70978-37-9

Basic information

• Product Name: 4-Methoxybenzyl azide
• Synonyms: Benzene, 1-(azidomethyl)-4-methoxy-
• CAS NO: 70978-37-9
• Molecular Formula: C₈H₉N₃O
• Molecular Weight: 163.17656
• Mol File: 70978-37-9.mol
• Article Data: 159

Chemical Properties

• Melting Point: 70-71℃
• Boiling Point: 126 °C(Press: 14 Torr)
• Appearance: /
• Density: 1.063 g/cm3 (420 ºC)
• Refractive Index: 1.5272 (589.3 nm 20℃)
• CAS DataBase Reference: 4-Methoxybenzyl azide(CAS DataBase Reference)
• NIST Chemistry Reference: 4-Methoxybenzyl azide(70978-37-9)
• EPA Substance Registry System: 4-Methoxybenzyl azide(70978-37-9)

Safety Data

• Hazardous Substances Data: 70978-37-9(Hazardous Substances Data)

Usage

General Description

4-Methoxybenzyl azide is a chemical compound with the molecular formula C8H9N3O. It is an organic compound with a methoxy group (-OCH3) attached to a benzene ring and an azide functional group (-N3). 4-Methoxybenzyl azide is commonly used in organic synthesis as a reagent for the introduction of azide groups into molecules. It is also used in the preparation of pharmaceuticals, agrochemicals, and other organic compounds. 4-Methoxybenzyl azide is known for its potential as a precursor in click chemistry reactions to produce diverse chemical compounds. Additionally, 4-Methoxybenzyl azide plays a crucial role as a building block in the production of compounds used in the pharmaceutical and material science industries.

Upstream product

• 824-94-2 p-methoxybenzyl chloride 
• 70887-29-5 4-methoxybenzyl iodide 
• 18494-82-1 2-(4-methoxy-benzyloxy)-tetrahydro-pyran 
• 2393-23-9 4-methoxy-benzylamine 
• 90673-97-5 methanesulfonic acid 4-methoxybenzyl ester 
• 4648-54-8 trimethylsilylazide 
• 2746-25-0 p-Methoxybenzyl bromide 
• 623-05-2 (4-hydroxyphenyl)methanol 
• 104-93-8 p-methylanizole 
• 100-66-3 methoxybenzene 
• 92567-07-2 1-(diazidomethyl)-4-methoxybenzene 
• 123-11-5 4-methoxy-benzaldehyde 
• 104-21-2 p-methoxybenzyl acetate 
• 105-13-5 4-Methoxybenzyl alcohol 

Downstream Products

• 81581-08-0 ethyl 1-(4-methoxybenzyl)-4-phenyl-1H-1,2,3-triazole-5-carboxylate 
• 81581-07-9 ethyl 1-(4-methoxybenzyl)-5-phenyl-v-triazole-4-carboxylate 
• 874-90-8 4-methoxybenzonitrile 
• 120157-94-0 N-(tert-butoxycarbonyl)p-methoxybenzylamine 
• 853017-03-5 {2-[((E)-Hex-2-enyl)oxy]-5,5-dimethyl-2λ⁵-[1,3,2]dioxaphosphinan-2-ylidene}-(4-methoxy-benzyl)-amine 
• 81581-05-7 ethyl 1-(4-methoxybenzyl)-1H-1,2,3-triazole-4-carboxylate 
• 944480-99-3 C₁₆H₁₆N₄O₃S 
• 99451-35-1 1-p-Methoxybenzyl-5-p-Toluenesulfonyltetrazole 
• 70978-35-7 ethyl 1-(4-methoxybenzyl)-1H-tetrazole-5-carboxylate 
• 944480-96-0 C₁₁H₁₂N₄O₂ 
• 862112-28-5 ethyl 5-amino-1-(4-methoxybenzyl)-1H-1,2,3-triazole-4-carboxylate 
• 942060-31-3 ethyl 1-(4-methoxybenzyl)-5-(trifluoromethyl)-1H-1,2,3-triazole-4-carboxylate 
• 942060-32-4 ethyl 1-(4-methoxybenzyl)-4-(trifluoromethyl)-1H-1,2,3-triazole-5-carboxylate 
• 947505-31-9 1-(4-methoxybenzyl)-5-methyl-1H-[1,2,3]|triazole-4-carboxylic acid methyl ester 

Relevant articles and documents

Regioselectivity in the 1,3-dipolar cycloaddition reactions of nitrile oxides and organic azides with bromocarbazole-1,4-diones

The effect exerted by the presence of a bromine atom in 2 or 3 position of a carbazole-1,4-dione on the regiocontrol of 1,3-dipolar cycloaddition reactions with nitrile oxides and organic azides was investigated. Comparison with the results obtained with

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.

Discovery of triazolyl thalidomide derivatives as anti-fibrosis agents

Fibrosis with excessive accumulation of extracellular matrix (ECM) often causes progressive organ dysfunction and results in many inflammatory and metabolic diseases, including systemic sclerosis, pulmonary fibrosis, advanced liver disease and advanced kidney disease. The store-operated calcium entry (SOCE) pathway and the related signaling pathway were both found to be the important routes for fibrogenesis. Our aim in this study was to discover novel compounds to inhibit fibrogenesis. A number of triazolyl thalidomide derivatives were synthesized and evaluated for their anti-fibrosis activities. Compounds 7b-e, 8c-d, 10a-b and 10e inhibited intracellular Ca2+ activation and showed no cytotoxicity. Among them, 6-{4-[(3-(1,3-dioxoisoindolin-2-yl)-2,6-dioxopiperidin-1-yl)methyl]-1H-1,2,3-triazol-1-yl}hexanoic acid (10e) with the most potent inhibitory effect was chosen for further examination. The results revealed that compound 10e, a SOCE inhibitor, reversed the migratory ability of TGF-β1-induced myofibroblasts, dedifferentiated myofibroblasts to fibroblasts due to cytoskeleton remodeling, and restrained myofibroblast activation by targeting Orai1 and TGF-β1/SMAD2/3 signaling pathways. The in silico study indicated that compound 10e, with the appropriate lipophilic carbon chain and carboxylic acid, showed a good drug-likeness model score. Conclusively, the SOCE inhibitor, compound 10e, is used as a promising lead compound for the development of a new treatment for fibrosis. This journal is