1347692-68-5

Basic information

• Product Name: 5-bromomethyl-1-phenylpyridine-2(1H)-one
• Synonyms: 5-bromomethyl-1-phenylpyridine-2(1H)-one
• CAS NO: 1347692-68-5
• Molecular Weight: 264.121
• Mol File: 1347692-68-5.mol

Chemical Properties

• CAS DataBase Reference: 5-bromomethyl-1-phenylpyridine-2(1H)-one(CAS DataBase Reference)
• NIST Chemistry Reference: 5-bromomethyl-1-phenylpyridine-2(1H)-one(1347692-68-5)
• EPA Substance Registry System: 5-bromomethyl-1-phenylpyridine-2(1H)-one(1347692-68-5)

Safety Data

• Hazardous Substances Data: 1347692-68-5(Hazardous Substances Data)

Upstream product

• 53179-13-8 Pirfenidone 
• 1003-68-5 5-methyl-2-pyridone 

Downstream Products

• 1347692-36-7 5-((4-acetylphenylamino)methyl)-1-phenylpyridin-2(1H)-one 
• 1347692-34-5 1-phenyl-5-((p-tolylamino)methyl)pyridin-2(1H)-one 
• 1347692-33-4 1-phenyl-5-((o-tolylamino)methyl)pyridin-2(1H)-one 
• 1347692-42-5 5-((4-chlorophenylamino)methyl)-1-phenylpyridin-2(1H)-one 
• 1347692-39-0 1-phenyl-5-((phenylamino)methyl)pyridin-2(1H)-one 

Relevant articles and documents

Metabolic Activation of Pirfenidone Mediated by Cytochrome P450s and Sulfotransferases

Pirfenidone is approved for the treatment of idiopathic pulmonary fibrosis. Idiosyncratic drug reactions, due to clinical application of pirfenidone, have been documented, even along with death cases resulting from acute liver failure. The present study aimed at the investigation of metabolic activation of pirfenidone possibly participating in the reported adverse reactions. Pirfenidone-derived glutathione/N-acetylcysteine (GSH/NAC) conjugates were detected in microsomal/primary hepatocyte incubations after exposure to pirfenidone. The GSH/NAC conjugates were also observed in bile and urine of rats given pirfenidone, respectively. The observation of the conjugates suggests the formation of a quinone methide intermediate derived from pirfenidone. The intermediate was possibly generated through two pathways. First, pirfenidone was directly metabolized to the quinone methide intermediate via dehydrogenation; second, pirfenidone was oxidized to 5-hydroxymethyl pirfenidone, followed by sulfation to a benzyl alcohol-sulfate derivative. The findings facilitate the understanding of the mechanisms of pirfenidone-induced idiosyncratic toxicity and assist medicinal chemists to minimize toxicities in the development of new pharmaceutical agents.

Pirfenidone-related substance as well as preparation method and application of pirfenidone-related substance

The invention discloses a pirfenidone-related substance as well as a preparation method and application of the pirfenidone-related substance. The pirfenidone-related substance is a compound with a structure as shown in a formula I.

Synthesis, pharmacophores, and mechanism study of pyridin-2(1H)-one derivatives as regulators of translation initiation factor 3A

Twenty-seven 1,5-disubstituted-pyridin-2(1H)-one derivatives were synthesized and evaluated for their anti-cancer and anti-fibrosis activity by A549 and NIH3T3 cell viability assays, respectively. To study the selectivity between the cancer and fibrosis cell lines, pharmacophore models (F 1-F4) were built in advance for compounds with pyridin-2(1H)-one scaffold, which revealed the relationship between the occupation of the aromatic sub-site F4 and potent anti-cancer activity. The relationship between structure and anti-cancer activity for all target compounds is also reported herein: 1-Phenyl-5-((m-tolylamino)methyl) pyridine-2(1H)-one (22) displayed both potency and selectivity (IC50 = 0.13 mM) toward the A549 cell line through the inhibition of translation initiation, especially by eIF3a suppression, and can be treated as a lead for the design of novel eIF3a regulators and anti-lung cancer agents. A series of pyridin-2(1H)-one derivatives were synthesized. Elucidation of their pharmacophores and mechanism of action suggested that structures with F 4 occupation displayed more selective anti-cancer than anti-fibrosis activity and that they interrupt the initiation phase of translation by acting on the eukaryotic translation initiation factor 3, subunit A.