101563-66-0

Basic information

• Product Name: 3(2H)-Pyridazinone, 5-(hydroxymethyl)-6-phenyl-
• CAS NO: 101563-66-0
• Molecular Formula: C11H10N2O2
• Molecular Weight: 202.213
• Mol File: 101563-66-0.mol
• Article Data: 7

Chemical Properties

• CAS DataBase Reference: 3(2H)-Pyridazinone, 5-(hydroxymethyl)-6-phenyl-(CAS DataBase Reference)
• NIST Chemistry Reference: 3(2H)-Pyridazinone, 5-(hydroxymethyl)-6-phenyl-(101563-66-0)
• EPA Substance Registry System: 3(2H)-Pyridazinone, 5-(hydroxymethyl)-6-phenyl-(101563-66-0)

Safety Data

• Hazardous Substances Data: 101563-66-0(Hazardous Substances Data)

Upstream product

• 132814-17-6 6-phenyl-5-hydroxymethyl-4,5-dihydro-2H-pyridazin-3-one acetate 
• 132814-18-7 6-phenyl-5-hydroxymethyl-2H-pyridazin-3-one acetate 
• 23239-13-6 6-phenyl-5-hydroxymethyl-4,5-dihydro-2H-pyridazin-3-one 

Downstream Products

• 87769-60-6 5-carboxy-6-phenyl-3(2H)-pyridazinone 
• 132814-15-4 6-phenyl-5-(N⁴-(2-furoyl)-N¹-piperazinylmethyl)-2H-pyridazin-3-one 
• 252920-10-8 5-methoxycarbonyl-6-phenyl-3(2H)-pyridazinone 
• 132814-14-3 6-phenyl-5-(N⁴-benzoyl-N¹-piperazinylmethyl)-2H-pyridazin-3-one 
• 277300-08-0 4-cyano-5-methoxycarbonyl-6-phenyl-3(2H)-pyridazinone 
• 252920-09-5 5-cyano-6-phenyl-3(2H)-pyridazinone 
• 101563-68-2 6-oxo-3-phenyl-1,6-dihydropyridazine-4-carbaldehyde 
• 132814-23-4 6-phenyl-5-bromomethyl-2H-pyridazin-3-one 
• 101563-70-6 5-aldehydo-6-phenyl-4,5-dihydro-4-methylpyridazin-3(2H)-one 
• 101563-72-8 6-phenyl-5(α-hydroxyethyl)-pyridazin-3(2H)-one 
• 101563-74-0 4-aldehydo-3-phenyl-6-methylpyridazine 

Relevant articles and documents

Ureido-Pyridazinone Derivatives: Insights into the Structural and Conformational Properties for STAT3 Inhibition

Three new ureido-pyridazinone derivatives, which are structurally related to the known STAT3 inhibitor AVS-0288, were designed by taking into account the structure-activity relationships determined for several ureido-oxadiazole derivatives previously studied by our group. Their synthesis was first attempted through suitable 5-aminopyridazinone intermediates (6a and 6b), which molecular structures were confirmed by means of X-ray diffraction data on 6a. Amine functionalization was unsuccessful, therefore, an alternative method was devised. Dual-luciferase and AlphaScreen-based assays were used to test their activity. The obtained data were rationalized on the basis of a modeling study, which focused our attention on the geometrical preferences of the ureido moiety. Computational results seem to indicate that both the 1,2,5-oxadiazole ring and the extended ZZ arrangement are essential and probably act in a synergistic way to confer significant activity against STAT3.

Efficient aromatization of 4,5-dihydro-3(2H)-pyridazinones substituted at 5 position by using anhydrous copper (II) chloride

An efficient conversion of 5-substituted-4,5-dihydro-3(2H)-pyridazinones into their corresponding dehydrogenated derivatives was achieved by treatment with anhydrous copper(II) chloride in acetonitrile.

Pyridazines. XIII. Synthesis of 6-aryl-5-oxygenated substituted-3(2H)- pyridazinones and evaluation as platelet aggregation inhibitors

Several 6-aryl-5-oxygenated substituted pyridazinones have been synthesized and evaluated in vitro for inhibition of platelet aggregation induced by adenosine 5'-diphosphate (ADP), thrombin and collagen. All the tested compounds (except 8 and 9) inhibited platelet aggregation in a dose- dependent manner. The IC50 of the most active substance compound 2b, was around 60 μM against ADP and collagen as inducers. The inhibition of platelet aggregation caused by test compounds was dependent on the level of oxidation of the function at the 5-position, with the order of IC50 values being R-OH (2a, b, 5) R-CHO (6, 7)R-COOH (8, 9). None of the tested compounds increased the intracellular levels of cAMP, indicating a lack of inhibitory activity on cAMP phosphodiesterase (PDE III) in intact cells. These results suggest that the group present at the 5 position of 6-aryl-5- substituted pyridazinones determines the platelet aggregation-inhibitory activity, and that a mechanism other than PDE inhibition is responsible for this effect.