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329231

Sigma-Aldrich

4,5-Dimethoxy-2-nitrobenzoic acid

99%

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Linear Formula:
O2NC6H2(OCH3)2CO2H
CAS Number:
Molecular Weight:
227.17
EC Number:
MDL number:
UNSPSC Code:
12352100
PubChem Substance ID:
NACRES:
NA.22

Quality Level

Assay

99%

mp

195-197 °C (lit.)

SMILES string

COc1cc(C(O)=O)c(cc1OC)[N+]([O-])=O

InChI

1S/C9H9NO6/c1-15-7-3-5(9(11)12)6(10(13)14)4-8(7)16-2/h3-4H,1-2H3,(H,11,12)

InChI key

WWCMFGBGMJAJRX-UHFFFAOYSA-N

General description

4,5-Dimethoxy-2-nitrobenzoic acid is a nitroaromatic compound.

Application

4,5-Dimethoxy-2-nitrobenzoic acid was used in the synthesis of 4,5-dimethoxy-2-nitrobenzamide and 6,7-dimethoxyquinazoline derivatives.

Pictograms

Exclamation mark

Signal Word

Warning

Hazard Statements

Hazard Classifications

Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

Target Organs

Respiratory system

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Regulatory Information

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J Navrátilová et al.
Folia microbiologica, 49(5), 613-615 (2005-02-11)
Two bacterial strains were isolated from forest soil by selective enrichment of the mineral medium containing 4-nitropyrocatechol as the sole carbon and energy source. Both strains could utilize 4-nitropyrocatechol and 5-nitroguaiacol. Degradation of 5-nitroguaiacol and stoichiometric release of nitrites was
R K Narla et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 4(6), 1405-1414 (1998-06-17)
The novel quinazoline derivative 4-(3'-bromo-4'-hydroxylphenyl)-amino-6,7-dimethoxyquinazoline (WHI-P154) exhibited significant cytotoxicity against U373 and U87 human glioblastoma cell lines, causing apoptotic cell death at micromolar concentrations. The in vitro antiglioblastoma activity of WHI-P154 was amplified > 200-fold and rendered selective by conjugation
P A Goodman et al.
The Journal of biological chemistry, 273(28), 17742-17748 (1998-07-04)
Exposure of B-lineage lymphoid cells to ionizing radiation induces an elevation of c-jun proto-oncogene mRNA levels. This signal is abrogated by protein-tyrosine kinase (PTK) inhibitors, indicating that activation of an as yet unidentified PTK is mandatory for radiation-induced c-jun expression.

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