52347-72-5

Usage

Uses

Used in Pharmaceutical Industry:
6-Amino-3-bromo (1H)indazole is utilized as a building block for the synthesis of biologically active molecules, particularly in the development of anticancer and antiviral drugs. Its unique structure and functional groups contribute to the creation of novel therapeutic agents with enhanced efficacy and selectivity.
Used in Organic Electronic Devices and Materials:
6-Amino-3-bromo (1H)indazole has been studied for its potential applications in organic electronic devices and materials due to its electronic and structural properties. Its incorporation into these systems can lead to improved performance and novel functionalities in areas such as organic light-emitting diodes (OLEDs), organic field-effect transistors (OFETs), and organic photovoltaics (OPVs).

InChI:InChI=1/C7H6BrN3/c8-7-5-2-1-4(9)3-6(5)10-11-7/h1-3H,9H2,(H,10,11)

Upstream product

• 70315-68-3 3-Bromo-6-nitro-1H-indazole 

Downstream Products

• 1415681-54-7 C₂₁H₁₈BrN₃O₄S₂ 
• 1415681-55-8 C₁₄H₁₂BrN₃O₂S 
• 117883-42-8 3-bromo-6-hydroxyl-1H-indazole 

Relevant academic research and scientific papers

Synthesis, antiproliferative and apoptotic activities of N-(6(4)-indazolyl)-benzenesulfonamide derivatives as potential anticancer agents

Recently, it has been reported that compounds bearing a sulfonamide moiety possess many types of biological activities, including anticancer activity. The present work reports the synthesis and antiproliferative evaluation of some N-(6(4)-indazolyl)benzenesulfonamides and 7-ethoxy-N-(6(4)-indazolyl) benzenesulfonamides. All compounds were evaluated for their in vitro antiproliferative activity against three tumor cell lines: A2780 (human ovarian carcinoma) A549 (human lung adenocarcinoma) and P388 (murine leukemia). The results indicated that sulfonamides 2c, 3c, 6d, 8, 13, 3b and 16 were endowed with a pharmacologically interesting antiproliferative activity with compounds 2c and 3c showing the lower IC50 (from 0.50 ± 0.09 to 1.83 ± 0.52 μM and from 0.58 ± 0.17 to 5.83 ± 1.83 μM, respectively). Moreover, these indazoles were able to trigger apoptosis through the upregulation of the typical apoptosis markers p53 and bax. As regard to the hypothetic targets of these compounds, a preliminary docking analysis showed that all compounds seemed to interact with β-tubulin, in particular compound 3b that showed the lower Ki. The cytofluorimetric analysis of the cell cycle phases indicates that all compounds, when administered at their IC 75, caused a block in the G2/M phase of the cell cycle with the generation of subpopulations of cells with a number of chromosome >4n. When the IC50s were applied we observed a prevalent block in the G0/G1 phase except for compounds 16 and 8 where a partial G2/M block was present with a concomitant decrease of cells in the G0/G1 and S phases of the cell cycle. Altogether these results suggest a possible, but not exclusive, interaction with microtubules.