242792-95-6

Basic information

• Product Name: 7-Phenylisatin
• Synonyms: 7-Phenylisatin
• CAS NO: 242792-95-6
• Molecular Formula: C₁₄H₉NO₂
• Molecular Weight: 223.22676
• Mol File: 242792-95-6.mol

Chemical Properties

• Appearance: /
• CAS DataBase Reference: 7-Phenylisatin(CAS DataBase Reference)
• NIST Chemistry Reference: 7-Phenylisatin(242792-95-6)
• EPA Substance Registry System: 7-Phenylisatin(242792-95-6)

Safety Data

• Hazardous Substances Data: 242792-95-6(Hazardous Substances Data)

Upstream product

• 20780-74-9 7-bromoisatin 
• 98-80-6 phenylboronic acid 
• 117500-16-0 2'-hydroxyimino-2-iodoacetanilide 
• 615-43-0 2-iodophenylamine 
• 20780-78-3 7-iodoisatin 
• 728-70-1 α-oximino-2-phenylacetanilide 

Downstream Products

• 242793-05-1 1-(4-Bromobutyl)-7-phenyl-1H-indole-2,3-dione 
• 136131-60-7 2-benzyl-5-phenyl-1-naphthol 
• 136131-55-0 2-benzyl-8-phenyl-1-naphthol 
• 136131-40-3 5-phenyl-1,4-dihydro-1,4-epoxynaphthalene 
• 129957-20-6 8-phenylnaphthalen-1-ol 
• 61982-94-3 5-phenyl-1-naphthol 

Relevant articles and documents

Design, synthesis, and biological evaluation of structurally modified isoindolinone and quinazolinone derivatives as hedgehog pathway inhibitors

The Hedgehog (Hh) signaling pathway is associated with diverse aspects of cellular events, such as cell migration, proliferation, and differentiation throughout embryonic development and tissue patterning. An abnormal Hh signaling pathway is linked to numerous human cancers, including basal cell carcinoma (BCC), medulloblastoma (MB), lung cancer, prostate cancer, and ovarian cancer, and it is therefore a promising target in cancer therapy. Using a structure-hopping approach, we designed new Hh signaling pathway inhibitors with isoindolinone or quinazolinone moieties, which were synthesized and biologically evaluated using an 8xGli-luciferase (Gli-Luc) reporter assay in NIH3T3 cells. Compounds 9–11 and 14 with isoindolinone scaffolds demonstrated moderate Hh inhibitory activity; whereas quinazolinone derivatives 24, 29, 32, 34, and 35 exhibited good potency with submicromolar IC50values and the analog 28 showed nanomolar IC50value. Although sonidegib shows a decrease in inhibitory effect on vismodegib resistance-conferring Smo mutants, the structurally modified new compounds not only possess the pharmacophoric properties of Hh pathway inhibition but also preserve the suppressive potency in drug-resistant Smo mutants. Mechanistically, quinazolinone derivatives 28 and 34 suppress Hh signaling by blocking Smo and Gli translocation into the cilia, similar to vismodegib and sonidegib. Additionally, the human microsomal stability of the representative analogs 28 and 34 were determined to be comparable to that of the reference compound sonidegib. Thus, these new scaffolds can serve as a platform for the development of novel cancer therapeutics targeting the Hh pathway.

Synthesis of 3-aryl-4-methyl-1,2-benzenedisulfonimides, new chiral Bronsted acids. A combined experimental and theoretical study

We have recently reported the use, in catalytic amounts, of 1,2-benzenedisulfonimide as a safe Bronsted acid in some acid-catalyzed organic reactions. With the design of new and chiral acid organocatalysts with the structure of 1,2-benzenedisulfonimide in

Methods and Compositions for Selectin Inhibition

The present teachings relate to novel compounds of formula I: wherein the constituent variables are as defined herein. Compounds of the present teachings can act as antagonists of the mammalian adhesion proteins known as selecting. Methods for treating or preventing selectin-mediated disorders are provided, which include administration of these compounds in a therapeutically effective amount.

Synthesis and biological evaluation of quinoline salicylic acids as P-selectin antagonists

Leukocyte recruitment of sites of inflammation and tissue injury involves leukocyte rolling along the endothelial wall, followed by firm adherence of the leukocyte, and finally transmigration of the leukocyte across cell junctions into the underlying tissue. The initial rolling step is mediated by the interaction of leukocyte glycoproteins containing active moieties such as sialyl Lewisx (sLex) with P-selectin expressed on endothelial cells. Consequently, inhibition of this interaction by means of a small molecule P-selectin antagonist is an attractive strategy for the treatment of inflammatory diseases such as arthritis. High-throughput screening of the Wyeth chemical library identified the quinoline salicylic acid class of compounds (1) as antagonists of P-selectin, with potency in in vitro and cell-based assays far superior to that of sLex. Through iterative medicinal chemistry, we identified analogues with improved P-selectin activity, decreased inhibition of dihydrooratate dehydrogenase, and acceptable CYP profiles. Lead compound 36 was efficacious in the rat AIA model of rheumatoid arthritis.

2-(4-Chlorobenzyl)-3-hydroxy-7,8,9,10-tetrahydrobenzo[H] quinoline-4-carboxylic acid (PSI-697): Identification of a clinical candidate from the quinoline salicylic acid series of P-selectin antagonists

P-selectin-PSGL-1 interaction causes rolling of leukocytes on the endothelial cell surface, which subsequently leads to firm adherence and leukocyte transmigration through the vessel wall into the surrounding tissues. P-selectin is upregulated on the surface of both platelets and endothelium in a variety of atherosclerosis-associated conditions. Consequently, inhibition of this interaction by means of a small molecule P-selectin antagonist is an attractive strategy for the treatment of atherosclerosis. High-throughput screening and subsequent analoging had led to the identification of compound 1 as the lead candidate. Herein, we report the continuation of this work and the discovery of a second-generation series, the tetrahydrobenzoquinoline salicylic acids. These compounds have improved pharmacokinetic properties, and a number of them have shown oral efficacy in mouse and rat models of atherogenesis and vascular injury. The lead 31 (PSI-697), is currently in clinical development for the treatment of atherothrombotic vascular events.

Methods and compositions for selectin inhibition

The present invention relates to the field of anti-inflammatory substances, and more particularly to novel compounds that act as antagonists of the mammalian adhesion proteins known as selectins. In some embodiments, methods for treating selectin mediated