76746-19-5

Usage

Chemical compound

2-amino-5-fluoro-benzohydrazide

Structure

Consists of a benzene ring with a fluorine atom at the 5th position and an amino group at the 2nd position

Common use

Reagent in organic synthesis to form hydrazones

Importance

Hydrazones are important intermediates in the production of pharmaceuticals and agrochemicals

Potential biological activities

Investigated for antimicrobial and antiviral properties

Potential application

Studied as a corrosion inhibitor for metals

Versatility

A versatile and multifunctional chemical compound with various potential applications in different fields

Upstream product

• 321-69-7 5-fluoroisatoic anhydride 
• 446-08-2 2-amino-5-fluorobenzoic acid 
• 319-24-4 2-amino-5-fluoro-benzoic acid methyl ester 

Downstream Products

• 1403672-16-1 2-(9-fluoro-2-pyridin-2-yl-5,6-dihydro[1,5-c]quinazolin-5-yl)phenol 
• 1403672-20-7 C₁₃H₁₀FN₅ 

Relevant academic research and scientific papers

Discovery of phthalazino[1,2-b]-quinazolinone derivatives as multi-target HDAC inhibitors for the treatment of hepatocellular carcinoma via activating the p53 signal pathway

In view of histone deacetylases (HDACs) as a promising target for cancer therapy, a series of phthalazino[1,2-b]-quinazolinone units were hybrided with ortho-aminoanilide or hydroxamic acid to serve as multi-target HDAC inhibitors for the treatment of solid tumors. Among the target compounds, 8h possessed nano-molar IC50 values toward the tested cancer cells and HDAC subtypes, which was more potent than the HDAC inhibitor SAHA (vorinostat). Mechanism study revealed that compound 8h could suppress the HepG2 cell proliferation via prompting the acetylation of histone 3 (H3) and α-tubulin, and activating the p53 signal pathway as designed. In addition, compound 8h exhibited much stronger in vivo antitumor efficacy than SAHA in the HepG2 xenograft tumor model with negligible toxicity. As a novel multi-target HDAC inhibitor, compound 8h deserves further development as a potential anticancer agent.

ARYL HYDROCARBON RECEPTOR (AHR) ACTIVATOR COMPOUNDS AS CANCER THERAPEUTICS

The present disclosure relates to compositions and methods for the diagnosis and treatment or prevention of cancers, particularly cancers that exhibit elevated expression of FOXA1 and/or FOXA1 gene targets, such as certain breast, liver and/or prostate cancers, including luminal and/or ER-positive forms of breast cancer. Three previously identified adenosine receptor antagonists, CGS-15943, MRS-1220 and SCH-58261, as well as furan ring moiety-possessing derivatives of CGS-15943 are specifically provided for killing cancer cells in a manner that appears to involve activation of the aryl hydrocarbon receptor (AHR) by such compounds. The instant disclosure therefore provides for selecting and/or administering CGS-15943, MRS-1220, SCH-58261 and/or a furan-possessing derivative of CGS-15943, MRS-1220 and/or SCH-58261 as a therapeutic agent to target a cancer cell and/or subject having or at risk of developing a cancer. Methods and compositions for therapies that include such compounds are also provided

Phthalazino[1,2-b]quinazolinones as p53 Activators: Cell Cycle Arrest, Apoptotic Response and Bak-Bcl-xl Complex Reorganization in Bladder Cancer Cells

p53 inactivation is a clinically defined characteristic for cancer treatment-nonresponsiveness. It is therefore highly desirable to develop anticancer agents by restoring p53 function.1 Herein the synthesized phthalazino[1,2-b]quinazolinones were discovered as p53 activators in bladder cancer cells. 10-Bromo-5-(2-dimethylamino-ethylamino)phthalazino[1,2-b]quinazolin-8-one (5da) was identified as the most promising candidate in view of both its anticancer activity and mechanisms of action. 5da exhibited strong anticancer activity on a broad range of cancer cell lines and significantly reduced tumor growth in xenograft models at doses as low as 6 mg/kg. Furthermore, 5da caused cell cycle arrest at S/G2 phase, induced apoptosis, changed cell size, and led to cell death by increasing the proportion of sub-G1 cells. Molecular mechanism studies suggested that accumulation of phospho-p53 in mitochondria after 5da treatment resulted in conformational activation of Bak, thereby evoking cell apoptosis, finally leading to irreversible cancer cell inhibition. Our present studies furnish new insights into the molecular interactions and anticancer mechanisms of phospho-p53-dependent quinazolinone compound.

Synthesis of diverse azolo[c]quinazolines by palladium(II)- catalyzed aerobic oxidative insertion of isocyanides

We report the palladium(II)-catalyzed aerobic oxidative coupling of isocyanides with various (2-aminophenyl)azoles using air as the stoichiometric oxidant. A diverse range of medicinally valuable azolo[c]quinazolines was obtained by this new approach.

A diversity oriented synthesis of 2,10-dioxo-10H-1,2,3,4,4a,5-hexahydropyridazino[3,2-b]quinazolines

A parallel method for the synthesis of the title compounds is described. Thus, methyl anthranilates (5) are transformed into 2-aminobenzohydrazides (3) which were treated with 4-oxo acids (4) to afford in high yields and acceptable purity of piridazino[3,2-b]quinazolines (1). Compounds (1) present four diversity centers (R1, R2, R3, and R4). The range of chemically acceptable substituents at each center has been evaluated. The isolation of a possible intermediate in the formation of 1, which presents an amino structure (10), has allowed proposing a complete mechanistic rationalization for the formation of structures (1).

Pyrazoloquinazolin-9-ones: A New Series of Antiallergic Agents

A new series of antiallergic agents, pyrazoloquinazolin-9-ones, was synthesized and evaluated for inhibitory effects in the rat reaginic passive cutaneous anaphylaxis (PCA) screen.Several analogues were found to be more potent than cromolyn sodium intravenously.Structure-activity relationships are discussed.One of the compounds, 4,9-dihydro-5-methoxy-9-oxopyrazoloquinazoline-2-carboxylic acid (36), was found to be approximately 250 times more potent than cromolyn sodium intravenously.