85-45-0

Basic information

• Product Name: 3-nitro-o-anisidine
• Synonyms: 3-nitro-o-anisidine;2-Methoxy-3-nitrobenzenamine;2-Methoxy-3-nitrophenylamine hydrochloride
• CAS NO: 85-45-0
• Molecular Formula: C₇H₈N₂O₃
• Molecular Weight: 168.15002
• EINECS: 201-608-0
• Mol File: 85-45-0.mol
• Article Data: 4

Chemical Properties

• Melting Point: 75-76 °C
• Boiling Point: 340.2°C at 760 mmHg
• Flash Point: 159.5°C
• Appearance: /
• Density: 1.318g/cm³
• Vapor Pressure: 8.76E-05mmHg at 25°C
• Refractive Index: 1.601
• Storage Temp.: Keep in dark place,Inert atmosphere,Room temperature
• PKA: 2.40±0.10(Predicted)
• CAS DataBase Reference: 3-nitro-o-anisidine(CAS DataBase Reference)
• NIST Chemistry Reference: 3-nitro-o-anisidine(85-45-0)
• EPA Substance Registry System: 3-nitro-o-anisidine(85-45-0)

Safety Data

• Hazardous Substances Data: 85-45-0(Hazardous Substances Data)

Usage

General Description

3-nitro-o-anisidine, also known as 3-nitro-2-methoxyaniline, is a chemical compound with the molecular formula C7H8N2O3. It is a yellow to brown solid that is used as an intermediate in the synthesis of dyes, pharmaceuticals, and other organic compounds. 3-nitro-o-anisidine is considered to be a hazardous substance, as it is toxic if swallowed, inhaled, or absorbed through the skin. Exposure to this chemical can cause irritation to the respiratory system, skin, and eyes, and may also have harmful effects on the liver, kidneys, and blood. It is important to handle and dispose of 3-nitro-o-anisidine with caution and in accordance with safety guidelines.

InChI:InChI=1/C7H8N2O3/c1-12-7-5(8)3-2-4-6(7)9(10)11/h2-4H,8H2,1H3

Upstream product

• 317-46-4 2-fluoro-3-nitro-benzoic acid 
• 85-38-1 3-nitrosalicylic acid 
• 40751-88-0 2-methoxy-3-nitrobenzoic acid 
• 90564-26-4 2-methoxy-3-nitro-benzoic acid methyl ester 
• 64-17-5 ethanol 
• 3535-67-9 2,6-dinitroanisole 
• 7783-06-4 hydrogen sulfide 

Downstream Products

• 521074-24-8 4-bromo-N-[3-(hydroxymethyl)-8-methoxy-7-quinolinyl]benzamide 
• 521074-25-9 4-bromo-N-[3-(chloromethyl)-8-methoxy-7-quinolinyl]benzamide hydrochloride 
• 521071-28-3 4'-fluoro-N-[8-methoxy-3-(1-pyrrolidinylmethyl)-7-quinolinyl]-[1,1'-biphenyl]-4-carboxamide 
• 67291-71-8 2-Chloro-N-(2-methoxy-3-nitro-phenyl)-acetamide 
• 116496-80-1 acetic acid-(2-methoxy-3-nitro-anilide) 

Relevant articles and documents

H-bonding directed one-step synthesis of novel macrocyclic peptides from ε-aminoquinolinecarboxylic acid

Two macrocyclic peptides 1a and 1b were synthesized directly from ε-aminoquinolinecarboxylic acid 2a and 2b, respectively. The preorganization of the uncyclized intermediates mediated by hydrogen bonding assisted the cyclization. The structures of 1a and 1b were characterized by 1H and 13C NMR spectroscopy and MALDI-TOF MS analysis. Solid state structure of 1a was investigated by single crystal X-ray studies. Their aggregation behaviors in solution were studied by both variable concentration and temperature 1H NMR experiments.

Drug Design Targeting T-Cell Factor-Driven Epithelial-Mesenchymal Transition as a Therapeutic Strategy for Colorectal Cancer

Metastasis is the cause of 90% of mortality in cancer patients. For metastatic colorectal cancer (mCRC), the standard-of-care drug therapies only palliate the symptoms but are ineffective, evidenced by a low survival rate of ～11%. T-cell factor (TCF) transcription is a major driving force in CRC, and we have characterized it to be a master regulator of epithelial-mesenchymal transition (EMT). EMT transforms relatively benign epithelial tumor cells into quasi-mesenchymal or mesenchymal cells that possess cancer stem cell properties, promoting multidrug resistance and metastasis. We have identified topoisomerase IIα (TOP2A) as a DNA-binding factor required for TCF-transcription. Herein, we describe the design, synthesis, biological evaluation, and in vitro and in vivo pharmacokinetic analysis of TOP2A ATP-competitive inhibitors that prevent TCF-transcription and modulate or reverse EMT in mCRC. Unlike TOP2A poisons, ATP-competitive inhibitors do not damage DNA, potentially limiting adverse effects. This work demonstrates a new therapeutic strategy targeting TOP2A for the treatment of mCRC and potentially other types of cancers.