CNSDose
(Comprehensive+)

Unlike conventional pharmacogenetic tests that focus solely on hepatic drug metabolism (for example CYP2D6 and CYP2C19), CNSDose uniquely analyses both liver metabolism and blood-brain barrier transport genetics. This enables clinicians to better understand factors influencing medication access to the central nervous system and the dose likely to reach therapeutic targets.

CNSDose delivers practical guidance on whether standard doses are likely to be sub‑therapeutic, appropriate or excessive for an individual patient. These insights can support initial medication and dose selection, explanation of prior non-response or adverse effects, and dose optimisation during ongoing treatment.

CNSDose is a once‑only test analysing 19 clinically relevant genes to provide guidance for 174 medications, including 96 psychotropics. Results remain applicable for lifetime prescribing decisions.

In a retrospective analysis of 1,100 CNSDose test results, 19% of patients with mental illness had normal liver metabolic genetics (e.g. CYP2D6 and CYP2C19), which would not assist clinicians in psychotropic medication selection. Of these patients, 40% had blood-brain barrier genetic variants affecting psychotropic medication transport into the brain, with significant implications for medication selection and dosing. These findings highlight the clinical value of CNSDose beyond standard metabolism‑only pharmacogenetic testing.

CNSDose is particularly useful when patients experience treatment resistance, medication intolerance, or when initiating or optimising antidepressants, anxiolytics, antipsychotics or other psychotropic therapies in both general practice and specialist care.

CNSDose was the first pharmacogenetic test to demonstrate positive outcomes in a randomised controlled trial for antidepressant treatment, with recovery rates of 72% in CNSDose guided prescribing compared to 28% with unguided prescribing.¹

A 2017 study published in Pharmacogenetics and Genomics found that patients with major depressive disorder whose treatment was guided by CNSDose were 2.5 times more likely to achieve remission compared with unguided prescribing.²

The user-friendly CNSDose report, developed by Australian psychiatrists, covers 174 medications and includes:

The CNSDose report is available to download from eResults.

Download Sample Report

The CNSDose report provides practical guidance for 174 medications, 96 of which are used in mental health care, including:

• Antidepressants (e.g. sertraline, escitalopram, fluoxetine)
• Antipsychotics (e.g. olanzapine, quetiapine)
• Anxiolytics (e.g. diazepam)
• ADHD medications (e.g. methylphenidate, lisdexamfetamine)
• Dementia medication (e.g. donepezil)

The CNSDose report also includes 78 non‑psychotropic medications across cardiology, oncology, pain management, gastroenterology and other clinical areas.

View Medications List

Case 1: Anti-depressant intolerance

A 22-year-old female university student who had struggled with depression and anxiety since high school. She had experienced multiple side effects, even at half-doses of antidepressant medication.

She reported that her previous doctor had described her as overly anxious and a hypochondriac. She subsequently researched pharmacogenetics online and asked her new general practitioner whether testing might be appropriate.

CNSDose testing revealed that she was a poor metaboliser at cytochrome P450 2D6 and 2C19, along with a low blood-brain barrier block based on the CNSDose algorithm estimate. This was consistent with an increased risk of inadvertent overdose, even at low doses of antidepressant medication.

She was commenced on sertraline 12.5 mg (one quarter of the lowest-strength tablet). The dose was not increased. She experienced no side effects and reported an improvement in mood after one month. Her ability to study improved as did her academic performance.

Case 2: Partial treatment response

A 43‑year‑old male accountant with recurrent depression that had partially responded to escitalopram 20 mg. He was otherwise medically well and was not taking any other medications. His general practitioner was apprehensive about escalating the dose.

The wait to see a psychiatrist exceeded six months, and the psychiatrist recommended ordering a CNSDose test in the interim to assist with treatment optimisation.

CNSDose testing demonstrated that the patient was an ultra-rapid metaboliser and appeared to have high efflux status at the blood-brain barrier. This suggested that either an alternate agent or a supra‑therapeutic dose of escitalopram may be required for adequate clinical effect. The patient preferred to avoid a medication change and was willing to trial escitalopram 30 mg.

An ECG was performed before and after dose escalation to monitor the QTc interval, given the known risk of QTc prolongation with citalopram, a medication structurally related to escitalopram. The ECG remained stable and within normal limits.

After three weeks on escitalopram 30 mg, his residual depressive symptoms, including low drive and ambivalence towards life, fully remitted. The scheduled psychiatry appointment was no longer required.