1245575-37-4

Basic information

• Product Name: 3-(phenylsulfonyl)-4-(2-(piperazin-1-yl)ethoxy)-1,2,5-oxadiazole-2-oxide
• Synonyms: 3-(phenylsulfonyl)-4-(2-(piperazin-1-yl)ethoxy)-1,2,5-oxadiazole-2-oxide
• CAS NO: 1245575-37-4
• Molecular Weight: 354.387
• Mol File: 1245575-37-4.mol
• Article Data: 12

Chemical Properties

• CAS DataBase Reference: 3-(phenylsulfonyl)-4-(2-(piperazin-1-yl)ethoxy)-1,2,5-oxadiazole-2-oxide(CAS DataBase Reference)
• NIST Chemistry Reference: 3-(phenylsulfonyl)-4-(2-(piperazin-1-yl)ethoxy)-1,2,5-oxadiazole-2-oxide(1245575-37-4)
• EPA Substance Registry System: 3-(phenylsulfonyl)-4-(2-(piperazin-1-yl)ethoxy)-1,2,5-oxadiazole-2-oxide(1245575-37-4)

Safety Data

• Hazardous Substances Data: 1245575-37-4(Hazardous Substances Data)

Upstream product

• 77279-24-4 tert-butyl 4-(2-hydroxyethyl)piperazine-1-carboxylate 
• 66074-00-8 3,4-bis(phenylsulfonyl)-1,2,5-oxadiazole 2-oxide 
• 103-76-4 1-(2-hydroxyethyl)piperazine 

Downstream Products

• 1245575-23-8 3-(phenylsulfonyl)-4-(2-(4-(2-((2E,6E)-3,7,11-trimethyldodeca-2,6,10-trienylthio)benzoyl)piperazin-1-yl)ethoxy)-1,2,5-oxadiazole-2-oxide 
• 1588522-96-6 4-(2-(4-(3-((3-((5-chloro-2-((2-methoxy-4-(4-methylpiperazin-1-yl)phenyl)amino)pyrimidin-4-yl)oxy)phenyl)amino)-3-oxopropyl)piperazin-1-yl)ethoxy)-3-(phenylsulfonyl)-1,2,5-oxadiazole 2-oxide 
• 1436851-33-0 C₄₀H₄₃ClN₁₀O₉S 

Relevant articles and documents

Chromone 3-piperazine linked furazan derivative as well as preparation method and application thereof

The invention relates to the fields of natural medicines and medicinal chemistry, and relates to a preparation method of a series of chromone 3-piperazine linked furazan derivatives with antitumor activity and a new application of the chromone 3-piperazine linked furazan derivatives in preparation of antitumor medicines. The chromone 3-piperazine linked furazan derivative and the pharmaceutically acceptable salt thereof disclosed by the invention are as shown in a general formula I in the specification. Wherein R is described in the claims and the specification.

Discovery of β-carboline-(phenylsulfonyl)furoxan hybrids as potential anti-breast cancer agents

The cytotoxicity properties of the β-carboline alkaloids have been broadly investigated. However, the potential application of β-carbolines was hindered due to the moderate activity in cancer. In the present study, thirty β-carboline-(phenylsulfonyl)furoxan hybrids (11a–j, 12a–j and 13a–j) were designed and synthesized through esterification and amidation reaction strategy, and their inhibitory activities against the human breast cancer cell lines MCF-7 and MDA-MB-231 were evaluated by CCK-8 assay. Biological evaluation presented that the most promising amide derivative 13h, substituted with p-methoxyphenyl group at position 1, generated high concentration of NO and evidently depressed the MCF-7 (IC50 = 0.89 μM) and MDA-MB-231 (IC50 = 0.62 μM) cells proliferation. Particularly, the wound healing and transwell assays demonstrated that 13h significantly inhibited the migration and invasion of MDA-MB-231cells. Furthermore, the preliminary mechanisms studies indicated that 13h induced G2/M phase arrest and apoptosis possibly causing by ROS accumulation and ROS-mediated DNA damage. Based on these considerations, 13h may be a promising antimetastatic agent for breast cancer, which is noteworthy for further exploration.

Antiproliferative chromone derivatives induce K562 cell death through endogenous and exogenous pathways

A series of furoxan derivatives of chromone were prepared. The antiproliferative activities were tested against five cancer cell lines HepG2, MCF-7, HCT-116, B16, and K562, and two normal human cell lines L-02 and PBMCs. Among them, compound 15a exhibited the most potent antiproliferative activity. It was also found 15a produced more than 8 μM of NO at the peak time of 45 min by Griess assay. Generally, antiproliferative activity is positively related to NO release to some extent. Further in-depth studies on apoptosis-related mechanisms showed that 15a caused S-phase cell cycle arrest in a concentration-dependent manner and induced apoptosis significantly through mitochondria-related pathways. Human apoptosis protein array assay also demonstrated 15a increased the expression levels of pro-apoptotic Bax, Bad, HtrA2 and Trail R2/DR5. The expression of catalase and cell cycle blocker claspin were similarly up-regulated. In balance, 15a induced K562 cells death through both endogenous and exogenous pathways.