38267-96-8

Basic information

• Product Name: 6-Bromo-4-chloroquinazoline
• Synonyms: 6-BROMO-4-CHLOROQUINAZOLINE;6-BROMO-4-CHLOROQUINAZOLINE, 95+%;4-Chloro-6-bromoquinazoline;6-Bromo-4-chloroquinazoli...;6-Bromo-4-chloro-quinazoline hydrochloride
• CAS NO: 38267-96-8
• Molecular Formula: C₈H₄BrClN₂
• Molecular Weight: 243.49
• EINECS: 202-766-3
• Product Categories: CHIRAL CHEMICALS
• Mol File: 38267-96-8.mol
• Article Data: 43

Chemical Properties

• Melting Point: 160-163 °C
• Boiling Point: 339.695 °C at 760 mmHg
• Flash Point: 159.242 °C
• Appearance: /
• Density: 1.763
• Vapor Pressure: 0mmHg at 25°C
• Refractive Index: 1.691
• Storage Temp.: under inert gas (nitrogen or Argon) at 2–8 °C
• PKA: 0.07±0.30(Predicted)
• CAS DataBase Reference: 6-Bromo-4-chloroquinazoline(CAS DataBase Reference)
• NIST Chemistry Reference: 6-Bromo-4-chloroquinazoline(38267-96-8)
• EPA Substance Registry System: 6-Bromo-4-chloroquinazoline(38267-96-8)

Safety Data

• Hazardous Substances Data: 38267-96-8(Hazardous Substances Data)

Usage

General Description

6-Bromo-4-chloroquinazoline is a chemical compound with the molecular formula C8H5BrClN2. It is a heterocyclic aromatic compound that belongs to the quinazoline family. 6-Bromo-4-chloroquinazoline is characterized by the presence of bromine and chlorine atoms on the quinazoline ring, which gives it unique properties and reactivity. 6-Bromo-4-chloroquinazoline is commonly used as a building block in the synthesis of pharmaceuticals, agrochemicals, and other organic compounds. Its structure and reactivity make it a valuable intermediate in organic synthesis, and it is utilized in the development of a variety of products with diverse applications in the chemical industry.

InChI:InChI=1/C8H4BrClN2/c9-5-1-2-7-6(3-5)8(10)12-4-11-7/h1-4H

Upstream product

• 32084-59-6 6-bromoquinazolin-4(3H)-one 
• 16313-66-9 5-bromoanthranilamide 
• 5794-88-7 5-Bromo-2-aminobenzoic acid 
• 32084-59-6 6-bromo-4-hydroxyquinazoline 
• 32084-59-6 6-bromo-4-quinazolone 
• 118-92-3 anthranilic acid 
• 134-20-3 2-carbomethoxyaniline 
• 52727-57-8 5-bromo-2-aminobenzoic acid methyl ester 

Downstream Products

• 102467-63-0 1-(6-bromo-quinazolin-4-yl)-5-(4-chloro-phenyl)-biguanide 
• 195457-61-5 6-bromo-N-(3-chloro-4-fluorophenyl)-4-quinazolinamine 
• 474707-54-5 6-bromo-4-{4-[3-(trifluoromethyl)phenyl]piperazin-1-yl}quinazoline 
• 307538-54-1 6-bromo-4-(4-N-methylpiperazin-1-yl)quinazoline 
• 474710-32-2 methyl 3-[4-(6-bromo-4-quinazolinyl)piperazino]benzoate 
• 474710-17-3 methyl-{3-[4-(6-bromo-4-quinazolinyl)-1,4-diazepan-1-yl]phenyl}sulfone 
• 474710-10-6 6-Bromo-4-[4-(2-fluoro-5-methylsulfonylphenyl)piperazin-1-yl]quinazoline 
• 179246-97-0 (4-benzyloxyphenyl)-(6-bromoquinazolin-4-yl)-amine hydrochloride 
• 32084-59-6 6-bromo-4-quinazolone 
• 307538-52-9 4-(6-bromoquinazolin-4-yl)morpholine 
• 307538-20-1 6-bromo-N-(3-chlorophenyl)quinazolin-4-amine 
• 944549-41-1 N-[3-chloro-4-[(3-fluorobenzyl)oxy]phenyl]-6-bromo-quinazolin-4-amine 
• 1135238-69-5 C₁₆H₁₄BrN₃O 
• 307538-42-7 SMER28 

Relevant articles and documents

Discovery of BPR1R024, an Orally Active and Selective CSF1R Inhibitor that Exhibits Antitumor and Immunomodulatory Activity in a Murine Colon Tumor Model

Colony-stimulating factor-1 receptor (CSF1R) is implicated in tumor-associated macrophage (TAM) repolarization and has emerged as a promising target for cancer immunotherapy. Herein, we describe the discovery of orally active and selective CSF1R inhibitors by property-driven optimization of BPR1K871 (9), our clinical multitargeting kinase inhibitor. Molecular docking revealed an additional nonclassical hydrogen-bonding (NCHB) interaction between the unique 7-aminoquinazoline scaffold and the CSF1R hinge region, contributing to CSF1R potency enhancement. Structural studies of CSF1R and Aurora kinase B (AURB) demonstrated the differences in their back pockets, which inspired the use of a chain extension strategy to diminish the AURA/B activities. A lead compound BPR1R024 (12) exhibited potent CSF1R activity (IC50 = 0.53 nM) and specifically inhibited protumor M2-like macrophage survival with a minimal effect on antitumor M1-like macrophage growth. In vivo, oral administration of 12 mesylate delayed the MC38 murine colon tumor growth and reversed the immunosuppressive tumor microenvironment with the increased M1/M2 ratio.

Discovery of quinazoline derivatives as a novel class of potent and in vivo efficacious LSD1 inhibitors by drug repurposing

Histone lysine-specific demethylase 1 (LSD1) is an important epigenetic modulator, and is implicated in malignant transformation and tumor pathogenesis in different ways. Therefore, the inhibition of LSD1 provides an attractive therapeutic target for cancer therapy. Based on drug repurposing strategy, we screened our in-house chemical library toward LSD1, and found that the EGFR inhibitor erlotinib, an FDA-approved drug for lung cancer, possessed low potency against LSD1 (IC50 = 35.80 μM). Herein, we report our further medicinal chemistry effort to obtain a highly water-soluble erlotinib analog 5k (>100 mg/mL) with significantly enhanced inhibitory activity against LSD1 (IC50 = 0.69 μM) as well as higher specificity. In MGC-803 cells, 5k suppressed the demethylation of LSD1, indicating its cellular activity against the enzyme. In addition, 5k had a remarkable capacity to inhibit colony formation, suppress migration and induce apoptosis of MGC803 cells. Furthermore, in MGC-803 xenograft mouse model, 5k treatment resulted in significant reduction in tumor size by 81.6% and 96.1% at dosages of 40 and 80 mg/kg/d, respectively. Our findings indicate that erlotinib-based analogs provide a novel structural set of LSD1 inhibitors with potential for further investigation, and may serve as novel candidates for the treatment of LSD1-overexpressing cancers.

SUBSTITUTED IMIDAZOLES FOR THE INHIBITION OF TGF-BETA AND METHODS OF TREATMENT

This disclosure relates to low molecular weight substituted imidazoles that inhibit the TGF-b signaling pathway. More specifically, this disclosure relates to methods of using said imidazoles for the treatment of diseases related to the TGF-b signaling pathways including, but not limited to, atherosclerosis, Marfan syndrome, Loeys-Dietz syndrome, obesity, diabetes, multiple sclerosis, keratoconus, idiopathic pulmonary fibrosis, Alzheimer's Disease, chronic kidney disease, and scleroderma.