286371-64-0

Usage

Uses

Used in Pharmaceutical Research:
7-Methoxy-6-benzyloxyquinazolin-4-one is utilized as a building block in the synthesis of novel pharmaceuticals, contributing to the development of new drugs with potential therapeutic applications.
Used in Medicinal Chemistry:
As a chemical probe, 7-Methoxy-6-benzyloxyquinazolin-4-one aids in biological studies, facilitating the understanding of various biological processes and the discovery of new therapeutic targets.
Used in Anti-Inflammatory Applications:
7-Methoxy-6-benzyloxyquinazolin-4-one may be employed for its potential anti-inflammatory properties, offering a new avenue for the treatment of inflammatory conditions.
Used in Anticancer Applications:
Possessing potential anticancer activity, 7-Methoxy-6-benzyloxyquinazolin-4-one could be developed into a therapeutic agent targeting various types of cancer.
Used in Antimicrobial Applications:
Due to its possible antimicrobial properties, 7-Methoxy-6-benzyloxyquinazolin-4-one may be used in the development of new antimicrobial agents to combat resistant infections.

InChI:InChI=1/C16H14N2O3/c1-20-14-8-13-12(16(19)18-10-17-13)7-15(14)21-9-11-5-3-2-4-6-11/h2-8,10H,9H2,1H3,(H,17,18,19)

Upstream product

• 645-08-9 Isovanillic acid 
• 855793-63-4 methyl 2-amino-5-(benzyloxy)-4-methoxybenzoate 
• 77287-34-4 formamide 
• 215659-03-3 methyl 5-hydroxy-4-methoxy-2-nitrobenzoate 
• 164161-49-3 methyl 5-(benzyloxy)-4-methoxy-2-nitrobenzoate 
• 100-39-0 benzyl bromide 
• 57535-57-6 methyl 3-(benzyloxy)-4-methoxy-benzoate 
• 6702-50-7 3-hydroxy-4-methoxybenzoate 
• 621-59-0 isovanillin 
• 3473-63-0 formamidine acetic acid 
• 26791-93-5 methyl 4,5-dimethoxy-2-nitrobenzoate 
• 122-51-0 orthoformic acid triethyl ester 
• 634197-80-1 2-amino-5-benzyloxy-4-methoxybenzoic acid benzyl ester 
• 1042978-66-4 5-benzyloxy-4-methoxy-2-aminobenzaldehyde 

Downstream Products

• 1006890-01-2 7-methoxy-4-pyridin-3-yl-6-(2-quinolin-2-ylethoxy)quinazoline 
• 1006890-13-6 6-(benzyloxy)-7-methoxy-N,N-dimethylquinazolin-4-amine 
• 1006889-93-5 6-(benzyloxy)-7-methoxy-4-(pyridin-3-yl)quinazoline 
• 1638151-52-6 (R)-2-((7-methoxy-4-(3-(quinoxaline-2-yloxy)-pyrrolidine-1-yl)-quinazoline-6-yl)-oxy)ethyl 4-methylbenzenesulphonate 
• 184475-35-2 gefitinib 
• 913819-12-2 6-(benzyloxy)-N-(3-chloro-4-fluorophenyl)-7-methoxyquinazolin-4-amine 
• 184475-71-6 4-(3-chloro-4-fluorophenylamino)-6-hydroxy-7-methoxyquinazoline 
• 1188908-25-9 1-(5-tert-butylisoxazol-3-yl)-3-(3-(6-hydroxy-7-methoxyquinazolin-4-yloxy)phenyl)urea 
• 1188908-26-0 C₂₂H₁₉N₃O₃ 
• 1188908-27-1 4-(3-aminophenoxy)-7-methoxyquinazolin-6-ol 
• 286371-65-1 6-(benzyloxy)-4-chloro-7-methoxyquinazoline 
• 634197-88-9 4-(6-benzyloxy-7-methoxy-quinazolin-4-yl)-piperazine-1-carboxylic acid (4-cyano-phenyl)-amide 

Relevant academic research and scientific papers

Synthesis, biological evaluation and molecular docking studies of novel 1,2,3-triazole-quinazolines as antiproliferative agents displaying ERK inhibitory activity

ERK1/2 inhibitors have attracted special attention concerning the ability of circumventing cases of innate or log-term acquired resistance to RAF and MEK kinase inhibitors. Based on the 4-aminoquinazoline pharmacophore of kinases, herein we describe the synthesis of 4-aminoquinazoline derivatives bearing a 1,2,3-triazole stable core to bridge different aromatic and heterocyclic rings using copper-catalysed azide-alkyne cycloaddition reaction (CuAAC) as a Click Chemistry strategy. The initial screening of twelve derivatives in tumoral cells (CAL-27, HN13, HGC-27, and BT-20) revealed that the most active in BT-20 cells (25a, IC50 24.6 μM and a SI of 3.25) contains a more polar side chain (sulfone). Furthermore, compound 25a promoted a significant release of lactate dehydrogenase (LDH), suggesting the induction of cell death by necrosis. In addition, this compound induced G0/G1 stalling in BT-20 cells, which was accompanied by a decrease in the S phase. Western blot analysis of the levels of p-STAT3, p-ERK, PARP, p53 and cleaved caspase-3 revealed p-ERK1/2 and p-STA3 were drastically decreased in BT-20 cells under 25a incubation, suggesting the involvement of these two kinases in the mechanisms underlying 25a-induced cell cycle arrest, besides loss of proliferation and viability of the breast cancer cell. Molecular docking simulations using the ERK-ulixertinib crystallographic complex showed compound 25a could potentially compete with ATP for binding to ERK in a slightly higher affinity than the reference ERK1/2 inhibitor. Further in silico analyses showed comparable toxicity and pharmacokinetic profiles for compound 25a in relation to ulixertinib.

Novel amide analogues of quinazoline carboxylate display selective antiproliferative activity and potent EGFR inhibition

In the present study, a novel series of quinazoline derivatives is developed for cancer therapy. All the synthesised analogues were evaluated against a panel of 60 human cancer cell lines for the antiproliferative activity. Significant and selective growth inhibition of several solid tumour cell lines such as NCI-H322M, NCI-H522 (non-small cell lung cancer), IGROV1, SK-OV-3 (ovarian cancer), TK-10 (renal cancer) and MDA-MB-468 (breast cancer) was observed. Further, all the new amide analogues strongly inhibited EGFR in low nanomolar range with morpholino quinazoline 10 producing activity (IC50 = 6.12 nM) comparable to standard drugs erlotinib and gefitinib. In addition, western blot analysis depicted inhibition of phosphorylation of EGFR by compounds 10 and 11 in MDA-MB-468 cells at 10 μM. Molecular docking studies showed the strong binding interactions with the active site of the EGFR protein. The current investigation could be extremely helpful for the development of newer therapeutically useful quinazoline based molecules for cancer therapy.

Structure–activity relationship study of novel quinazoline-based 1,6-naphthyridinones as MET inhibitors with potent antitumor efficacy

As a privileged scaffold, the quinazoline ring is widely used in the development of EGFR inhibitors, while few quinazoline-based MET inhibitors are reported. In our ongoing efforts to develop new MET-targeted anticancer drug candidates, a series of quinaz

A simple and highly efficient process for synthesis of Gefitinib and its intermediate

A highly efficient one pot conversion of 4-methoxy-3-benzyloxy-6-nitro benzoate to 6-benzoyloxy-7-methoxy quinazoline-4-one using Fe/acetic acid and formamidine acetate followed by debenzylation of 4-(3-chloro-4-flurophenylamino)-6-benzoyloxy-7-methoxy quinazoline using methanesulfonic acid in chloroform is described. Additionally the desmethyl impurity formation is controlled using oxalyl chloride and DIPEA.

Fluorine-containing 6,7-dialkoxybiaryl-based inhibitors for phosphodiesterase 10 A: Synthesis and in vitro evaluation of inhibitory potency, selectivity, and metabolism

Based on the potent phosphodiesterase 10 A (PDE10A) inhibitor PQ-10, we synthesized 32 derivatives to determine relationships between their molecular structure and binding properties. Their roles as potential positron emission tomography (PET) ligands were evaluated, as well as their inhibitory potency toward PDE10A and other PDEs, and their metabolic stability was determined in vitro. According to our findings, halo-alkyl substituents at position 2 of the quinazoline moiety and/or halo-alkyloxy substituents at positions 6 or 7 affect not only the compounds′ affinity, but also their selectivity toward PDE10A. As a result of substituting the methoxy group for a monofluoroethoxy or difluoroethoxy group at position 6 of the quinazoline ring, the selectivity for PDE10A over PDE3A increased. The same result was obtained by 6,7-difluoride substitution on the quinoxaline moiety. Finally, fluorinated compounds (R)-7-(fluoromethoxy)-6-methoxy-4-(3-(quinoxaline-2-yloxy)pyrrolidine-1-yl) quinazoline (16 a), 19 a-d, (R)-tert-butyl-3-(6-fluoroquinoxalin-2-yloxy) pyrrolidine-1-carboxylate (29), and 35 (IC50 PDE10A 11-65 nM) showed the highest inhibitory potential. Further, fluoroethoxy substitution at position 7 of the quinazoline ring improved metabolic stability over that of the lead structure PQ-10. Fluor your health: Phosphodiesterase 10 A (PDE10A) has emerged as an attractive target for the development of 18F-labelled brain imaging agents for positron emission tomography. A series of fluorinated dialkoxybiaryl compounds were synthesized and evaluated as PDE10A inhibitors, assisted by QSAR docking studies. The 7-fluoromethoxy derivative appears to be a promising candidate for further development.

Facile and efficient oxidation of quinazolines into quinazolin-4(3 H)-ones by peracetic acid

A new approach to synthesize quinazoline-4(3H)-ones was achieved by oxidation of quinazolines using peracetic acid, which possesses some advantages of economic reagents, simplified operation, high efficiency, and environmental friendliness. Application of this method allowed us to synthesize a series of quinazolin-4(3H)-ones with different substituents at 6 and 7 positions in good to excellent yields, including the key intermediates of tyrosine kinase inhibitors such as PD153035, Erlotinib, and Gefitinib. [Supplementary materials are available for this article. Go to the publisher's online edition of Synthetic Communications for the following free supplemental resource(s): Full experimental and spectral details.]

4-Quinazolinyloxy-diaryl ureas as novel BRAFV600E inhibitors

Aryl phenyl ureas with a 4-quinazolinoxy substituent at the meta-position of the phenyl ring are potent inhibitors of mutant and wild type BRAF kinase. Compound 7 (1-(5-tert-butylisoxazol-3-yl)-3-(3-(6,7-dimethoxyquinazolin-4-yloxy) phenyl)urea hydrochloride) exhibits good pharmacokinetic properties in rat and mouse and is efficacious in a mouse tumor xenograft model following oral dosing.

Use of structure-based design to discover a potent, selective, in vivo active phosphodiesterase 10A inhibitor lead series for the treatment of schizophrenia

Utilizing structure-based virtual library design and scoring, a novel chimeric series of phosphodiesterase 10A (PDE10A) inhibitors was discovered by synergizing binding site interactions and ADME properties of two chemotypes. Virtual libraries were docked and scored for potential binding ability, followed by visual inspection to prioritize analogs for parallel and directed synthesis. The process yielded highly potent and selective compounds such as 16. New X-ray cocrystal structures enabled rational design of substituents that resulted in the successful optimization of physical properties to produce in vivo activity and to modulate microsomal clearance and permeability.

HETEROAROMATIC QUINOLINE-BASED COMPOUNDS

The invention pertains to heteroaromatic compounds that serve as effective phosphodiesterase (PDE) inhibitors. The invention also relates to compounds which are selective inhibitors of PDE10. The invention further relates to intermediates for preparation of such compounds; pharmaceutical compositions comprising such compounds; and the use of such compounds in methods for treating certain central nervous system (CNS) or other disorders. The invention relates also to methods for treating neurodegenerative and psychiatric disorders, for example psychosis and disorders comprising deficient cognition as a symptom.

Spiro compounds and methods of use

The present invention relates to spiro compounds of formula I, processes for their preparation, pharmaceutical compositions containing them as active ingredient, methods for the treatment of disease states such as cancers associated with protein tyrosine kinases, especially epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF), to their method of use as medicaments and to their method of use in the manufacture of medicaments for use in the production of inhibition of tyrosine kinase reducing effects in warm-blooded animals such as humans.