Pharmacogenetics (PGx)
A 10-gene panel covering drug metabolism across 34 medications in cardiometabolic, GI, psychiatric, and other therapeutic areas. Identifies poor, intermediate, normal, and ultra-rapid metabolizers.
Clinical Area · Pharmacogenomics
Right drug, right dose — informed by genomics
Pharmacogenomic testing examines how a patient's genetic profile may affect their response to certain medications — information that can support more informed prescribing and help reduce trial-and-error. Preventive genomic panels can extend this to inherited disease-risk assessment. Results are intended to inform, not replace, clinical judgment.
Preventive genomic risk
Genome-wide polygenic risk scores across 40+ disease categories including cardiovascular disease, metabolic conditions, and cancer — stratified separately for male and female patients.
Multi-cancer early detection
Cell-free DNA analysis covering five or six cancer types from a single blood draw. Appropriate for high-risk populations under physician guidance, not as a population screening tool.
Clinical indications
When to consider PGx or preventive genomics
Drug non-response or adverse reaction — identifying a pharmacogenetic basis
Polypharmacy — assessing drug-gene interactions across a medication regimen
Starting a new drug in a class with known PGx variation (antidepressants, anticoagulants, analgesics)
Preventive health — polygenic disease risk across cardiovascular, metabolic, and cancer categories
Multi-cancer early detection — cfDNA screening in appropriate risk-group populations
Cardiology — hereditary arrhythmia risk screening in individuals with family history of sudden death
Available tests
Pharmacogenomics & preventive panels through AC
GC Genome
ai-CANCERCH®
Multi-cancer early detection from cfDNA; includes five cancer types for males and six cancer types for females, including ovarian cancer.
Method: NGS
Specimen: Streck cfDNA tube
TAT: 14–21 days
GC Genome
Genome Health (Female)
Polygenic risk assessment across 45 disease categories for females, including 14 cancer types.
Method: NGS
Specimen: EDTA whole blood
TAT: 12–14 days
GC Genome
Genome Health (Male)
Polygenic risk assessment across 44 disease categories for males, including neurological, cardiovascular, metabolic, and cancer risks.
Method: NGS
Specimen: EDTA whole blood
TAT: 12–14 days
GC Genome
Genome Screen — Cancer
Genomic screening focused on inherited cancer predisposition and risk stratification.
Specimen: EDTA whole blood
GC Genome
Genome Screen — Cardiac Arrest
A 40-gene screen covering 15 disease types, including hereditary arrhythmia syndromes.
Method: NGS
Specimen: EDTA whole blood
TAT: 17–21 days
GC Genome
Pharmacogenetics (34 drugs)
Ten-gene pharmacogenetic panel predicting response across 34 drugs used in cardiometabolic, gastrointestinal, inflammatory, and other conditions.
Method: Real-time PCR
Specimen: EDTA whole blood
TAT: 10–12 days
GC Genome
Telorisk®
Telomere-related risk assessment from peripheral blood.
Specimen: EDTA whole blood
Result interpretation
Understanding PGx metabolizer phenotypes
PGx results classify patients into phenotype categories based on predicted enzyme activity for specific drug-metabolizing genes. Results should be interpreted by the prescribing clinician alongside the full clinical picture.
Poor metabolizer (PM)
— Little or no functional enzyme activity
Medications metabolized by this enzyme pathway may accumulate at standard doses, increasing the risk of adverse effects or toxicity. Dose reduction or an alternative medication not dependent on this pathway is often clinically indicated. The prescribing clinician should review relevant drug labeling and clinical guidelines.
Intermediate metabolizer (IM)
— Reduced enzyme activity compared to normal
Enzyme activity is lower than expected. Some medications may accumulate or respond differently depending on the drug, dose, and clinical context. Closer monitoring or dose adjustment may be appropriate. Clinical significance varies by specific gene-drug pair.
Normal metabolizer (NM)
— Expected enzyme activity — also called extensive metabolizer
Enzyme activity is within the expected range. Standard dosing guidelines generally apply. This is the most common phenotype for most drug-metabolizing genes. NM status does not rule out other pharmacokinetic or pharmacodynamic factors affecting drug response.
Ultra-rapid metabolizer (UM)
— Significantly higher-than-normal enzyme activity
Some medications may be cleared too rapidly to be effective at standard doses, reducing therapeutic benefit. For prodrugs activated by the same enzyme, conversion to the active form may be accelerated, increasing pharmacodynamic effect. Drug-specific guidance should be reviewed before prescribing.
PGx panels through AC currently cover selected CYP450 and other drug-metabolizing genes. Coverage varies by panel — confirm the specific genes and medications included before ordering.
Pharmacogenomics · clinical detail
Acceptance, limitations & reporting
General guidance to support ordering decisions. Specific thresholds, specimen requirements, and assay availability are confirmed per case with the reference laboratory before testing.
Sample acceptance criteria
- Specimen per the specimen guide (e.g., peripheral blood or a buccal/saliva collection kit), collected and shipped per instructions.
- Current medication list and relevant clinical context support actionable interpretation; consent appropriate to the test.
Assay limitations
- PGx panels genotype defined variants and star alleles; genes or alleles not on the panel are not assessed, and phenotype prediction does not capture all factors affecting drug response (drug–drug interactions, organ function, adherence).
- Polygenic risk scores estimate population-level risk, are not diagnostic, and perform differently across ancestries.
- Multi-cancer early detection is not a population screening tool and does not replace guideline-recommended screening; a negative result does not rule out cancer.
What's reportable
- Metabolizer phenotypes and gene–drug guidance for covered genes and medications.
- Risk estimates for covered conditions where applicable, framed as non-diagnostic.
- Variant and allele coverage and any limitations affecting interpretation.
Prescribing decisions remain with the treating clinician; PGx results inform but do not dictate therapy.
Pharmacogenomics · common questions
Pharmacogenomics — questions clinicians ask
What does a pharmacogenomic (PGx) test actually tell me?
PGx genotyping predicts a metabolizer phenotype — poor, intermediate, normal, or ultra-rapid — for specific drug-metabolizing genes, which informs how a patient may process certain medications. It supports more informed prescribing and can reduce trial-and-error, but it informs rather than dictates therapy; the prescribing clinician integrates it with the full clinical picture.
What are the limitations of PGx results?
Panels genotype defined variants and star alleles, so genes or alleles not on the panel are not assessed. Phenotype prediction also does not capture every factor affecting drug response — drug–drug interactions, organ function, and adherence all matter. Coverage varies by panel, so confirm the specific genes and medications included before ordering.
Are polygenic risk scores diagnostic?
No. Polygenic risk scores estimate population-level risk, are not diagnostic, and can perform differently across ancestries. They are intended to support preventive discussion and risk stratification, not to establish or exclude a diagnosis.
Can multi-cancer early detection replace standard screening?
No. Multi-cancer early detection (cfDNA) is not a population screening tool and does not replace guideline-recommended screening. A negative result does not rule out cancer. It is appropriate for defined higher-risk populations under physician guidance, alongside — not instead of — established screening.
Pharmacogenomics
Discuss a PGx or preventive genomics case
Share the clinical scenario, current medications, or preventive health question. AC can help identify the most appropriate panel and interpretation pathway.
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