591-33-3

Basic information

• Product Name: 3'-ETHOXYACETANILIDE
• Synonyms: 3’-ethoxy-acetanilid;m-ethoxyacetanilide;n-(3-ethoxyphenyl)-acetamid;M-ACETOPHENETIDIDE;3'-ETHOXYACETANILIDE;3'-ETHOXYACETANILIDE 99+%;3-acetophenetidide;N-(3-Ethoxyphenyl)acetamide
• CAS NO: 591-33-3
• Molecular Formula: C₁₀H₁₃NO₂
• Molecular Weight: 179.22
• EINECS: 209-713-3
• Mol File: 591-33-3.mol
• Article Data: 7

Chemical Properties

• Melting Point: 95-98 °C
• Boiling Point: 311.75°C (rough estimate)
• Flash Point: 164.8°C
• Appearance: /
• Density: 1.1248 (rough estimate)
• Refractive Index: 1.4950 (estimate)
• PKA: 14.69±0.70(Predicted)
• CAS DataBase Reference: 3'-ETHOXYACETANILIDE(CAS DataBase Reference)
• NIST Chemistry Reference: 3'-ETHOXYACETANILIDE(591-33-3)
• EPA Substance Registry System: 3'-ETHOXYACETANILIDE(591-33-3)

Safety Data

• Hazard Codes: Xn
• Statements: 22
• Safety Statements: 22
• RTECS: AM4300000
• TSCA: Yes
• Hazardous Substances Data: 591-33-3(Hazardous Substances Data)

Usage

General Description

Gray plates (in H2O).

Air & Water Reactions

Water soluble.

Reactivity Profile

3'-ETHOXYACETANILIDE is an example of an amide. Amides/imides react with azo and diazo compounds to generate toxic gases. Flammable gases are formed by the reaction of organic amides/imides with strong reducing agents. Amides are very weak bases (weaker than water). Imides are less basic yet and in fact react with strong bases to form salts. That is, they can react as acids. Mixing amides with dehydrating agents such as P2O5 or SOCl2 generates the corresponding nitrile. The combustion of these compounds generates mixed oxides of nitrogen (NOx).

Health Hazard

ACUTE/CHRONIC HAZARDS: When heated to decomposition 3'-ETHOXYACETANILIDE emits toxic fumes.

Fire Hazard

Flash point data for 3'-ETHOXYACETANILIDE are not available. 3'-ETHOXYACETANILIDE is probably combustible.

Safety Profile

Moderately toxic by ingestion. Seealso p-ACETOPHENETIDIDE. When heated todecomposition it emits toxic fumes of NOx.

Upstream product

• 108-24-7 acetic anhydride 
• 621-33-0 m-phenetidine 
• 591-27-5 m-Hydroxyaniline 
• 75-03-6 ethyl iodide 
• 64-19-7 acetic acid 
• 74-96-4 ethyl bromide 
• 621-42-1 meta-hydroxyacetanilide 

Downstream Products

• 4342-48-7 3-ethoxy-cyclohexylamine 
• 871895-08-8 acetic acid-(3-ethoxy-4-nitro-anilide) 
• 116496-78-7 N-(5-ethoxy-2-nitrophenyl)acetamide 
• 872819-78-8 acetic acid-(5-ethoxy-2,4-dinitro-anilide) 
• 861057-62-7 N-(3-ethoxy-cyclohexyl)-acetamide 
• 621-33-0 m-phenetidine 
• 79874-40-1 3-(m-ethoxyphenylamino)-1-butyne 
• 146680-74-2 N-vinylacetyl-m-phenetidine 
• 119416-54-5 4-Chlor-m-phenacetin 
• 65979-66-0 4,6-dichloro-3-ethoxyacetanilide 
• 139085-94-2 C₁₀H₁₂BrNO₂ 
• 129319-13-7 C₁₀H₁₁Br₂NO₂ 
• 104066-80-0 N-(4-bromo-3-methoxyphenyl)acetamide 
• 63549-06-4 (3-ethoxyphenyl)ammonium chloride 

Relevant articles and documents

REPLICATION PROTEIN A (RPA)-DNA INTERACTION INHIBITORS

This invention relates to RPA compounds or pharmaceutically acceptable salts thereof, and for the use of the compounds to treat cancer.

Quinoline Based Monocarbonyl Curcumin Analogs as Potential Antifungal and Antioxidant Agents: Synthesis, Bioevaluation and Molecular Docking Study

In search for new fungicidal and free radical scavenging agents, we synthesized a focused library of 2-chloroquinoline based monocarbonyl analogs of curcumin (MACs). The synthesized MACs were evaluated for in vitro antifungal and antioxidant activity. The antifungal activity was evaluated against five different fungal strains such as Candida albicans, Fusarium oxysporum, Aspergillus flavus, Aspergillus niger, and Cryptococcus neoformans, respectively. Most of the synthesized MACs displayed promising antifungal activity compared to the standard drug Miconazole. Furthermore, molecular docking study on a crucial fungal enzyme sterol 14α-demethylase (CYP51) could provide insight into the plausible mechanism of antifungal activity. MACs were also screened for in vitro radical scavenging activity using butylated hydroxytoluene (BHT) as a standard. Almost all MACs exhibited better antioxidant activity compared to BHT.

MATERIALS AND METHOD FOR INHIBITING REPLICATION PROTEIN A AND USES THEREOF

Targeting uncontrolled cell proliferation and resistance to DNA damaging chemotherapeutics with at least one reagent has significant potential in cancer treatment. Replication Protein A, the eukaryotic single-strand (ss) DNA binding protein, is essential for genomic maintenance and stability via roles in both DNA replication and repair. Reported herein are small molecules that inhibit the in vitro, in vivo, and cellular ssDNA binding activity of RPA, thereby disrupting the eukaryotic cell cycle, inducing cytotoxicity and increasing the efficacy of chemotherapeutic agents damage DNA, and/or disrupt its replication and/or function. These results provide new insights into the mechanism of RPA-ssDNA interactions in chromosome maintenance and stability. This represents a molecularly targeted eukaryotic DNA binding inhibitor and demonstrates the utility of targeting a protein-DNA interaction as a means of studying the cell cycle and providing a therapeutic strategy for cancer treatment.