• The INFINITI UGT1A1 Assay is CE Marked.
  • The INFINITI UGT1A1 is designed to identify UGT1A1 genetic variants.
  • The INFINITI UGT1A1 utilizes the UGT1A1 Intellipac, UGT1A1 Amp Mix and UGT1A1 BioFilmChip Microarray.
  • The INFINITI UGT1A1 Assay is automated by the INFINITI Analyzer.

Analytes Detected: 
  • UGT1A1: *1, *28, *36, *37
  • Multiplexed determination of 4 genetic variants on one BioFilmChip Microarray

  • Detection of duplications in the TATA box promoter region provides accurate analysis

  • Load & Go automated on the INFINITI/INFINITI PLUS Analyzer.

  • Replicate determinations on a single BioFilmChip Microarray ensures quality results.

Sample Type and Volume: 
  • Uses 0.2 - 2.0 mL of peripheral whole blood in EDTA (purple top) tube.
  • Requires 50ng DNA / reaction
Clinical Relevance: 
  • UGT 1A1 is responsible for conjugating SN 38, the active metabolite of irinotecan HCl.
  • UGT 1A1*28 genotype (heterozygous *1/*28 or wild type *28/*28) increases risk of irinotecan related toxicity due to a higher exposure to SN 38 in the liver.
  • UGT 1A1*37 polymorphism also results in high levels of active metabolite SN 38, thus *37 also presents a risk for neutropenia.
  • UGT 1A1*36 polymorphism enhances the metabolism of SN 38, thus *36 tolerate a higher irinotecan dosage
Clinical Utility: 

  • Studies have shown that testing an individual for UGT1A1*28 polymorphism will allow the physician to determine the specific dosage of irinotecan per the individual
  • This will reduce toxicity associated with the polymorphism, as well as the severity of the side effects of irinotecan HC1.
  • Approximately 10% of the North American population inherits two copies of UGT1A1*28 and are at a much higher risk of having a toxic reaction to the drug interacation HC1.
  1. How Long Will It Take For Oncologists To Embrace UGT1A1 Testing?”  Diagnostic Testing and Technology Report.  Feb. 2006.  VI(6): 5-7

  2. Tukey RH, Strassburg CP (2000). "Human UDP-glucuronosyltransferases: metabolism, expression, and disease.". Annu. Rev. Pharmacol. Toxicol. 40: 581–616. doi:10.1146/annurev.pharmtox.40.1.581. PMID 10836148. 
  3. Kadakol A, Ghosh SS, Sappal BS, et al. (2000). "Genetic lesions of bilirubin uridine-diphosphoglucuronate glucuronosyltransferase (UGT1A1) causing Crigler-Najjar and Gilbert syndromes: correlation of genotype to phenotype.". Hum. Mutat. 16 (4): 297–306. doi:10.1002/1098-1004(200010)16:4<297::AID-HUMU2>3.0.CO;2-Z. PMID 11013440.