1393477-75-2

Basic information

• Product Name: 4-(4-((3-carboxypropanoyl)oxy)n-propoxy)-3-benzenesulfonyl-1,2,5-oxadiazole-2-oxide
• Synonyms: 4-(4-((3-carboxypropanoyl)oxy)n-propoxy)-3-benzenesulfonyl-1,2,5-oxadiazole-2-oxide
• CAS NO: 1393477-75-2
• Molecular Weight: 400.366
• Mol File: 1393477-75-2.mol
• Article Data: 16

Chemical Properties

• Boiling Point: 691.6±65.0 °C(Predicted)
• Density: 1.53±0.1 g/cm3(Predicted)
• CAS DataBase Reference: 4-(4-((3-carboxypropanoyl)oxy)n-propoxy)-3-benzenesulfonyl-1,2,5-oxadiazole-2-oxide(CAS DataBase Reference)
• NIST Chemistry Reference: 4-(4-((3-carboxypropanoyl)oxy)n-propoxy)-3-benzenesulfonyl-1,2,5-oxadiazole-2-oxide(1393477-75-2)
• EPA Substance Registry System: 4-(4-((3-carboxypropanoyl)oxy)n-propoxy)-3-benzenesulfonyl-1,2,5-oxadiazole-2-oxide(1393477-75-2)

Safety Data

• Hazardous Substances Data: 1393477-75-2(Hazardous Substances Data)

Upstream product

• 108-30-5 succinic acid anhydride 
• 361541-87-9 3-(4-benzenesulfonyl-5-oxy-furazan-3-yloxy)-propan-1-ol 
• 66074-00-8 3,4-bis(phenylsulfonyl)-1,2,5-oxadiazole 2-oxide 
• 110-15-6 succinic acid 

Downstream Products

• 1446816-86-9 C₃₅H₃₈N₄O₁₂S 

Relevant articles and documents

Evaluation of novel paclitaxel-loaded NO-donating polymeric micelles for an improved therapy for gastroenteric tumor

This study reports the design and synthesis of NO-donating polymer to generate biodegradable polymeric micelle containing paclitaxel (NO/PTX) as a nanomedicine delivery system aimed to enhance the solubility and anti-cancer activity of paclitaxel (PTX). NO/PTX showed greater NO-releasing performance than nitroglycerin, displaying excellent tolerance in KM mice, and exhibited a two-fold stronger antiproliferative activity than PTXin vitroagainst HCT116, SW480, and SGC-7901 cell lines.In vivotumor growth inhibition assay results indicated that NO/PTX displayed lightly stronger activities against tumor growth than PTX at a dose of 10 mg kg?1, while the anti-tumor effect of NO/PTX was significantly improved than that of PTX and Genexol-PM groups at a dose of 15 mg kg?1(the inhibition rate: 67%vs.53% and 41%). In addition, NO/PTX showed an improved area under the plasma concentration-time curve and drug deposition in tumors in comparison to PTX. Wound healing assay and western blot analysis of EMT-related markers suggested that NO/PTX could inhibit the potential of HCT116 migration. Western blot analysis also demonstrated that NO/PTX dampened efflux activity of P-gp and up-regulated apoptosis-related proteins. Overall, these promising results suggested that the synergism between PTX and NO-donating micelles could contribute to the potent anti-cancer activity of NO/PTX.

A class of chelidonine nitric oxide donor derivatives, preparation method and applications

The invention relates to the field of natural medicines and medicinal chemistry, and relates to a chelidonine nitric oxide donor derivative, a preparation method and applications, particularly to a preparation method of a series of chelidonine nitric oxide donor derivatives with antitumor activity, and new applications of the chelidonine nitric oxide donor derivatives in preparation of antitumor drugs. The chelerythrine nitric oxide donor derivative and the pharmaceutically acceptable salt thereof disclosed by the invention are represented by a general formula, wherein n1, n2, n3 and X are defined in the claims and the specification.

Design, synthesis and apoptosis-related antiproliferative activities of chelidonine derivatives

To get chelidonine derivatives with enhanced antiproliferative activity and selectivity, a series of nitric oxide donating derivatives (10a-f and 11a-j) were designed, synthesized and biologically evaluated. Compared with chelidonine, these compounds exhibited lower IC50 values against human hepatoma cells HepG2, breast cancer cells MCF-7, colon cancer cells HCT-116, as well as leukemia cells K562. Compound 11j displayed the strongest antiproliferative activity with IC50 values of 3.91, 6.90, 4.36 and 1.12 μM against the above four cells, respectively. Nevertheless, it showed an IC50 value >40 μM against human peripheral blood mononuclear cells (PBMCs), which demonstrated high selectivity between normal and cancer blood cells. In further mechanism studies, 11j showed the capability to induce K562 cells apoptosis, S phase cell cycle arrest and mitochondrial membrane potential disorder. Besides, 11j was found to be effective in promoting the expression of proapoptotic protein Bad and suppressing the expression of anti-apoptotic proteins Bcl-xL, catalase, survivin, claspin and clusterin.