524955-09-7

Basic information

• Product Name: AKOS B033273
• Synonyms: AKOS B033273;3-CHLORO-4-(PYRIDIN-2-YLMETHOXY)-BENZENAMINE;3-CHLORO-4-(PYRIDIN-2-YLMETHOXY)-PHENYLAMINE;ART-CHEM-BB B033273;UKRORGSYN-BB BBV-019513;3-chloro-4-(2-pyridinylMethoxy)- BenzenaMine;3-Chloro-4-[(pyridin-2-yl)Methoxy]benzenaMine [3-Chloro-4-(pyridin-2-ylMethoxy)phenyl]aMine;BenzenaMine, 3-chloro-4-(2-pyridinylMethoxy)-
• CAS NO: 524955-09-7
• Molecular Formula: C₁₂H₁₁ClN₂O
• Molecular Weight: 234.685
• EINECS: 1592732-453-0
• Mol File: 524955-09-7.mol
• Article Data: 29

Chemical Properties

• Melting Point: 91.0 to 95.0 °C
• Boiling Point: 402.5±35.0 °C(Predicted)
• Appearance: /
• Density: 1.292±0.06 g/cm3(Predicted)
• Storage Temp.: Keep in dark place,Inert atmosphere,Room temperature
• PKA: 3.88±0.10(Predicted)
• CAS DataBase Reference: AKOS B033273(CAS DataBase Reference)
• NIST Chemistry Reference: AKOS B033273(524955-09-7)
• EPA Substance Registry System: AKOS B033273(524955-09-7)

Safety Data

• Hazardous Substances Data: 524955-09-7(Hazardous Substances Data)

Usage

Description

AKOS B033273, also known as 3-Chloro-4-(2-pyridylmethoxy)aniline, is a chemical compound with potential applications in the pharmaceutical industry. It is characterized by its unique molecular structure, which allows it to interact with specific biological targets and exhibit various biological activities.

Uses

Used in Pharmaceutical Industry:
AKOS B033273 is used as a key intermediate in the synthesis of disubstituted (arylamino)quinolinecarbonitriles. These compounds have demonstrated potent and selective inhibition of human epidermal growth factor receptor-2 (HER2) kinase activity, making them promising candidates for the development of orally active antitumor agents.
In the context of cancer treatment, AKOS B033273 contributes to the development of novel therapeutics that target the HER2 receptor, which is overexpressed in various types of cancer, including breast, ovarian, and gastric cancers. By inhibiting the HER2 receptor, these agents can potentially halt tumor growth and progression, offering a new treatment option for patients with HER2-overexpressing cancers.
Furthermore, the use of AKOS B033273 in the synthesis of disubstituted (arylamino)quinolinecarbonitriles highlights its potential in the development of targeted therapies, which aim to minimize side effects and improve the overall efficacy of cancer treatment.

Upstream product

• 586-98-1 2-Hydroxymethylpyridine 
• 3964-52-1 2-chloro 4-aminophenol 
• 4377-33-7 2-chloromethylpyridine 
• 619-08-9 2-chloro-4-nitrophenol 
• 6959-47-3 2-chloromethylpyridine hydrochloride 
• 55401-97-3 2-(Bromomethyl)pyridine 
• 350-30-1 3-chloro-4-fluoronitrobenzene 
• 179687-79-7 2-((2-chloro-4-nitrophenoxy)methyl)pyridine 

Downstream Products

• 1439373-52-0 C₂₃H₁₉ClN₄O₄ 
• 915941-95-6 N-(4-[3-chloro-4-(pyridin-2-ylmethoxy)phenylamino]-3-cyano-7-ethoxyquinoline-6-yl)acetamide 
• 892142-92-6 2-[(4-{[3-chloro-4-(pyridin-2-ylmethoxy)phenyl]amino}-1H-pyrazolo[3,4-d]pyrimidin-3-yl)oxy]ethanol 
• 1260402-49-0 3-chloro-4-(N-oxidepyridine-2-methoxyl)-phenylamine TFA salt 
• 179688-70-1 N-(3-chloro-4-(pyridin-2-ylmethoxy)phenyl)-6-nitroquinazolin-4-amine 
• 1351942-60-3 4-(3-chloro-4(pyridin-2-yl-methoxy)phenylamino)-6-nitro-7-(tetrahydrofuran-3-yl-oxy)quinoline-3-carbonitrile 
• 1351943-50-4 6-amino-4-(3-chloro-4-(pyridin-2-yl-methoxy)phenylamino)-7-(tetrahydrofuran-3-yl-oxy)quinoline-3-carbonitrile 
• 1351940-20-9 (E)-4-bromo-N-(4-(3-chloro-4-(pyridin-2-yl-methoxy)phenylamino)-3-cyano-7-(tetrahydrofuran-3-yl-oxy)quinolin-6-yl)-but-2-enamide 
• 1351940-21-0 (E)-N-(4-(3-chloro-4-(pyridin-2-yl-methoxy)phenylamino)-3-cyano-7-(tetrahydrofuran-3-yl-oxy)quinolin-6-yl)-4-(dimethylamino)-but-2-enamide 
• 1351940-22-1 (E)-N-(4-(3-chloro-4-(pyridin-2-yl-methoxy)phenylamino)-3-cyano-7-(tetrahydrofuran-3-yl-oxy)quinolin-6-yl)-4-(dimethylamino)-but-2-enamide hydrochloride 
• 1351940-53-8 N-(4-(3-chloro-4-(pyridin-2-yl-methoxy)phenylamino)-3-cyano-7-(tetrahydrofuran-3-yl-oxy)quinolin-6-yl)acrylamide 
• 1351940-60-7 tert-butyl 4-(2-(4-(3-chloro-4-(pyridin-2-yl-methoxy)phenylamino)-3-cyano-7-(tetrahydrofuran-3-yl-oxy)quinolin-6-yl-amino)-2-oxoethylidene)piperidine-1-carboxylate 
• 1351940-61-8 N-(4-(3-chloro-4-(pyridin-2-yl-methoxy)phenylamino)-3-cyano-7-(tetrahydrofuran-3-yl-oxy)quinolin-6-yl)-2-(piperidin-4-ylidene)acetamide 
• 1351940-63-0 N-(4-(3-chloro-4-(pyridin-2-yl-methoxy)phenylamino)-3-cyano-7-(tetrahydrofuran-3-yl-oxy)quinolin-6-yl)-2-(1-methylpiperidin-4-ylidene)acetamide 

Relevant articles and documents

Novel heteroaryl amide derivatives as MAO-B inhibitors and pharmaceutical compositions for preventing, ameliorating or treating neurodegenerative diseases comprising the same

A novel heteroaryl amide derivative compound useful as MAO-B inhibitors. The present invention relates to a compound selected from a pharmaceutically acceptable salt thereof, a hydrate thereof, or a stereoisomer thereof, and a pharmaceutical composition comprising the compound as an active ingredient for preventing, alleviating, or treating neurodegenerative diseases such MAO as B's disease, 's disease, 's disease, and the like.

Targeting Her2-insYVMA with Covalent Inhibitors - A Focused Compound Screening and Structure-Based Design Approach

Mutated or amplified Her2 serves as a driver of non-small cell lung cancer or mediates resistance toward the inhibition of its family member epidermal growth factor receptor with small-molecule inhibitors. To date, small-molecule inhibitors targeting Her2 which can be used in clinical routine are lacking, and therefore, the development of novel inhibitors was undertaken. In this study, the well-established pyrrolopyrimidine scaffold was modified with structural motifs identified from a screening campaign with more than 1600 compounds, which were applied against wild-type Her2 and its mutant variant Her2-A775_G776insYVMA. The resulting inhibitors were designed to covalently target a reactive cysteine in the binding site of Her2 and were further optimized by means of structure-based drug design utilizing a set of obtained complex crystal structures. In addition, the analysis of binding kinetics and absorption, distribution, metabolism, and excretion parameters as well as mass spectrometry experiments and western blot analysis substantiated our approach.

Discovery of anilino-furo[2,3-d]pyrimidine derivatives as dual inhibitors of EGFR/HER2 tyrosine kinase and their anticancer activity

Being responsible for the development of many cancer types, EGFR (Epidermal Growth Factor Receptor) and HER2 (Human Epidermal growth factor Receptor 2) were the focus of this study where a series of novel 4-anilino-furo[2,3-d]pyrimidine derivatives was designed, synthesized and biologically evaluated. Modification of the solvent accessible 5-position side chain greatly affected the in-vitro EGFR/HER2 inhibitory activity. Three derivatives bearing 5-carboxylic acid side chain, namely the 3-chloroanilino derivative (8c), the 3-bromoaniline (8d) and the lapatinib analogue (10) demonstrated the most significant submicromolar EGFR inhibition. Surprisingly, the in-vitro assay of the ester 7h and its acid analogue 10 showed a significant variation of results between the antiproliferative activity against A549 cell line (IC50 0.5 and 21.4 μM) respectively and EGFR inhibitory activity (18% and 100%) respectively, suggesting that 7h might be a prodrug for 10. This assumption was also affirmed by the in-vivo results, where the in-vivo antitumor assessment against EAC (Ehrlich Ascites Carcinoma) solid tumor model revealed that 7h and 8d (10 mg/kg dose) exhibited antitumor activity comparable to that of gefitinib at the same dose, exhibiting TGI% of 67%, 71% and 70%, respectively. This effect could be explained, at least partly, via activation of apoptosis, where 7h and 8d caused more than 2-fold increase of caspase 3 and cytochrome c expression than the control group which is comparable to that of gefitinib-treated group. Finally, 7h was the most effective apoptotic inducer, resulting in a significant elevation in annexin V–FITC-positive apoptotic cells (both early and late apoptosis) by 25 and 79-folds, respectively, compared to control, which is higher than that of gefitinib (22 and 61-folds, respectively).