Use pharmacogenomic testing when you need clearer guidance on dose, tolerability, medication switching, or likely gene-drug issues in complex psychopharmacology. Reports are built for specialist review and returned in 2 to 3 weeks.
Psychiatry is the deepest coverage area in the TBMH-PGx panel, with meaningful overlap into pain, neurology, and general medicine prescribing that often complicates specialist psychiatric treatment plans.
The deepest coverage area in the panel, spanning antidepressants, antipsychotics, anxiolytics, stimulants, and mood stabilisers.
Representative coverage: Aripiprazole, risperidone, escitalopram, sertraline, venlafaxine, nortriptyline, bupropion, mirtazapine, dexamphetamine, lisdexamfetamine, lithium, carbamazepine, lamotrigine, and sodium valproate.
Common genes: Key genes include CYP2D6, CYP2C19, CYP3A4, CYP1A2, CYP2B6, CES1, HLA-A, HLA-B, UGT1A4, UGT1A6, and POLG.
Useful for clinicians managing cognition, seizure disorders, sleep-wake prescribing, and movement-related therapy.
Representative coverage: Donepezil, galantamine, phenytoin, primidone, phenobarbital, modafinil, and tetrabenazine.
Common genes: Most frequently implicated genes are CYP2D6, CYP2C19, CYP2C9, and CYP3A4.
Captures several high-impact analgesic pathways where under-response and toxicity risk are both clinically relevant.
Representative coverage: Codeine, tramadol, oxycodone, fentanyl, methadone, morphine, celecoxib, ibuprofen, and ketamine/esketamine.
Common genes: Common drivers include CYP2D6, CYP3A4, CYP2B6, CYP2C9, ABCB1, and UGT2B7.
Smaller in scope, but relevant where psychiatric care intersects with sleep, cardiovascular, and behavioural prescribing.
Representative coverage: Melatonin, propranolol, and guanfacine.
Common genes: Coverage includes CYP1A2, CYP2C19, CYP2D6, and CYP3A4.
The quick-reference guide ranks these genes by the number of medications they influence within the panel.
Broadest influence across antidepressants, antipsychotics, stimulants, opioids, and tetrabenazine.
High relevance for antipsychotics, anxiolytics, ketamine/esketamine, donepezil, and several analgesics.
Prominent in SSRIs, TCAs, diazepam, modafinil, and selected anticonvulsants.
Important for NSAIDs, phenytoin, phenobarbital, primidone, and valproate-related interpretation.
Frequently relevant for clozapine, olanzapine, duloxetine, melatonin, and propranolol.
Key for bupropion, methadone, tramadol, sertraline, and ketamine/esketamine metabolism.
The highest-yield referrals are the ones where you need the next prescribing decision to be more defensible, not just more informed.
Useful when antidepressants, antipsychotics, or ADHD agents have produced limited benefit despite reasonable sequencing and adherence.
Helps explain adverse effects at standard doses, active-metabolite burden, or the need for slower titration than expected.
Particularly relevant when you are deciding whether to change class, reduce dose, avoid a drug, or choose a more tolerable next option.
Useful where interacting inhibitors or inducers may shift functional phenotype and alter the interpretation of a usual prescribing plan.
Helpful where CYP2D6 or CYP2C19 findings may change the risk-benefit balance across atomoxetine, antidepressants, and adjunctive strategies.
Supports broader panel selection and interaction review when ketamine sits within a more complex medication pathway.
These two enzymes sit behind many of the prescribing problems psychiatrists actually see in clinic: early side effects, partial response, difficult dose finding, and surprising medication-switch outcomes.
Clinical references: CPIC serotonin reuptake inhibitor guideline, CPIC atomoxetine guideline, and FDA pharmacogenetic associations for CYP2D6-codeine safety.
CYP2D6 is one of the body's most important drug-metabolising enzymes. Found mainly in the liver, it helps process many commonly prescribed psychiatric medications, including antidepressants, antipsychotics, and ADHD medicines.
In precision psychiatry, CYP2D6 acts like a metabolic "speed controller." Genetic differences in CYP2D6 explain why one person gets side effects at a low dose, why another seems to get little benefit, or why a medication that is "standard" on paper turns out to be either ineffective or poorly tolerated for a particular individual.
CYP2D6-relevant psychiatric medications include:
3D ribbon model of the CYP2D6 enzyme
CYP2C19 is equally important in psychiatric prescribing. It metabolises several first-line antidepressants including citalopram, escitalopram, sertraline, and amitriptyline. CYP2C19 intermediate metabolisers (a very common finding) may require slower titration and lower maintenance doses for these SSRIs.
The report is built to shorten interpretation time in clinic. It is not just a genotype dump.
Clear metaboliser calls and activity interpretation for the genes most likely to alter psychiatric prescribing.
Medication cards highlight avoid, caution, moderate, or use-as-directed pathways, with dose or alternative flags where relevant.
CPIC, DPWG, FDA PGx, FDA label, and BaMH synthesis are shown together so you can judge strength and differences quickly.
Flags multi-gene and drug-gene-drug issues that can change phenotype in practice, especially in polypharmacy.
Helps identify when plasma-level monitoring or closer early review is worth building into the plan.
Designed to support the next prescribing decision alongside comorbidity, adverse-effect history, organ function, and treatment goals.
TBMH-PGx reports draw from internationally recognised pharmacogenomic sources so you can separate strong prescribing guidance from background PGx context.
CPIC (Clinical Pharmacogenomics Implementation Consortium) provides evidence-based, peer-reviewed guidelines for gene–drug pairs. CPIC uses a strong/moderate/optional/no recommendation framework and is considered the gold standard for clinical PGx implementation. CPIC guidelines undergo regular systematic evidence review and are published in Clinical Pharmacology & Therapeutics.
Visit the Clinical Pharmacogenomics Implementation Consortium (CPIC)
DPWG (Dutch Pharmacogenomics Working Group) provides European guidelines for gene–drug interactions. DPWG and CPIC often agree but may frame recommendations differently. DPWG guidelines are embedded in Dutch clinical pharmacy infrastructure, providing a complementary evidence source. The PGx report shows both, allowing clinicians to compare evidence provenance.
FDA PGx labelling identifies pharmacogenomic information mentioned in approved drug prescribing information (US market). Not all FDA PGx entries carry the same level of actionability as CPIC guidelines — the "Unspecified" label often indicates informational content rather than a specific dosing recommendation. Useful for regulatory context but should not be the primary driver of prescribing changes.
When ketamine or esketamine is part of the treatment pathway, the clinically relevant PGx landscape shifts beyond the usual SSRI and antipsychotic focus.
Clinical references: FDA Spravato prescribing information and PubMed review of pharmacogenetic and drug-interaction aspects of ketamine safety.
Ketamine is primarily metabolised by CYP3A4 and CYP2B6, with CYP2C9 playing a secondary role. Genetic variation in these enzymes may influence ketamine clearance, active metabolite accumulation, and both therapeutic response and dissociative side-effect burden.
Most psychiatric PGx centres on CYP2D6 and CYP2C19. Ketamine planning shifts attention to CYP3A4/5 and CYP2B6, especially when the patient is already on a complex regimen.
Recommendation: If ketamine or esketamine is likely to remain part of the pathway, the Comprehensive Panel is the more clinically useful option.
Use the form below to start the patient workflow. The patient receives purchase and kit instructions directly, while the completed report comes back to you for specialist review.
The referral only needs the clinical essentials required to start patient contact and route the final report back to you.
After referral, the patient receives clear steps for purchase, home swab collection, and return shipping.
The PGx result is designed for psychiatrist interpretation in the context of current medications, adverse effects, and treatment goals.
Please review the details below. When you click "Send Referral", an email will be generated to:
Your referral email has been opened in your email client. A copy will be delivered to:
Use the report in this order when you need to interpret it quickly in specialist practice: Dashboard, Medications, Genotypes, GGD Interactions, TDM, then the source notes on each drug card.
Start with Key Findings plus the Preferred and Avoid panels. This gives you the actionable genotypes, priority drugs, and phenoconversion risks in under a minute.
Search the Medications tab for the proposed drug or class. Start with the report risk level: Significant, Moderate, Caution, or Use as Directed.
Interpret the risk tag, impacted genes, phenotype chips, and any DOSE or ALT markers before opening the full clinical note and source-by-source recommendations.
Compare CPIC, DPWG, FDA PGx, FDA Label, and the BaMH synthesis. When sources diverge, use the indication and patient context to decide whether to titrate, monitor, or switch.
Open GGD Interactions for phenoconversion and multi-gene effects, then use the TDM tab where flagged to plan plasma level monitoring after initiation or dose change.
PGx is prescribing decision support, not a prescription. Reconcile the report with current medicines, comorbidities, renal or hepatic function, adverse effect history, and treatment goals before acting.
The clinician guide describes six core report areas - Dashboard, Medications, Genotypes, GGD Interactions, TDM, and How to Read. Drug-level risk tags tell you how actionable the prescribing issue is, while phenotype labels, activity scores, and gene-specific notes explain why that recommendation appears.
Use this as a refresher for report language and phenotype terminology. Most psychiatrists will only need it for occasional reference.
Numeric value quantifying expected enzyme activity (e.g. CYP2D6 AS 1.0 = Normal Metaboliser).
Naming system for gene variants, e.g. CYP2D6*1 (normal function) or *4 (no function).
Predicted functional effect: Poor, Intermediate, Normal, Rapid, or Ultrarapid Metaboliser.
Your specific diplotype result for a gene, e.g. *1/*4 (one functional + one non-functional allele).
A medication converted to its active form by a metabolising enzyme; ultrarapid metabolisers may overproduce active metabolite.
Single Nucleotide Polymorphism — the smallest type of genetic variation, and the most common type tested in PGx.
A genetic finding that may guide a clinical decision — dose adjustment, alternative medication, or enhanced monitoring.
The combination of two alleles (one from each parent) that determines your overall enzyme function for a given gene.
A specific gene-medication combination for which clinical pharmacogenomic guidelines exist (e.g. CYP2D6–aripiprazole).