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N8509

Sigma-Aldrich

N-Nitroso-N-ethylurea

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Synonym(s):
ENU, N-Ethyl-N-nitrosourea
Empirical Formula (Hill Notation):
C3H7N3O2
CAS Number:
759-73-9
Molecular Weight:
117.11
EC Number:
212-072-2
MDL number:
MFCD00053635
UNSPSC Code:
12352200
PubChem Substance ID:
24897681
NACRES:
NA.25

Quality Level

100

form

powder

contains

aqueous acetic acid as stabilizer

storage temp.

−20°C

SMILES string

CCN(N=O)C(N)=O

InChI

1S/C3H7N3O2/c1-2-6(5-8)3(4)7/h2H2,1H3,(H2,4,7)

InChI key

FUSGACRLAFQQRL-UHFFFAOYSA-N

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Application


  • Genetic determinants of blood pressure and heart rate identified through ENU-induced mutagenesis with automated meiotic mapping.: This study identifies genetic factors affecting blood pressure and heart rate using N-ethyl-N-nitrosourea (ENU)-induced mutagenesis. The research utilizes automated meiotic mapping to reveal the genetic underpinnings of these cardiovascular traits, providing insights that could inform therapeutic targets (Teixeira et al., 2024).

  • Clonality, trafficking, and molecular alterations among Hprt mutant T lymphocytes isolated from control mice versus mice treated with N-ethyl-N-nitrosourea.: This study examines the effects of ENU on T lymphocyte clonality and trafficking in mice. The findings provide insights into the mutagenic and immunological impacts of ENU, contributing to our understanding of chemical-induced mutations (Judice et al., 2023).

  • Adopting duplex sequencing technology for genetic toxicity testing: A proof-of-concept mutagenesis experiment with N-ethyl-N-nitrosourea (ENU)-exposed rats.: This proof-of-concept study integrates duplex sequencing technology to test genetic toxicity in rats exposed to ENU. The results demonstrate the feasibility and effectiveness of this approach in detecting mutagenic effects, highlighting its potential for genetic toxicity assessment (Smith-Roe et al., 2023).

Biochem/physiol Actions

DNA alkylating agent that is carcinogenic in many animal species. Induces benign and malignant tumors of numerous types, including the nervous tissue, stomach, esophagus, pancreas, respiratory tract, intestine, lymphoreticular tissues, skin, and kidney.

Packaging

Weight on dry basis.

Pictograms

Skull and crossbonesHealth hazard
GHS06,GHS08

Signal Word

Danger

Hazard Classifications

Acute Tox. 3 Oral - Carc. 1B - Repr. 1B

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Certificates of Analysis (COA)

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Katherine R Bull et al.
The Journal of pathology, 233(1), 18-26 (2013-12-03)
The study of mutations causing the steroid-resistant nephrotic syndrome in children has greatly advanced our understanding of the kidney filtration barrier. In particular, these genetic variants have illuminated the roles of the podocyte, glomerular basement membrane and endothelial cell in
Peng Huang et al.
Journal of genetics and genomics = Yi chuan xue bao, 39(9), 421-433 (2012-10-02)
Zebrafish (Danio rerio) is a well-established vertebrate animal model. A comprehensive collection of reverse genetics tools has been developed for studying gene function in this useful organism. Morpholino is the most widely used reagent to knock down target gene expression
Ryohei Katayama et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 21(1), 166-174 (2014-10-30)
ROS1 rearrangement leads to constitutive ROS1 activation with potent transforming activity. In an ongoing phase I trial, the ALK tyrosine kinase inhibitor (TKI) crizotinib shows remarkable initial responses in patients with non-small cell lung cancer (NSCLC) harboring ROS1 fusions; however
Jinjun Dang et al.
Blood, 125(23), 3609-3617 (2015-04-10)
Alterations of genes encoding transcriptional regulators of lymphoid development are a hallmark of B-progenitor acute lymphoblastic leukemia (B-ALL) and most commonly involve PAX5, encoding the DNA-binding transcription factor paired-box 5. The majority of PAX5 alterations in ALL are heterozygous, and
Georgina Caruana et al.
PloS one, 8(3), e55429-e55429 (2013-03-08)
Mice harbouring gene mutations that cause phenotypic abnormalities during organogenesis are invaluable tools for linking gene function to normal development and human disorders. To generate mouse models harbouring novel alleles that are involved in organogenesis we conducted a phenotype-driven, genome-wide
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