What you carry at this position in your DNA and what research says about it.
Chemotherapy Drug Safety: 8/10 evidence, 0 publications.
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Sample genotype (not yours): TG/TG
Typical Chemotherapy Toxicity Risk
Normal DPD enzyme activity allows standard processing of fluoropyrimidine chemotherapy drugs. Standard dosing of medications like fluorouracil or capecitabine carries a typical risk of side effects.
What this genotype means: Normal DPD enzyme activity; Typical risk of chemotherapy side effects.
Sample genotype (not yours): T/T
Severe Chemotherapy Toxicity Risk
Absent DPD enzyme activity is linked to an extremely high risk of severe or fatal toxicity from standard fluoropyrimidine doses. The CPIC DPYD guideline classifies this genotype as a poor metabolizer.
What this genotype means: Complete DPD enzyme deficiency; Extremely high risk of fatal chemotherapy toxicity; CPIC: poor metabolizer, fluoropyrimidines flagged high-toxicity.
Sample genotype (not yours): TG/T
Increased Chemotherapy Toxicity Risk
Reduced DPD enzyme activity is linked to a higher risk of severe, potentially life-threatening toxicity from standard doses of fluorouracil or capecitabine. The CPIC DPYD guideline classifies this genotype as an intermediate metabolizer.
What this genotype means: Reduced DPD enzyme activity; High risk of severe chemotherapy toxicity; CPIC: intermediate metabolizer.
Gene function and biological role
Gene Function: The DPYD gene provides instructions for making dihydropyrimidine dehydrogenase (DPD), an enzyme essential for breaking down pyrimidines. DPD is also the primary enzyme responsible for metabolizing fluoropyrimidine chemotherapy drugs, such as fluorouracil and capecitabine. When DPD activity is reduced or absent, these drugs can accumulate to toxic levels in the body. This can lead to severe, life-threatening side effects during cancer treatment.
Variant Impact: The rs72549303 variant, also known as DPYD*3, is a frameshift mutation in the DPYD gene that results in a non-functional enzyme. This specific genetic change disrupts the reading frame of the gene, leading to a premature stop codon or an unstable protein. Consequently, the dihydropyrimidine dehydrogenase enzyme is unable to perform its normal role in breaking down pyrimidines and fluoropyrimidine drugs. Individuals carrying this variant have significantly reduced or completely absent DPD enzyme activity.
Key Insight: Standard doses of common chemotherapy drugs can act as a massive overdose in individuals with this variant due to the body's inability to clear the medication.
Location: DPYD. Chromosome 1 · 1p21.3 · 97.5 Mb
Estimated prevalence by population
No frequency data available
This variant is not present in the gnomAD database.
Showing effects for TG/TG genotype
Pharmacogenomics
Chemotherapy Response
Fluorouracil Toxicity. Evidence: 8/10. Typical Risk.
Capecitabine Toxicity. Evidence: 8/10. Typical Risk.
Tegafur Toxicity. Evidence: 8/10. Typical Risk.
Drug Metabolism Enzyme Activity
DPD Enzyme Activity. Evidence: 6/10. Normal Function.
Showing effects for T/T genotype
Fluorouracil Toxicity. Evidence: 8/10. Severe/Fatal Risk.
Capecitabine Toxicity. Evidence: 8/10. Severe/Fatal Risk.
Tegafur Toxicity. Evidence: 8/10. Severe/Fatal Risk.
DPD Enzyme Activity. Evidence: 6/10. Absent Function.
Showing effects for TG/T genotype
Fluorouracil Toxicity. Evidence: 8/10. High Risk.
Capecitabine Toxicity. Evidence: 8/10. High Risk.
Tegafur Toxicity. Evidence: 8/10. High Risk.
DPD Enzyme Activity. Evidence: 6/10. Reduced Function.
What this genotype means for the people who carry it
Sample genotype: TGTG (Homozygous)
Normal dihydropyrimidine dehydrogenase (DPD) enzyme function is expected with these genetic markers. The DPD enzyme is responsible for breaking down more than 80% of fluorouracil and its oral prodrug capecitabine into inactive metabolites. Because the enzyme functions normally, standard doses of these chemotherapy drugs do not pose an elevated risk of severe toxicity. However, typical chemotherapy side effects may still occur depending on other clinical factors.
Normal DPD enzyme activity; Typical risk of chemotherapy side effects.
Sample genotype: TT (Homozygous)
Inheriting two copies of the non-functional DPYD*3 variant leads to complete dihydropyrimidine dehydrogenase (DPD) deficiency, classifying this genotype as a poor metabolizer. Without active DPD enzymes, the body is completely unable to clear fluoropyrimidine chemotherapies like fluorouracil or capecitabine, resulting in a massive drug overdose from standard doses. This leads to an extremely high risk of severe, life-threatening, or fatal toxicities, such as profound bone marrow suppression, severe mucosal damage, and organ failure. The CPIC DPYD guideline classifies this genotype as a poor metabolizer.
Complete DPD enzyme deficiency; Extremely high risk of fatal chemotherapy toxicity; CPIC: poor metabolizer, fluoropyrimidines flagged high-toxicity.
Sample genotype: TGT (Heterozygous)
Presence of one copy of the DPYD*3 non-functional variant results in reduced dihydropyrimidine dehydrogenase (DPD) enzyme activity, classifying this genotype as an intermediate metabolizer. When treated with standard doses of fluoropyrimidines like fluorouracil or capecitabine, the body cannot break down the drugs efficiently, leading to toxic accumulation. This significantly increases the risk of severe, potentially life-threatening side effects, including severe diarrhea, hand-foot syndrome, and myelosuppression (dangerously low blood cell counts). The CPIC DPYD guideline classifies this genotype as an intermediate metabolizer.
Reduced DPD enzyme activity; High risk of severe chemotherapy toxicity; CPIC: intermediate metabolizer.
Variants with shared genetic architecture
rs56038477 · DPYD Gene · Chr 1 · Chemotherapy Toxicity Risk
rs75017182 · DPYD Gene · Chr 1 · Chemotherapy Drug Toxicity
rs17376848 · DPYD Gene · Chr 1 · Chemotherapy Toxicity Risk
Content updated August 2026.
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