This is the practical walkthrough. If you have Nebula Genomics WGS data and you want to know what a drug response report looks like when run against your VCF, here's the actual output: which medications get flagged, what the recommendations say, what WGS specifically adds over consumer-array data for drug response calls.
Pharmacogenetic reports inform prescribing decisions; they do not replace clinical judgment. Never start, stop, or change a medication based solely on a report. Always discuss with your prescribing clinician.
This is the most concrete place where WGS data changes your drug response report. CYP2D6 is the gene behind dozens of common medication decisions: codeine, tramadol, paroxetine, venlafaxine, fluoxetine, atomoxetine, aripiprazole, tamoxifen, metoprolol. Its phenotype depends not only on single-nucleotide variants but on gene copy number (duplications and deletions), which genotyping arrays cannot reliably detect. With Nebula WGS you get CYP2D6 called with duplications and deletions resolved, which means the report correctly identifies ultrarapid and poor metabolizers that a consumer-array report might miss or call as normal.
A typical output: a metabolizer phenotype card for each pharmacogene (CYP2D6, CYP2C19, CYP2C9, CYP3A5, CYP2B6, SLCO1B1, VKORC1, DPYD, TPMT, UGT1A1, HLA-B), followed by a per-medication recommendations section. A patient who turns out to be a CYP2D6 ultrarapid metabolizer with a DPYD intermediate metabolizer finding, for example, would see: tramadol flagged with a do-not-use warning (risk of severe toxicity from over-activation), codeine flagged similarly, and capecitabine flagged with a 25-50 percent dose reduction recommendation if chemotherapy ever comes up. Each flag links back to the specific CPIC or FDA guideline that produced it.
For medications you're currently on or about to be prescribed: share the relevant section with your clinician before the next dose decision. For medications you're not currently taking: save the report. It's a reference document. A patient who discovers they're DPYD intermediate at age 40 is storing information that will matter enormously if they ever get a colorectal cancer diagnosis and their oncologist is about to order capecitabine. Same for pain management: knowing your CYP2D6 status before you need opioids after surgery is materially different from finding out after a bad reaction.
Beyond CYP2D6 resolution, WGS improves confidence on several other pharmacogenes. DPYD has several rare loss-of-function variants that consumer arrays may not include; WGS catches them all. TPMT deficiency (critical for azathioprine and mercaptopurine safety) is similarly rare but important; WGS won't miss a deficient patient. For patients whose ancestry is not well-represented in consumer-array design (non-European populations), WGS is meaningfully better at catching pharmacogenetic variants than array-based tests.
Specific phenotype outputs you'll see in a Nebula WGS drug response report, with the practical implications for each.
Roughly 1 to 3 percent of people. WGS is particularly good at catching this phenotype because it involves gene duplications. For prodrugs like codeine and tramadol, this is the dangerous end of the phenotype range: the drug activates too quickly, producing dangerously high opioid levels from standard doses. The FDA has a boxed warning specifically for CYP2D6 ultrarapid metabolizers and codeine.
Roughly 7 percent of people of European descent. Tramadol and codeine don't activate effectively, so patients get little pain relief but keep taking the drug hoping it will work. For non-prodrug CYP2D6 medications (paroxetine, venlafaxine, atomoxetine, aripiprazole), poor metabolizers reach higher-than-expected plasma levels on standard doses and often report more side effects.
About 3 to 5 percent of people carry reduced-function DPYD variants. Clinically critical if chemotherapy with 5-FU or capecitabine ever comes up; standard doses in DPYD-deficient patients can cause severe, sometimes fatal toxicity. WGS is preferred over consumer arrays for DPYD because some of the consequential variants are rare.
Rare but serious for azathioprine, mercaptopurine, and thioguanine therapy (used in IBD, lupus, organ transplant, and some leukemias). Standard doses in TPMT- or NUDT15-deficient patients can cause life-threatening bone marrow suppression within weeks. WGS catches the full panel of known loss-of-function variants; consumer arrays may not.
The WGS data advantage is most meaningful at the edges of the phenotype distribution: ultrarapid and poor metabolizers, and rare-variant carriers. For patients who turn out to be normal metabolizers for everything, WGS and consumer-array data give the same answer. The WGS advantage shows up when it matters.
Highest-value moments to pull up your Nebula drug response report: before any new antidepressant trial, before a procedure where opioid prescribing is likely, before starting statin therapy (SLCO1B1 muscle pain risk), before starting clopidogrel after a cardiac event, before starting warfarin (both CYP2C9 and VKORC1 matter), and before any chemotherapy regimen involving fluoropyrimidines (capecitabine, 5-FU) or thiopurines (azathioprine, mercaptopurine).
Learn how genetics may affect your response to these related medications:
That guide is the overview: why WGS is good for pharmacogenetics, why Gene2Rx is an option for analyzing your Nebula data, what CPIC and FDA guidelines cover. This guide is the walkthrough: what the report actually shows, what the phenotype calls mean in practice, how WGS-specific advantages show up in the output. If you're new to pharmacogenetics, read the pharmacogenetics guide first. If you have Nebula data and want to know what a report from it looks like, this guide is the right place.
Nebula provides various interpretation tools but does not produce a dedicated CPIC- and FDA-anchored pharmacogenetic report covering 103 medications. A dedicated analysis gives you a more complete drug-response picture than Nebula's built-in tools.
A VCF file, which Nebula provides as part of your WGS data package. Look for the 'Data' or 'Raw Data' section of your Nebula account. If your Nebula data is available as both BAM and VCF, the VCF is what Gene2Rx needs.
A few minutes. WGS data is larger than consumer genotyping data, so processing is slightly slower, but the end-to-end experience is still minutes-to-report rather than days or weeks like clinical pharmacogenetic tests.
Both reference genome builds are supported. Gene2Rx detects the build from the VCF header or infers it from variant positions, then maps pharmacogenetic loci correctly regardless. You don't need to lift over the file before uploading.
Your genotype calls don't change, but the clinical recommendations derived from them can shift as CPIC publishes new guidelines or revisions. For high-stakes prescribing decisions, re-running the report every few years catches any material updates. For most use cases, a report generated today will still be accurate years from now.
Find out how your DNA may influence your response to Sertraline and other medications with a Gene2Rx pharmacogenetics report.
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