1238116-48-7

Basic information

• Product Name: Kazinol U
• Synonyms: Kazinol U;4-[(2R)-3,4-Dihydro-7-hydroxy-2H-1-benzopyran-2-yl]-3-(3-methyl-2-buten-1-yl)-1,2-benzenediol
• CAS NO: 1238116-48-7
• Molecular Formula: C₂₀H₂₂O₄
• Molecular Weight: 326.38628
• Mol File: 1238116-48-7.mol
• Article Data: 1

Chemical Properties

• Boiling Point: 538.8±50.0 °C(Predicted)
• Appearance: /
• Density: 1.243±0.06 g/cm3(Predicted)
• PKA: 9.72±0.40(Predicted)
• CAS DataBase Reference: Kazinol U(CAS DataBase Reference)
• NIST Chemistry Reference: Kazinol U(1238116-48-7)
• EPA Substance Registry System: Kazinol U(1238116-48-7)

Safety Data

• Hazardous Substances Data: 1238116-48-7(Hazardous Substances Data)

Usage

General Description

Kazinol U is a synthetic chemical compound that has been developed by researchers for its potential anti-cancer and anti-inflammatory properties. It is a benzazepine derivative that has shown promising results in preclinical studies for its ability to inhibit cancer cell growth and reduce inflammation. Its mechanism of action involves targeting specific cellular pathways that are involved in tumor development and progression. Kazinol U also has potential applications in the treatment of other diseases and conditions related to inflammation and immune dysfunction. Further research and clinical studies are needed to better understand its efficacy and safety profile.

Relevant articles and documents

Autophagy antagonizes apoptosis induced by flavan enantiomers from Daphne giraldii in hepatic carcinoma cells in vitro

Enantiomers account for quite a large percentage of compounds in natural products. Our team is interested in the separation and biological activity of racemic compounds. In this report, four pairs of prenylated flavan enantiomers [(±)-1–(±)-4], including five new compounds, were isolated from the stem and root bark of Daphne giraldii, and separated successfully by using chiral chromatographic column. Their planar structures and absolute configurations were established by comprehensive spectroscopic analyses as well as circular dichroism (CD) spectroscopy. The isolates had a selective cytotoxicity towards hepatic carcinoma cell lines. Among them, new compound (+)-4 showed a more potent inhibitory effect on Hep3B cells with an IC50 value of 30.3 μM, compared with its racemic mixture 4. Therefore, the action mechanism of (+)-4 in vitro was subsequently investigated. The morphological observation and Western blot analysis demonstrated that (+)-4 could markedly induce apoptosis through intrinsic and extrinsic pathways, and also cause autophagy by increasing the phosphorylation of AMP-activated protein kinase (AMPK) in Hep3B cells. After treatment with the autophagic inhibitor bafilomycin A1 (Baf A1), (+)-4-induced apoptosis increased significantly, suggesting that the autophagy induced by (+)-4 performed a protective effect on apoptotic cell death.