Ask about this productRelated genes to: UGT1A1 Blocking Peptide
- Gene:
- UGT1A1 NIH gene
- Name:
- UDP glucuronosyltransferase family 1 member A1
- Previous symbol:
- UGT1, GNT1
- Synonyms:
- UGT1A
- Chromosome:
- 2q37.1
- Locus Type:
- complex locus constituent
- Date approved:
- 1989-02-13
- Date modifiied:
- 2019-04-23
Related products to: UGT1A1 Blocking Peptide
Related articles to: UGT1A1 Blocking Peptide
- To evaluate the effect of homozygosity on the safety profile of NALIRIFOX (liposomal irinotecan + 5-fluorouracil/leucovorin + oxaliplatin) in patients with metastatic pancreatic ductal adenocarcinoma (mPDAC) in NAPOLI 3 (NCT04083235). - Source: PubMed
Publication date: 2026/05/04
Abdelrahim MaenKhan GazalaHatoum HassanZervoudakis AliceDayyani FarshidZhang LiLi JiaMaxwell FionaO'Reilly Eileen MWainberg Zev ABullock Andrea - 5-Fluorouracil (5-FU) is a widely utilized antimetabolite in colorectal cancer chemotherapy, primarily exerting its cytotoxic effects by irreversibly inhibiting thymidylate synthase (TS). This inhibition leads to a reduction in deoxythymidine monophosphate (dTMP), which disrupts DNA synthesis and repair. A major challenge in 5-FU treatment is the dose-limiting toxicity of chemotherapeutic-induced intestinal mucositis. Da-Bu-Pi Decoction (DBPD), a well-established formula in traditional Chinese medicine for treating spleen-stomach deficiency, is often used to enhance spleen qi and balance the middle jiao. While growing clinical evidence points to the therapeutic benefits of DBPD in alleviating 5-FU-induced mucositis, the underlying molecular mechanisms remain largely undefined. - Source: PubMed
Publication date: 2026/04/30
Wang ShunZhiLi YalingMa JingLi JunJieHuang DanWa XiaoXiaZhou YuCenLiu YongQi - Interindividual variations in drug metabolism involve various factors, including posttranscriptional gene regulation mechanisms controlled by microRNAs (miRNAs or miRs) derived from the genome. The aim of this study was to use RNA bioengineering technology to produce novel recombinant human miR-491-5p, miR-491-3p, and pre-miR-491 molecules, namely BioRNA/miR-491-5p, BioRNA/miR-491-3p, and BioRNA/pre-miR-491, respectively, and define their functional difference in regulating UDP-glucuronosyltransferase 1A1 (UGT1A1) expression and drug-metabolizing capacity. All 6 BioRNAs were heterologously overexpressed in Escherichia coli (>30% of total RNA) and isolated by fast protein liquid chromatography to high purity (>97%). As BioRNA/pre-miR-491 agents were processed to both 5p and 3p strands in Hep3B and HepG2 cells, BioRNA/miR-491-5p and -3p were selectively processed to 5p and 3p, respectively, and each accumulated to greater levels. Immunoblotting and immunofluorescence studies demonstrated the efficacy of BioRNA/miR-491-3p to suppress UGT1A1 protein levels in Hep3B and HepG2 cells, localized on the endoplasmic reticulum, exhibiting monomeric (∼55 kDa) and oligomeric (∼150 kDa) bands under different conditions, whereas BioRNA/pre-miR-491 and miR-491-5p had no effects. Using a fluorescent substrate, N-butyl-4-(4-hydroxyphenyl)-1,8-naphthalimide, lower UGT1A1 drug-metabolizing capacities were found in cells treated with BioRNA/miR-491-3p. In addition, liquid chromatography-tandem mass spectrometry analysis revealed a 45% reduction of estradiol 3-glucuronidation activity by BioRNA/miR-491-3p in Hep3B cells, whereas formation of estradiol 17-glucuronidation mediated by other UGTs was unchanged. Together, these results underline the role of miR-491-3p in regulating UGT1A1 and its impact on cellular drug-metabolizing capacity while demonstrating the applications of recombinant miRNA agents to delineating the importance of posttranscriptional gene regulation in drug metabolism. SIGNIFICANT STATEMENT: Research on posttranscriptional gene regulation mainly uses miRNA mimics chemically synthesized in vitro. This study successfully produced 6 novel recombinant miR-491 molecules through in vivo fermentation with transfer RNA scaffold and transfer RNA-fused pre-miRNA carrier-based technologies, which were further utilized to delineate the biogenesis and function of miR-491-3p versus -5p in modulating UDP-glucuronosyltransferase 1A1 protein levels and drug-metabolizing capacity. The findings demonstrate the role of miR-491-3p in regulating UDP-glucuronosyltransferase 1A1 and value of recombinant miRNA agents for studying drug metabolism. - Source: PubMed
Publication date: 2026/04/04
Wang YimeiTu Mei-JuanBatra NeeluGuan SuZhou YufanYu Ai-Ming - Crigler-Najjar Syndrome (CNS) is a rare autosomal recessive disorder caused by uridine diphosphate glucuronosyltransferase (UGT1A1) deficiency, leading to unconjugated hyperbilirubinemia. Without treatment, patients are at high risk of kernicterus and irreversible neurological damage. Liver transplantation (LT) is the only curative option. This study aims to evaluate long-term outcomes of LT in CNS patients over a 20-year period in Iran. - Source: PubMed
Publication date: 2026/04/27
Teimoury SajadBeyzaei ZahraShamsaeefar AlirezaKazemi KuroshNikeghbalian SamanMalekhosseini Seyed-AliGeramizadeh Bita - Bemnifosbuvir is a novel oral guanosine nucleotide prodrug with potent pan-genotypic inhibitory activity against hepatitis C virus. In vitro studies assessing the inhibition or induction potential of bemnifosbuvir on the CYP450 and UGT1A1 enzymes demonstrated that bemnifosbuvir is a weak inducer and a reversible and time-dependent inhibitor of CYP3A4. These results prompted further evaluation in a Phase 1 clinical study in healthy participants who received midazolam (a sensitive CYP3A4 substrate) without and with simultaneous or staggered doses of bemnifosbuvir. A single simultaneous 550 mg bemnifosbuvir dose increased the total plasma exposure of a single 2 mg midazolam dose by 24% via reversible inhibition. Simultaneous coadministration of bemnifosbuvir 550 mg twice daily increased the total plasma exposure to midazolam by 98% as an outcome of reversible/time-dependent inhibition and induction. Simultaneous coadministration of a single and repeat dose of bemnifosbuvir increased the total plasma exposure to 1-hydroxymidazolam (primary metabolite of midazolam) by 22% and 27%, respectively. Staggered coadministration generally had a lower effect on plasma exposure to both midazolam and 1-hydroxymidazolam. Conversely, midazolam had no significant effect on the pharmacokinetics of bemnifosbuvir. Overall, bemnifosbuvir was a weak clinical inhibitor (geometric mean ratio <2) of CYP3A4. - Source: PubMed
Zhou Xiao-JianVo AlexMorelli GaetanoMontrond MaureenLynch ShannanPietropaolo KeithBelanger BruceGood StevenHorga ArantxaAgrawal NancyHammond Janet