Pharmacogenomic screening is an, at home cheek-swab test that helps your doctor or psychiatrist choose safer, better-matched medication options with less guesswork.
Best suited for people who have had side effects, limited benefit, or repeated medication changes and want a more informed conversation with their clinician.
The offer is a complete PGx testing package: home collection, accredited lab analysis, and a report built to support a clinical prescribing discussion.
Targets clinically useful pharmacogenomic markers rather than broad consumer ancestry-style screening.
Cheek-swab collection kit posted to your address with prepaid return packaging.
Medication-response findings organised for use by your doctor or psychiatrist, not just raw gene data.
From laboratory receipt of your sample to report delivery for clinical review.
Pharmacogenomics helps explain why one person gets side effects at a low dose, another gets little benefit, and another responds as expected.
Most medications are prescribed using population-level guidance, yet real-world response varies widely. Genetic differences can influence how quickly a medication is broken down, whether the dose runs too high or too low, and whether a medicine is more likely to be poorly tolerated.
In psychiatry, this matters because many people spend months or years cycling through medication changes before finding a workable fit. PGx testing does not replace clinical judgment, but it can make the next prescribing decision more informed and more personalised.
Clinical references: RCPA Pharmacogenomic Indications in Australia, CPIC serotonin reuptake inhibitor guideline, and CPIC atomoxetine guideline.
Ramsey CM, Lynch KG, Thase ME, et al. "Prevalence of predicted gene-drug interactions for antidepressants in the treatment of major depressive disorder in the Precision Medicine in Mental Health Care Study." Journal of Affective Disorders. 2021;282:1272-1277. https://doi.org/10.1016/j.jad.2021.01.034
It works best when you and your doctor are trying to choose a better next step, not when you are simply curious about your genetics.
You have tried two or more psychiatric medications with limited benefit, or your treatment has been changed more than once.
You have had side effects at standard doses or found previous medications hard to tolerate.
Your doctor is considering a new medication and wants more guidance before more trial-and-error prescribing.
You want results that can be reviewed with a GP or psychiatrist as part of a treatment plan, not used on their own.
Answer a few quick questions to find out whether pharmacogenomic testing may be relevant to your situation.
The purchase process is simple. Clinical intake and consent happen after checkout, so you do not need to prepare your full medication history to buy the kit.
Purchase your PGx swab kit through our dedicated secure checkout page.
A simple cheek swab collection kit will be mailed to your address, including a prepaid return envelope to send your sample back to our NATA-accredited laboratory.
After purchase, TBMH completes clinical onboarding and confirms the doctor or psychiatrist who should receive the report. If you do not already have a preferred clinician, TBMH can help arrange review options.
Your clinician receives the report for interpretation in the context of your treatment history, medications, and care plan.
You can then schedule an appointment with your doctor to review the results of your personalised PGx report.
Knowing exactly which genes are tested helps clinicians and patients understand the scope of the report and which medications are covered.
Your genetic profile determines how quickly your liver enzymes break down specific medications. Click on any metaboliser type below to learn what it means for you.
The enzyme works very slowly, so medication can build up in the body. This increases the risk of side effects and adverse reactions, even at standard doses.
If you are a poor metaboliser and are prescribed a medication affected by your genotype, your clinician will consider:
You break down certain medications somewhat more slowly than average. This is a very common finding and often results in moderate caution rather than major prescribing changes.
For escitalopram in a CYP2C19 intermediate metaboliser, CPIC recommends starting with the standard dose but considering a slower titration and lower maintenance dose compared to a normal metaboliser. This is a "use thoughtfully" result — not a "do not use" result.
Your enzyme processes certain medications at the expected rate. Standard prescribing guidelines apply in most cases.
A normal metaboliser result for one gene does not mean there are no relevant pharmacogenomic findings in your report. Other genes (e.g. CYP2C19, HLA-B) may still have actionable results for different medications.
Always review your full PGx report alongside your clinician, not just a single gene result.
You break down certain medications faster than average. This means standard doses may leave you with lower-than-expected drug levels, potentially reducing effectiveness.
Rapid metabolism doesn't mean a medication won't work; it means achieving a therapeutic level may require dose adjustment. Your clinician will weigh this against safety and clinical context.
Your enzyme breaks down certain medications extremely quickly. This can make some medications less effective at standard doses, or in rare cases, create safety concerns when metabolites are active.
For prodrugs (medications that are converted into an active form by the enzyme), ultrarapid metabolism can actually increase active drug levels. This is clinically important for medications like codeine, which is why pharmacogenomics matters not just for under-response but for safety.
Clinical references: CPIC serotonin reuptake inhibitor guideline, CPIC guideline index, and FDA table of pharmacogenetic associations for CYP2D6-codeine safety.
The test is privately funded. For eligible patients, private-health rebates may materially reduce out-of-pocket cost. No Medicare rebate is currently available.
Best for patients who want a complete home test kit and clinician-ready prescribing report.
As of June 3, 2026, Medibank publishes a PGx claiming guide for eligible members.
As of June 3, 2026, the $47 AUD example reflects a full $150 Medibank benefit on a $197 test price. Always check current insurer terms before purchase.
These de-identified examples show the kind of prescribing decisions a PGx report can support when standard treatment is not going to plan.
Why testing was useful: Had trialled three SSRIs over two years without adequate response, and experienced marked side effects at standard doses, with dizziness, fatigue, and nausea, at doses her psychiatrist considered modest.
PGx Finding: CYP2D6 Poor Metaboliser · CYP2C19 Intermediate Metaboliser
What changed next: Switched to agomelatine (not significantly CYP2D6-dependent). Dose started low with monitoring. Reported effective symptom control and no significant side effects at 3 months.
Why testing was useful: Clinician considering dose increase due to persistent low-grade symptoms. Patient had no subjective complaints about his current dose but plasma levels had not been checked.
PGx Finding: CYP2D6 Ultrarapid Metaboliser
What changed next: Plasma aripiprazole level confirmed sub-therapeutic despite "standard" dosing. Dose adjusted upward per CPIC guidance. Clinician avoided unnecessarily switching to a different antipsychotic.
Why testing was useful: Patient had persistent low mood and poor sleep despite being prescribed escitalopram by her GP. Dose escalation was being considered because symptoms had only partially improved. A comprehensive PGx panel was ordered before increasing the antidepressant dose.
PGx Finding: CYP2C19 Poor Metaboliser — CPIC: for citalopram/escitalopram, consider an alternative antidepressant not predominantly metabolised by CYP2C19, or use dose adjustment if the drug remains clinically appropriate. Poor metabolism can increase drug exposure and adverse-effect risk.
What changed next: Escitalopram dose escalation was avoided. The GP discussed options with psychiatry and transitioned the patient to a more suitable antidepressant strategy. Sedation, gastrointestinal intolerance, and potential dose-related cardiac safety concerns were avoided before worsening.
All vignettes are de-identified composite cases for educational purposes. They do not represent specific individual patients.
Garrod first proposed that inherited differences in metabolism explain variability in disease and chemical responses, laying the conceptual foundation for what would become pharmacogenomics.
Adverse reactions to primaquine in patients with G6PD deficiency demonstrated that individual genetic variation could predict drug response.
Researchers identify CYP2D6 as a key enzyme responsible for debrisoquine metabolism, now central to psychiatric pharmacogenomics.
Completing the sequencing of the human genome unlocked a new era for personalised medicine, making broad pharmacogenomic testing feasible.
CPIC, DPWG and FDA PGx guidelines now provide clinically actionable gene–drug interaction recommendations used in practice globally, including at TBMH.
Sir Archibald Garrod (1857–1936) — pioneer of biochemical genetics
Purchase begins with a simple secure checkout. TBMH then completes clinical onboarding, consent, and clinician coordination after your order is confirmed.
Checkout collects payment and shipping details only. You do not need to prepare your referral information, medication list, or clinical history before ordering.