50892-99-4

Basic information

• Product Name: FURAN-2-AMIDOXIME
• CAS NO: 50892-99-4
• Molecular Formula: C₅H₆N₂O₂
• Molecular Weight: 126.115
• Mol File: 50892-99-4.mol
• Article Data: 17

Chemical Properties

• CAS DataBase Reference: FURAN-2-AMIDOXIME (CAS DataBase Reference)
• NIST Chemistry Reference: FURAN-2-AMIDOXIME (50892-99-4)
• EPA Substance Registry System: FURAN-2-AMIDOXIME (50892-99-4)

Safety Data

• Safety Statements: Explodes when heated above 100°C. Exothermic reaction if heated to 65°C. When heated to decomposition it emits toxic fumes of NOsub xmlns="">x/sub>.
• Hazardous Substances Data: 50892-99-4(Hazardous Substances Data)

Upstream product

• 617-90-3 2-furancarbonitrile 

Downstream Products

• 1117842-23-5 5-(4-chloro-2-methylphenyl)-3-(furan-2-yl)-1,2,4-oxadiazole 
• 61084-44-4 5-(4-Chloro-3-nitrophenyl)-3-(2-furanyl)-1,2,4-oxadiazole 
• 61051-44-3 5-(2-chloro-4-nitrophenyl)-3-(2-furanyl)-1,2,4-oxadiazole 
• 61051-42-1 [3-chloro-4-[3-(2-furanyl)-1,2,4-oxadiazol-5-yl]phenyl]carbamic acid, 2,2,2-trichloroethyl ester 
• 61051-39-6 [2-chloro-5-[3-(2-furanyl)-1,2,4-oxadiazol-5-yl]phenyl]carbamic acid, 2,2,2-trichloroethyl ester 
• 61051-41-0 [3-Chloro-4-[3-(2-furanyl)-1,2,4-oxadiazol-5-yl]phenyl]carbamic acid, phenyl ester 
• 61051-40-9 [2-chloro-5-[3-(2-furanyl)-1,2,4-oxadiazol-5-yl]phenyl]carbamic acid, phenyl ester 
• 61051-38-5 [2-chloro-5-[3-(2-furanyl)-1,2,4-oxadiazol-5-yl]phenyl]carbamic acid, methyl ester 
• 96898-38-3 3-(2-furanyl)-5-<3-nitro-4-(phenylthio)phenyl>-1,24-oxadiazole 
• 96913-34-7 N'-<3-chloro-4-<3-(furanyl)-1,2,4-oxadiazol-5-yl>phenyl>-N,N-diethylthiourea 
• 96898-51-0 N'-<2-chloro-5-<3-(furanyl)-1,2,4-oxadiazol-5-yl>phenyl>-N,N-diethylthiourea 
• 96898-67-8 5-(2-Chloro-4-isothiocyanato-phenyl)-3-furan-2-yl-[1,2,4]oxadiazole 
• 61051-45-4 5-(4-amino-2-chlorophenyl)-3-(2-furanyl)-1,2,4-oxadiazole 
• 96898-69-0 5-(4-chloro-3-isothiocyanophenyl)-3-(2-furyl)-1,2,4-oxadiazole 

Relevant articles and documents

Novel 5-(quinuclidin-3-ylmethyl)-1,2,4-oxadiazoles to investigate the activation of the α7 nicotinic acetylcholine receptor subtype: Synthesis and electrophysiological evaluation

α7 nicotinic acetylcholine receptors (nAChRs) are relevant therapeutic targets for a variety of disorders including neurodegeneration, cognitive impairment, and inflammation. Although traditionally identified as an ionotropic receptor, the α7 subtype showed metabotropic-like functions, mainly linked to the modulation of immune responses. In the present work, we investigated the structure-activity relationships in a set of novel α7 ligands incorporating the 5-(quinuclidin-3-ylmethyl)-1,2,4-oxadiazole scaffold, i.e. derivatives 21a-34a and 21b-34b, aiming to identify the structural requirements able to preferentially trigger one of the two activation modes of this receptor subtype. The new compounds were characterized as partial and silent α7 nAChR agonists in electrophysiological assays, which allowed to assess the contribution of the different groups towards the final pharmacological profile. Overall, modifications of the selected structural backbone mainly afforded partial agonists, among them tertiary bases 27a-33a, whereas additional hydrogen-bond acceptor groups in permanently charged ligands, such as 29b and 31b, favored a silent desensitizing profile at the α7 nAChR.

Synthesis of 2,4-Disubstituted Imidazoles via Nucleophilic Catalysis

A convergent, microwave-assisted protocol for the synthesis of disubstituted NH-imidazoles via nucleophilic catalysis is described. The substituted imidazoles are accessed via the intramolecular addition of a variety of amidoxime substrates to activated a

Small Molecule Inhibition of MicroRNA miR-21 Rescues Chemosensitivity of Renal-Cell Carcinoma to Topotecan

Chemical probes of microRNA (miRNA) function are potential tools for understanding miRNA biology that also provide new approaches for discovering therapeutics for miRNA-associated diseases. MicroRNA-21 (miR-21) is an oncogenic miRNA that is overexpressed in most cancers and has been strongly associated with driving chemoresistance in cancers such as renal cell carcinoma (RCC). Using a cell-based luciferase reporter assay to screen small molecules, we identified a novel inhibitor of miR-21 function. Following structure-activity relationship studies, an optimized lead compound demonstrated cytotoxicity in several cancer cell lines. In a chemoresistant-RCC cell line, inhibition of miR-21 via small molecule treatment rescued the expression of tumor-suppressor proteins and sensitized cells to topotecan-induced apoptosis. This resulted in a >10-fold improvement in topotecan activity in cell viability and clonogenic assays. Overall, this work reports a novel small molecule inhibitor for perturbing miR-21 function and demonstrates an approach to enhancing the potency of chemotherapeutics specifically for cancers derived from oncomir addiction.