797784-29-3

Basic information

• Product Name: 2-(3,5-DIFLUOROPHENYL)ACETOHYDRAZIDE
• Synonyms: 2-(3,5-DIFLUOROPHENYL)ACETIC ACID HYDRAZIDE;2-(3,5-DIFLUOROPHENYL)ACETOHYDRAZIDE
• CAS NO: 797784-29-3
• Molecular Formula: C₈H₈F₂N₂O
• Molecular Weight: 186.16
• Mol File: 797784-29-3.mol
• Article Data: 6

Chemical Properties

• Boiling Point: 347.2 °C at 760 mmHg
• Flash Point: 163.8 °C
• Appearance: /
• Density: 1.327 g/cm³
• Vapor Pressure: 5.48E-05mmHg at 25°C
• Refractive Index: 1.524
• Storage Temp.: 2-8°C
• CAS DataBase Reference: 2-(3,5-DIFLUOROPHENYL)ACETOHYDRAZIDE(CAS DataBase Reference)
• NIST Chemistry Reference: 2-(3,5-DIFLUOROPHENYL)ACETOHYDRAZIDE(797784-29-3)
• EPA Substance Registry System: 2-(3,5-DIFLUOROPHENYL)ACETOHYDRAZIDE(797784-29-3)

Safety Data

• Hazardous Substances Data: 797784-29-3(Hazardous Substances Data)

Usage

General Description

2-(3,5-Difluorophenyl)acetohydrazide, also known as 2-(3,5-Difluorophenyl)hydrazinecarboxamide, is a chemical compound with the molecular formula C8H8F2N2O. It is a hydrazide derivative of 3,5-difluorophenylacetic acid and is commonly used in the synthesis of various pharmaceutical compounds. It is a white to off-white powder with a melting point of 165-167°C and is soluble in organic solvents such as dimethylformamide and chloroform. Its potential uses include its antimicrobial properties and potential applications in pharmaceutical research.

InChI:InChI=1/C8H8F2N2O/c9-6-1-5(2-7(10)4-6)3-8(13)12-11/h1-2,4H,3,11H2,(H,12,13)

Upstream product

• 105184-38-1 3,5-difluorophenyl acetic acid 
• 210530-70-4 methyl 2-(3,5-difluorophenyl)acetate 
• 139368-37-9 ethyl 2-(3,5-difluorophenyl)acetate 

Relevant articles and documents

Synthesis and structure-activity relationships of 3,4,5-trisubstituted-1,2,4-triazoles: High affinity and selective somatostatin receptor-4 agonists for Alzheimer's disease treatment

Somatostatin receptor-4 (SST4) is highly expressed in brain regions affiliated with learning and memory. SST4 agonist treatment may act to mitigate Alzheimer's disease (AD) pathology. An integrated approach to SST4 agonist lead optimization is presented herein. High affinity and selective agonists with biological efficacy were identified through iterative cycles of a structure-based design strategy encompassing computational methods, chemistry, and preclinical pharmacology. 1,2,4-Triazole derivatives of our previously reported hit (4) showed enhanced SST4 binding affinity, activity, and selectivity. Thirty-five compounds showed low nanomolar range SST4 binding affinity, 12 having a Ki 500-fold affinity for SST4 as compared to SST2A. SST4 activities were consistent with the respective SST4 binding affinities (EC50 600-fold selectivity over SST2A) display a favorable physiochemical profile, and was advanced to learning and memory behavior evaluations in the senescence accelerated mouse-prone 8 model of AD-related cognitive decline. Chronic administration enhanced learning with i.p. dosing (1 mg kg-1) compared to vehicle. Chronic administration enhanced memory with both i.p. (0.01, 0.1, 1 mg kg-1) and oral (0.01, 10 mg kg-1) dosing compared to vehicle. This study identified a novel series of SST4 agonists with high affinity, selectivity, and biological activity that may be useful in the treatment of AD. This journal is

MrgprX2 ANTAGONISTS AND USES THEREOF

The present disclosure is directed to use of MrgprX2 antagonists in the treatment of inflammatory disorders, e.g., inflammatory disorders of the skin. This invention is also directed to pharmaceutical compositions comprising a MrgprX2 antagonist and a pha

A novel serine racemase inhibitor suppresses neuronal over-activation in vivo

Serine racemase (SRR) is an enzyme that produces D-serine from L-serine. D-Serine acts as an endogenous coagonist of NMDA-type glutamate receptors (NMDARs), which regulate many physiological functions. Over-activation of NMDARs induces excitotoxicity, which is observed in many neurodegenerative disorders and epilepsy states. In our previous works on the generation of SRR gene knockout (Srr-KO) mice and its protective effects against NMDA- and Aβ peptide-induced neurodegeneration, we hypothesized that the regulation of NMDARs’ over-activation by inhibition of SRR activity is one such therapeutic strategy to combat these disease states. In the previous study, we performed in silico screening to identify four compounds with inhibitory activities against recombinant SRR. Here, we synthesized 21 derivatives of candidate 1, one of four hit compounds, and performed screening by in vitro evaluations. The derivative 13J showed a significantly lower IC50 value in vitro, and suppressed neuronal over-activation in vivo.