrome P450. These are liver enzymes that break down many drugs, and the version you inherited can leave you with far more or far less active drug than the dose on the bottle implies.
The direction of that effect flips depending on the drug. For most medicines, slow clearance means the drug piles up and side effects follow. Some drugs arrive inactive and have to be switched on by your liver. For those, slow clearance means the drug barely works. Codeine and clopidogrel are the classic pair: a poor metabolizer gets little pain relief from one and little clot protection from the other.
A smaller group of genes isn't about dose at all. For a handful of drugs, a variant means a standard dose can put you in a hospital. That group covers fluorouracil chemotherapy, thiopurine immune-suppressing drugs, immune variants behind severe skin reactions to certain seizure and gout drugs, the red blood cell enzyme glucose-6-phosphate dehydrogenase, and the two genes behind a dangerous reaction to anesthesia. Several of these have testing instructions written into the drug labels themselves.
The clotting genes answer something different again. Factor V Leiden and the prothrombin variant don't describe how you handle a drug; they describe how readily your blood clots. In a United Kingdom Biobank study of more than 240,000 women, Factor V Leiden carriers had a clot-risk estimate close to six times higher in the first two years of oral contraceptive use.
The Two Tiers Inside One Report
Read your report as two documents. The first is the guideline tier. For a subset of genes here, the Clinical Pharmacogenetics Implementation Consortium and its Dutch counterpart publish specific dosing instructions by gene result, and the Food and Drug Administration references several of them on drug labels. These are results a pharmacist can act on today.
That tier has been tested head to head. In a European trial spanning seven countries, people whose prescribing followed a 12-gene panel had clinically relevant side effects drop from roughly 28 in 100 under usual care to about 21 in 100.
The second tier is the receptor and repair genes: serotonin and dopamine receptors, the opioid receptor, the dopamine-clearing enzyme COMT, and the DNA repair and detoxification genes studied in chemotherapy. The reasoning for including them is sound, since a drug's effect depends on its target as much as on its concentration. But in antidepressant studies, many target-side markers have not replicated consistently, and the guideline group for serotonin-reuptake antidepressants left HTR2A out of prescribing guidance.
Read them as context, not instruction. The target-side signal with the clearest support is the link between an HTR2C serotonin receptor variant and weight gain on antipsychotics. Even there, the result doesn't override how you're doing on the medicine.
How to Read Your Results Together
Almost everyone carries something. Across large preemptive testing programs, about 9 in 10 people have at least one result that could change a prescribing recommendation. In a 10,000-person biobank study, 79 percent carried actionable variants in three or more genes. An abnormal result is the norm, not the exception. What matters is which gene it's in and whether you'll ever take the matching drug.
| Pattern | What It Suggests |
|---|---|
| Poor metabolizer at CYP2C19 while you're taking clopidogrel | Your body may not be activating enough of the drug. This pair has prescribing guidance and a label warning, and alternatives exist. |
| Normal metabolizer at CYP2D6, but you take a drug that blocks CYP2D6 | Your genes and your real-world metabolism disagree. The medication list wins. |
| A variant in DPYD, TPMT or NUDT15 with no cancer or autoimmune diagnosis | Nothing to do today. This is the result worth having on file before anyone ever writes that prescription. |
| A receptor variant labeled reduced response while a medication is working fine | Context, not a reason to switch. These markers don't override how you're actually doing. |
When Results Can Be Misleading
Three things break the clean story, and each one affects the whole panel at once.
The first is phenoconversion. Phenoconversion means a medicine you're taking changes how your genes behave in practice. Plenty of ordinary drugs block the same enzymes this panel measures, so someone genetically normal can behave like a poor metabolizer while taking them. Among more than 4,000 people receiving psychiatric care, 42 percent had their CYP2D6 metabolizer status effectively changed by another drug they were on. Your gene result is the starting point. Your current medication list modifies it.
The second is coverage. Labs test a chosen list of variants and report anything they didn't look for as normal. Which variants a lab includes can change the metabolizer status it prints, and the gaps have fallen hardest on people whose ancestry was underrepresented in older genetic studies. Check variant coverage before you order.
The third is translation. Two reports can start from the same gene call and give different advice. In a comparison of commercial antidepressant reports against consortium guidelines, roughly 13 percent of metabolizer assignments and 43 percent of medication recommendations differed from the standard. The gene result is the durable fact. The interpretation printed next to it is not.
What to Do with Your Results
Sort the report into three piles. Results for drugs you take now go to whoever prescribes them this week, named by gene and metabolizer status rather than handed over as the whole 49-gene report. Results for high-risk drugs you might take later go in your chart: chemotherapy, thiopurine, anesthesia, immune-reaction and aminoglycoside-antibiotic warnings. The anesthesia and antibiotic warnings belong on a card you carry. Everything else is background.
You never need to repeat the test. DNA doesn't change, and no meal, medication or time of day alters the result. Interpretation does change, though: allele function calls get revised and panels add variants. If your report is several years old and you're about to start a drug with a serious genetic warning, get a fresh interpretation of the same data rather than a new sample.
A few blood tests make the gene result more useful. Kidney and liver function set your actual clearance, which the genes alone can't tell you. If statin muscle aches are the question, a creatine kinase level shows whether muscle is really being damaged. If glucose-6-phosphate dehydrogenase deficiency turns up, an enzyme activity measurement confirms how severe it is. And a Factor V Leiden or prothrombin result alongside a contraception decision is worth taking to a clinician who handles clotting risk.