20151-40-0

Basic information

• Product Name: 2,4-DIBROMOQUINOLINE
• Synonyms: 2,4-DIBROMOQUINOLINE;2,4-DibroMoquinoline 97%
• CAS NO: 20151-40-0
• Molecular Formula: C₉H₅Br₂N
• Molecular Weight: 286.9507
• Mol File: 20151-40-0.mol
• Article Data: 10

Chemical Properties

• Melting Point: 92-94 ºC
• Boiling Point: 344.3 °C at 760 mmHg
• Flash Point: 162 °C
• Appearance: /
• Density: 1.923 g/cm³
• Vapor Pressure: 0.000132mmHg at 25°C
• Refractive Index: 1.698
• Storage Temp.: under inert gas (nitrogen or Argon) at 2-8°C
• PKA: -1.12±0.50(Predicted)
• CAS DataBase Reference: 2,4-DIBROMOQUINOLINE(CAS DataBase Reference)
• NIST Chemistry Reference: 2,4-DIBROMOQUINOLINE(20151-40-0)
• EPA Substance Registry System: 2,4-DIBROMOQUINOLINE(20151-40-0)

Safety Data

• Hazard Codes: T
• Statements: 25-37/38-41
• Safety Statements: 26-39-45
• RIDADR: UN 2811
• WGK Germany: 3
• Hazardous Substances Data: 20151-40-0(Hazardous Substances Data)

Usage

General Description

2,4-Dibromoquinoline is a chemical compound comprising bromine and quinoline. It is characterized by the presence of two bromine atoms substituted at the 2nd and 4th positions of the heterocyclic quinoline ring. Quinolines are aromatic compounds which contain two fused rings, a benzene and pyridine ring. This chemical is utilized in various industrial and scientific applications, particularly in the field of organic synthesis. Information on its safety, toxicity or environmental impact may vary based on its usage and handling, thus appropriate precautions should always be taken.

InChI:InChI=1/C9H5Br2N/c10-7-5-9(11)12-8-4-2-1-3-6(7)8/h1-5H

Upstream product

• 20146-63-8 2-bromo-4-nitroquinoline 
• 56-57-5 4-nitroquinoline-N-oxide 
• 7789-60-8 phosphorus tribromide 
• 141-78-6 ethyl acetate 
• 67-66-3 chloroform 
• 22614-98-8 4-bromoquinoline-N-oxide 
• 10025-87-3 trichlorophosphate 
• 141-82-2 malonic acid 
• 62-53-3 aniline 
• 70254-43-2 4-Hydroxy-2-quinolone 
• 70254-44-3 2,4-dihydroxyquinoline 

Downstream Products

• 152570-22-4 4-(2'-bromo-4'-quinolyl)-2-phenyl-3-butyn-2-ol 
• 152570-21-3 1-(2'-bromo-4'-quinolyl)-2-phenylacetylene 
• 64658-05-5 2-bromo‐4‐chloroquinoline 
• 938-39-6 4-bromo-2-hydroxyquinoline 
• 703-61-7 2,4-dichloroquinoline 
• 532392-87-3 2,4-dibromoquinoline-3-carbaldehyde 
• 866831-75-6 2-bromo-4-quinolinecarboxaldehyde 
• 64658-04-4 2-bromo-4-methyl-quinoline 
• 866831-73-4 2-bromo-4-iodoquinoline 
• 1426532-71-9 (R)-(2-bromoquinolin-4-yl)((S)-1-tritylpyrrolidin-2-yl)methanol 
• 1426532-89-9 pyridin-2-yl(2-(4-(trifluoromethyl)phenyl)quinolin-4-yl)methanol 
• 1426532-91-3 (2-phenylquinolin-4-yl)(pyridin-2-yl)methanol 
• 1369590-98-6 (2-(4-methoxyphenyl)quinolin-4-yl)(pyridin-2-yl)methanol 
• 1426532-92-4 phenyl(2-(4-(trifluoromethyl)phenyl)quinolin-4-yl)methanol 

Relevant articles and documents

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Methoxyl regulation-based wide-band yellow phosphorescent 2-phenylquinoline iridium (III) complex and preparation method and application thereof

The invention discloses a methoxy regulation-based wide-band yellow phosphorescent 2-phenylquinoline iridium (III) complex and a preparation method and application thereof. The structural formula of the complex is shown in the specification, wherein R1 an

Design, synthesis and discovery of 2(1H)-quinolone derivatives for the treatment of pulmonary fibrosis through inhibition of TGF-β/smad dependent and independent pathway

Idiopathic pulmonary fibrosis (IPF) is a progressive, life-threatening and interstitial lung disease with the median survival of only 3–5 years. However, due to the unclear etiology and problems in accurate diagnosis, up to now only two drugs were approved by FDA for the treatment of IPF and their outcome responses are limited. Numerous studies have shown that TGF-β is the most important cytokine in the development of pulmonary fibrosis and plays a role through its downstream signaling molecule TGF-binding receptor Smads protein. In this paper, compounds bearing 2(1H)-quinolone scaffold were designed and their anti-fibrosis effects were evaluated. Of these compounds, 20f was identified as the most active one and could inhibit TGF-β-induced collagen deposition of NRK-49F cells and mouse fibroblasts migration with comparable activity and lower cytotoxicity than nintedanib in vitro. Further mechanism studies indicated that 20f reduced the expression of fibrogenic phenotypic protein α-SMA and collagen Ⅰ by inhibiting the TGF-β/Smad dependent pathways and ERK1/2 and p38 pathways. Moreover, compared with the nintedanib, 20f (100 mg/kg/day, p.o) more effectively alleviated collagen deposition in lung tissue and delayed the destruction of lung tissue structure both in bleomycin-induced prevention and treatment mice pulmonary fibrosis models. The immunohistochemical experiments further showed that 20f could block the expression level of phosphorylated Smad3 in the lung tissue cells, which resulted in its anti-fibrosis effects in vivo. In addition, 20f demonstrated good bioavailability (F = 41.55% vs 12%, compare with nintedanib) and an appropriate elimination half-life (T1/2 = 3.5 h), suggesting that 20f may be a potential drug candidate for the treatment of pulmonary fibrosis.