603-23-6

Basic information

• Product Name: 3-PHENYL-2,4(1H,3H)-QUINAZOLINEDIONE
• Synonyms: 3-PHENYL-2,4(1H,3H)-QUINAZOLINEDIONE;3-phenylquinazoline-2,4(1h,3h)-dione;2,4(1H,3H)-Quinazolinedione, 3-phenyl-;3-Phenyl-1H,3H-quinazoline-2,4-dione;3-Phenyl-1,2,3,4-tetrahydroquinazoline-2,4-dione;3-Phenylbenzoyleneurea;3-phenyl-1H-quinazoline-2,4-dione;3-phenyl-1H-quinazoline-2,4-quinone
• CAS NO: 603-23-6
• Molecular Formula: C₁₄H₁₀N₂O₂
• Molecular Weight: 238.2414
• Mol File: 603-23-6.mol
• Article Data: 47

Chemical Properties

• Melting Point: 281-283°C
• Boiling Point: 447.6°C at 760 mmHg
• Flash Point: 224.5°C
• Appearance: /
• Density: 1.319g/cm³
• Vapor Pressure: 8.51E-09mmHg at 25°C
• Refractive Index: 1.644
• CAS DataBase Reference: 3-PHENYL-2,4(1H,3H)-QUINAZOLINEDIONE(CAS DataBase Reference)
• NIST Chemistry Reference: 3-PHENYL-2,4(1H,3H)-QUINAZOLINEDIONE(603-23-6)
• EPA Substance Registry System: 3-PHENYL-2,4(1H,3H)-QUINAZOLINEDIONE(603-23-6)

Safety Data

• Hazard Codes: Xi
• HazardClass: IRRITANT
• Hazardous Substances Data: 603-23-6(Hazardous Substances Data)

Usage

Synthesis Reference(s)

Journal of the American Chemical Society, 79, p. 4405, 1957 DOI: 10.1021/ja01573a044Tetrahedron Letters, 6, p. 2597, 1965 DOI: 10.1016/S0040-4039(00)90214-4Synthetic Communications, 21, p. 285, 1991 DOI: 10.1080/00397919108020823

InChI:InChI=1/C14H10N2O2/c17-13-11-8-4-5-9-12(11)15-14(18)16(13)10-6-2-1-3-7-10/h1-9H,(H,15,18)

Upstream product

• 3391-37-5 o-Phenylureidobenzanilide 
• 2164-95-6 N-phenyl-N'-(2-carboxyphenyl)-urea 
• 94775-14-1 1,2-bis<2-(3-phenylureido)benzoyl>hydrazine 
• 3422-01-3 tert-butyl phenylcarbamate 
• 103-71-9 phenyl isocyanate 
• 79873-99-7 2-(3-Methyl-3-phenyl-ureido)-N-phenyl-benzamide 
• 57-13-6 urea 
• 4424-17-3 2-aminobenzanilide 
• 7446-70-0 aluminium trichloride 
• 95-50-1 1,2-dichloro-benzene 
• 17082-12-1 trans-azobenzene 
• 71-43-2 benzene 
• 124-38-9 carbon dioxide 
• 62-53-3 aniline 

Downstream Products

• 128650-95-3 ethyl-2-(3-phenyl-2,4-dioxo-3,4-dihydroquinazolin-1(2H)-yl)acetate 
• 106550-73-6 ethyl 3-phenyl-4(3H)-oxo-2-quinazolinoxyacetate 
• 106550-76-9 2-(2'-bromoethoxy)-3-phenylquinazolin-4(3H)-one 
• 106550-78-1 2-allyloxy-3-phenylquinazolin-4(3H)-one 
• 106550-74-7 2-phenacyloxy-3-phenylquinazolin-4(3H)-one 
• 106550-75-8 2-(p-bromophenacyloxy)-3-phenylquinazolin-4(3H)-one 
• 106550-77-0 2-acetylmethoxy-3-phenylquinazolin-4(3H)-one 
• 727-62-8 2-chloro-3-phenylquinazoline-4-(3H)-one 
• 62-53-3 aniline 
• 1904-58-1 anthranilic acid hydrazide 
• 221540-10-9 1-(4-bromobutyl)-2,4-dioxo-3-phenyl-1,2,3,4-tetrahydroquinazoline 
• 1562346-95-5 2-(6-methyl-5-oxo-3-thioxo-2,5-dihydro-3H-[1,2,4]triazin-4-ylimino)-3-phenyl-2,3-dihydro-1H-quinazoline-4-one 
• 18741-24-7 3-phenyl-2-thioxo-2,3-dihydro-1H-quinazolin-4-one 

Relevant articles and documents

Design, synthesis, biological evaluation, and molecular docking study of thioxo-2,3-dihydroquinazolinone derivative as tyrosinase inhibitors

Tyrosinase is known to be a key enzyme in melanogenesis and hyperpigmentation. In this study, a series of thioxo-dihydroquinazolinone compounds were designed and synthesized as tyrosinase inhibitors. Among the investigated compounds, 4m demonstrated the best inhibitory activity with an IC50 value of 15.48 μM compared to kojic acid as a positive control with IC50 value of 9.30 μM. In kinetic evaluation against tyrosinase, 4m depicted a mixed inhibition pattern. Additionally, antioxidant evaluations exhibited moderate to weak potency in 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay. The detailed interactions and binding mode toward tyrosinase of the most potent derivative were explicated by molecular docking study. Moreover, the computer-aided drug-likeness and pharmacokinetic studies were also carried out.

Synthesis, biological evaluation and molecular docking of 3-substituted quinazoline-2,4(1H, 3H)-diones

Abstract: The quinazoline-2,4-diones scaffold is found in bioactive compounds, commercial drugs and exhibit important biological activities. However, their antidiabetic activity is rarely explored. For this purpose, an easy one-pot three-components and straightforward synthesis of 3-substituted quinazoline-2,4-diones was designed, in both, the catalyst- and solvent-free conditions under microwave irradiation. Additionally, the synthesized compounds were screened for in vitro α-amylase and α-glucosidase inhibitory activity, as well as antioxidants and cytotoxicity. The quinazoline-2,4-diones were isolated, with yields in the range of 30-65percent. The compounds 3d, 3e, 3g and 3h displayed moderate activity against α-amylase and/or α-glucosidase enzymes compared with the acarbose drug. The molecular docking study revealed that all active compounds displayed a different type of intermolecular interaction in the pocked site of these enzymes. Interestingly, in the Artemia salina assay, the compound 3d exhibited a higher cytotoxic effect than 5-fluorouracil. All these results support the pharmacological potential of quinazoline-2,4-diones since all evaluated compounds behave as moderate inhibitors of the enzymes α-amylase and/or α-glucosidase. Graphic abstract: An easy one-pot three-components and straightforward synthesis of 3-substituted quinazoline-2,4-diones was designed, in both, the catalyst- and solvent-free conditions under microwave irradiation. Moreover, the in vitro α-amylase and α-glucosidase inhibitory activity, as well as antioxidants and cytotoxicity are reported.[Figure not available: see fulltext.]

High-selective HDAC6 inhibitor promotes HDAC6 degradation following autophagy modulation and enhanced antitumor immunity in glioblastoma

Glioblastoma is the most fatal type of primary brain cancer, and current treatments for glioblastoma are insufficient. HDAC6 is overexpressed in glioblastoma, and siRNA-mediated knockdown of HDAC6 inhibits glioma cell proliferation. Herein, we report a high-selective HDAC6 inhibitor, J22352, which has PROTAC (proteolysis-targeting chimeras)-like property resulted in both p62 accumulation and proteasomal degradation, leading to proteolysis of aberrantly overexpressed HDAC6 in glioblastoma. The consequences of decreased HDAC6 expression in response to J22352 decreased cell migration, increased autophagic cancer cell death and significant tumor growth inhibition. Notably, J22352 reduced the immunosuppressive activity of PD-L1, leading to the restoration of host anti-tumor activity. These results demonstrate that J22352 promotes HDAC6 degradation and induces anticancer effects by inhibiting autophagy and eliciting the antitumor immune response in glioblastoma. Therefore, this highly selective HDAC6 inhibitor can be considered a potential therapeutic for the treatment of glioblastoma and other cancers.