1038408-35-3

Basic information

• Product Name: 1,2-BenzenediaMine, 4-broMo-N2-(1-Methylethyl)-
• Synonyms: 1,2-BenzenediaMine, 4-broMo-N2-(1-Methylethyl)-;5-bromo-N1-isopropylbenzene-1,2-diamine
• CAS NO: 1038408-35-3
• Molecular Formula: C₉H₁₃BrN₂
• Molecular Weight: 229.11692
• Mol File: 1038408-35-3.mol
• Article Data: 9

Chemical Properties

• Appearance: /
• Storage Temp.: 2-8°C
• CAS DataBase Reference: 1,2-BenzenediaMine, 4-broMo-N2-(1-Methylethyl)-(CAS DataBase Reference)
• NIST Chemistry Reference: 1,2-BenzenediaMine, 4-broMo-N2-(1-Methylethyl)-(1038408-35-3)
• EPA Substance Registry System: 1,2-BenzenediaMine, 4-broMo-N2-(1-Methylethyl)-(1038408-35-3)

Safety Data

• Hazardous Substances Data: 1038408-35-3(Hazardous Substances Data)

Usage

General Description

1,2-Benzenediamine, 4-bromo-N2-(1-methylethyl)- is a chemical compound with the molecular formula C10H14BrN2. It is a brominated derivative of 1,2-benzenediamine and is also known as 4-Bromo-2-isopropylaminoaniline. 1,2-BenzenediaMine, 4-broMo-N2-(1-Methylethyl)- is commonly used in the synthesis of pharmaceuticals and agrochemicals, and it also has applications as a dye intermediate and in the production of hair dyes. It is important to handle this compound with care as it is a hazardous material and can cause skin and eye irritation, as well as being harmful if ingested or inhaled.

Upstream product

• 863604-71-1 5-bromo-N-isopropyl-2-nitroaniline 
• 321-23-3 4-bromo-2-fluoronitrobenzene 

Downstream Products

• 1038408-36-4 6-bromo-1-isopropyl-2-methyl-1H-benzo[d]imidazole 

Relevant articles and documents

Discovery of N-(4-(3-isopropyl-2-methyl-2 H-indazol-5-yl)pyrimidin-2-yl)-4-(4-methylpiperazin-1-yl)quinazolin-7-amine as a Novel, Potent, and Oral Cyclin-Dependent Kinase Inhibitor against Haematological Malignancies

Hematologic malignancies (HM) start in blood forming tissue or in the cells of the immune system. Cyclin-dependent kinases (CDKs) regulate cell cycle progression, and some of them control cellular transcription. CDK inhibition can trigger apoptosis and could be particularly useful in hematological malignancies. Herein, we describe our efforts toward the discovery of a novel series of quinazoline derivatives as CDK inhibitors. Intensive structural modifications lead to the identification of compound 37d as the most active inhibitors of CDKs 1, 2, 4, 8 and 9 with balancing potency and selectivity against CDKs. Further biological studies revealed that compound 37d can arrest the cell cycle and induce apoptosis via activating PARP and caspase 3. More importantly, compound 37d showed good antitumor efficacy in multiple HM mice xenograft models with no obvious toxicity. These results indicated that CDK 1, 2, 4, 8, and 9 inhibitors could be potentially used to treat certain hematologic malignancies.

THYROID HORMONE RECEPTOR BETA AGONIST COMPOUNDS

Provided herein are compounds, preferably thyroid hormone receptor beta (THR beta) agonist compounds, compositions thereof, and methods of their preparation, and methods of agonizing THR beta and methods for treating disorders mediated by THR beta.

Novel dual inhibitors targeting CDK4 and VEGFR2 synergistically suppressed cancer progression and angiogenesis

Based on the significantly synergistic effects of CDK4 and VEGFR2 inhibitors on growth of cancer cells, a series of novel multi-kinase inhibitors targeting CDK4 and VEGFR2 were designed, synthesized and evaluated, among which Roxyl-ZV-5J exhibited potent and balanced activities against both CDK4 and VEGFR2 with half-maximal inhibitory concentration at the nanomolar level. It effectively induced breast and cervical cancer cell cycle arrest and cell apoptosis. Roxyl-ZV-5J also inhibited the proliferation, tube formation and VEGFR2 downstream signaling pathways of HUVECs. Oral administration of Roxyl-ZV-5J led to significant tumor regression and anti-angiogenesis without obvious toxicity in SiHa xenograft mouse model. In addition, this compound showed good pharmacokinetics. This study confirmed a new tool for dual CDK-VEGFR2 pathways inhibition achieved with a single molecule, which provided valuable leads for further structural optimization and anti-angiogenesis and anti-tumor mechanism study.