2363-16-8

Usage

Chemical Properties

White crystalline powder

InChI:InChI=1/C8H6BrNO4/c1-14-8(11)5-2-3-6(9)7(4-5)10(12)13/h2-4H,1H3

Upstream product

• 619-42-1 4-methoxycarbonylphenyl bromide 
• 67-56-1 methanol 
• 335015-51-5 4-bromo-3-nitrobenzoyl chloride 
• 6319-40-0 4-bromo-3-nitrobenzoic acid 
• 586-75-4 4-chlorobenzoyl chloride 
• 186581-53-3 diazomethane 

Downstream Products

• 126759-36-2 methyl 4-ethenyl-3-nitrobenzoate 
• 82080-46-4 4-(methoxycarbonyl)-2-nitro-N,N-dimethylaniline 
• 925930-39-8 4'-fluoro-2-nitro-biphenyl-4-carboxylic acid methyl ester 
• 50820-65-0 indole-6-carboxylic acid methyl ester 
• 126759-44-2 2-<(4-methoxycarbonyl-2-nitrophenyl)methyl>-1,3-dioxane 

Relevant academic research and scientific papers

A 3D MOF showing unprecedented solvent-induced single-crystal-to-single-crystal transformation and excellent CO2 adsorption selectivity at room temperature

A water stable porous 3D metal-organic framework, [Cu3L2(μ3-OH)2(μ2-H2O)]·2DMA (1, mother crystal, H2L = 2,2′-dinitrobiphenyl-4,4′-dicarboxylic acid, DMA = N,N-dimethylacetamide), shows unprecedented irreversible solvent-induced substitutions of bridging aqua ligands and guest-exchanges in single-crystal-to-single-crystal (SCSC) transformations at room temperature (RT), producing quantitatively three daughter crystals, [Cu3L2(μ3-OH)2]·2S (2: 2A, S = acetone; 2B, S = 2-propanol; 2C, S = 2-butanol), which exhibit reversible interconversion by guest-exchanges at RT in SCSC transformations. MOF 1 shows excellent separation selectivity (128) of CO2/N2 at RT and is a better sorbent of micro-solid-phase extraction (μ-SPE) than currently known benchmark ZIF-8.

Creative Construction of a Series of Chiral 3D Indium-Organic Frameworks with a umy Topology

Using 2,2′-R2-biphenyl-4,4′-dicarboxylic acid to bind with a cis-[InO4(μ2-OH)2] octahedron, three novel chiral 3D indium-organic frameworks, [In(μ2-OH)L] [1, L1, R = N(CH3)2; 2, L2, R = OCH3; 3, L3, R = CH3], have been hydrothermally synthesized without chiral reagents. Crystal structure analyses reveal that 1-3 show an unprecedented 4-connected umy topology with the Schl?fli symbol (42·64). 1 exhibits high water stability and good sorption selectivity of CO2 over N2, while 3 displays high C2H2, C2H4, and C2H6 uptake capacity at 273 K.

Beta-carboboline GSK3beta/DYRK1A dual inhibitor and preparation method thereof and application of beta-carboboline GSK3beta/DYRK1A dual inhibitor in resisting Alzheimer's disease

The invention discloses a beta-carboline GSK3beta/DYRK1A dual inhibitor as shown in a general formula I, a preparation method of the beta-carboline GSK3beta/DYRK1A dual inhibitor and application of the beta-carboline GSK3beta/DYRK1A dual inhibitor in resi

Design, synthesis and biological evaluation of harmine derivatives as potent GSK-3β/DYRK1A dual inhibitors for the treatment of Alzheimer's disease

Alzheimer's disease (AD) is a chronic and progressive neurodegenerative disease, characterized by irreversible cognitive impairment, memory loss and behavioral disturbances, ultimately leading to death. Glycogen synthase kinase 3β (GSK-3β) and dual-specificity tyrosine phosphorylation regulated kinase1A (DYRK1A) have gained a lot of attention for its role in tau pathology. To search for potential dual GSK-3β/DYRK1A inhibitors, we focused on harmine, a natural β-carboline alkaloid, which has been extensively studied for its various biological effects on the prevention of AD. In this study, a new series of harmine derivatives were designed, synthesized and evaluated as dual GSK-3β/DYRK1A inhibitors for their multiple biological activities. The in vitro results indicated that most of them displayed promising activity against GSK-3β and DYRK1A. Among them, compound ZDWX-25 showed potent inhibitory effects on GSK-3β and DYRK1A with IC50 values of 71 and 103 nM, respectively. Molecular modelling and kinetic studies verified that ZDWX-25 could interact with the ATP binding pocket of GSK-3β and DYRK1A. Western blot analysis revealed that ZDWX-25 inhibited hyperphosphorylation of tau protein in okadaic acid (OKA)-induced SH-SY5Y cells. In addition, ZDWX-25 showed good blood-brain barrier penetrability in vitro. More importantly, ZDWX-25 could ameliorate the impaired learning and memory in APP/PS1/Tau transgenic mice. These results indicated that the harmine-based compounds could be served as promising dual-targeted candidates for AD.

Synthesis of multifunctional metal-organic frameworks and tuning the functionalities with pendant ligands

A series of multifunctional metal-organic frameworks (MOFs), SNU-170-SNU-176, has been synthesized using ligands, in which various functional pendants such as -NH2, -SMe, -OMe, -OEt, -OPr, and -OBu are attached to the phenyl ring of 4-(2-carboxyvinyl)benz

New Dual CK2/HDAC1 Inhibitors with Nanomolar Inhibitory Activity against Both Enzymes

Four potent CK2 inhibitors derived from CX-4945 are described. They also provided nanomolar activity against HDAC1, therefore having promising utility as dual-target agents for cancer. The linker length between the hydroxamic acid and the CX-4945 scaffold plays an important role in dictating balanced activity against the targeted enzymes. The seven-carbon linker (compound 15c) was optimal for inhibition of both CK2 and HDAC1. Remarkably, 15c showed 3.0 and 3.5 times higher inhibitory activity than the reference compounds CX-4945 (against CK2) and SAHA (against HDAC1), respectively. Compound 15c exhibited micromolar activity in cell-based cytotoxic assays against multiple cell lines.

Design and Synthesis of N1-Modified Imidazoquinoline Agonists for Selective Activation of Toll-like Receptors 7 and 8

A series of N1-modified imidazoquinolines were synthesized and screened for Toll-like receptors (TLR) 7 and 8 activities to identify recognition elements that confer high affinity binding and selectivity. These receptors are key targets in the development of immunomodulatory agents that signal the NF-κB mediated transcription of pro-inflammatory chemokines and cytokines. Results are presented showing both TLR7/8 activations are highly correlated to N1-substitution, with TLR8 selectivity achieved through inclusion of an ethyl-, propyl-, or butylamino group at this position. While the structure-activity relationship analysis indicates TLR7 activity is less sensitive to N1-modification, extension of the aminoalkyl chain length to pentyl and p-methylbenzyl elicited high affinity TLR7 binding. Cytokine profiles are also reported that show the pure TLR8 agonist [4-amino-2-butyl-1-(2-aminoethyl)-7-methoxycarbonyl-1H-imidazo[4,5-c]quinoline] induces higher levels of IL-1β, IL-12, and IFNγ when compared with TLR7 selective or mixed TLR7/8 agonists. The results are consistent with previous work suggesting TLR8 agonists are Th1 polarizing and may help promote cell-mediated immunity.

TrkA KINASE INHIBITORS, COMPOSITIONS AND METHODS THEREOF

The present invention is directed to bicyclic heteroaryl benzamide compounds of formulas (I) which are tropomyosin-related kinase (Trk) family protein kinase inhibitors, and hence are useful in the treatment of pain, inflammation, cancer, restenosis, atherosclerosis, psoriasis, thrombosis, a disease, disorder, injury, or malfunction relating to dysmyelination or demyelination or a disease or disorder associated with abnormal activities of nerve growth factor (NGF) receptor TrkA.

FUSED TETRA OR PENTA-CYCLIC PYRIDOPHTHALAZINONES AS PARP INHIBITORS

Provided are certain fused tetra or penta-cyclic compounds and salts thereof, compositions thereof, and methods of use thereof.

TrkA KINASE INHIBITORS,COMPOSITIONS AND METHODS THEREOF

The present invention is directed to substituted five membered heteroaryl benzamide compounds compounds of formula (I), which are tropomyosin-related kinase (Trk) family protein kinase inhibitors, and hence are useful in the treatment of pain, inflammation, cancer, restenosis, atherosclerosis, psoriasis, thrombosis, a disease, disorder, injury, or malfunction relating to dysmyelination or demyelination or a disease or disorder associated with abnormal activities of nerve growth factor (NGF) receptor TrkA.