95192-64-6

Usage

Uses

Used in Pharmaceutical Industry:
5-BROMO-2-METHYL-1,3-DINITROBENZENE is used as a synthetic intermediate for the production of various pharmaceuticals, leveraging its reactivity in chemical reactions to form complex organic molecules with therapeutic properties.
Used in Dye Industry:
In the dye industry, 5-BROMO-2-METHYL-1,3-DINITROBENZENE is utilized as a precursor in the synthesis of dyes, contributing to the development of colorants for various applications, such as textiles and printing inks.
Used in Chemical Research:
5-BROMO-2-METHYL-1,3-DINITROBENZENE serves as a valuable compound in chemical research, where its reactivity is exploited to study and develop new reaction pathways and mechanisms, furthering the understanding of organic chemistry.

InChI:InChI=1/C7H5BrN2O4/c1-4-6(9(11)12)2-5(8)3-7(4)10(13)14/h2-3H,1H3

Upstream product

• 16533-71-4 3,5-dinitro-p-toluic acid 
• 527-84-4 2-methylisopropylbenzene 
• 606-20-2 2,6-dinitrotoluene 
• 60956-26-5 4-bromo-2-nitrotoluene 
• 858843-71-7 2-bromo-4-methyl-3,5-dinitro-aniline 
• 101580-70-5 4,5-dibromo-2-nitro-toluene 
• 854403-39-7 1,2-dibromo-4-isopropyl-5-methyl-benzene 
• 101421-17-4 3,4-dibromo-2,6-dinitro-toluene 
• 100959-47-5 6-bromo-3-methyl-2,4-dinitro-aniline 
• 19406-51-0 4-Amino-2,6-dinitrotoluene 

Downstream Products

• 16533-71-4 3,5-dinitro-p-toluic acid 
• 95192-56-6 4-bromo-2,6-dinitrobenzoic acid 
• 1079039-13-6 C₇H₄BrClN₂O₄ 
• 864550-41-4 5-bromo-2-methyl-3-nitrophenol 
• 885519-07-3 5-bromo-1-methoxy-2-methyl-3-nitrobenzene 
• 393553-57-6 6-bromo-4-methoxyindole 
• 1198438-39-9 6-bromo-1-methyl-1H-indazol-4-amine 

Relevant academic research and scientific papers

X-ray Structure-Guided Discovery of a Potent, Orally Bioavailable, Dual Human Indoleamine/Tryptophan 2,3-Dioxygenase (hIDO/hTDO) Inhibitor That Shows Activity in a Mouse Model of Parkinson’s Disease

Human indoleamine 2,3-dioxygenase 1 (hIDO1) and tryptophan 2,3-dioxygenase (hTDO) have been closely linked to the pathogenesis of Parkinson’s disease (PD); nevertheless, development of dual hIDO1 and hTDO inhibitors to evaluate their potential efficacy against PD is still lacking. Here, we report biochemical, biophysical, and computational analyses revealing that 1H-indazole-4-amines inhibit both hIDO1 and hTDO by a mechanism involving direct coordination with the heme ferrous and ferric states. Crystal structure-guided optimization led to23, which manifested IC50values of 0.64 and 0.04 μM to hIDO1 and hTDO, respectively, and had good pharmacokinetic properties and brain penetration in mice.23showed efficacy against the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse motor coordination deficits, comparable to Madopar, an anti-PD medicine. Further studies revealed that different from Madopar,23likely has specific anti-PD mechanisms involving lowering IDO1 expression, alleviating dopaminergic neurodegeneration, reducing inflammatory cytokines and quinolinic acid in mouse brain, and increasing kynurenic acid in mouse blood.

4,6-Substituted-1H-Indazoles as potent IDO1/TDO dual inhibitors

Indoleamine 2,3-dioxygenase 1 (IDO1) and tryptophan 2,3-dioxygenase (TDO) are constitutively overexpressed in many types of cancer cells and exert important immunosuppressive functions. In this article, a series of 4,6-substituted-1H-indazole derivatives were synthesized and evaluated the inhibitory activities against IDO1 and TDO, as well as their structure-activity relationships (SARs). Among these, compound 35 displayed the most IDO1 inhibitory potency with an IC50 value of 0.74 μM in an enzymatic assay and 1.37 μM in HeLa cells. Quantitative analysis of the Western blot results indicated that 35 significantly decreased the INFγ-induced IDO1 expression in a concentration-dependent manner. In addition, 35 showed promising TDO inhibition with an IC50 value of 2.93 μM in the enzymatic assay and 7.54 μM in A172 cells. Moreover, compound 35 exhibited in vivo antitumor activity in the CT26 xenograft model. These findings suggest that 1H-indazole derivative 35 is a potent IDO1/TDO dual inhibitor, and has the potential to be developed for IDO1/TDO-related cancer treatment.

Method for preparing 1H-indazole derivative

The invention discloses a method for preparing a 1H-indazole derivative. The method takes a compound as a formula (A1) or a compound as a formula (A2) as raw materials, and the compound as the formula(A1) and the compound as the formula (A2) are subjected

Indazole compounds and application thereof to preparation of IDO inhibitors

The invention discloses indazole compounds as shown in a formula (i) or (II) which is described in the specification, and a preparation method thereof, and application of the compounds as IDO inhibitors. The compounds provided by the invention can be used for preventing and/or treating a plurality of diseases, such as Alzheimer's disease, cataract, infections related to cellular immune activation,autoimmune diseases, AIDS, cancers, depression, the metabolic disorder of tryptophan or the like.

Polysubstituted-indazole compounds and application of same as IDO inhibitors

The invention discloses polysubstituted-indazole compounds as shown in a formula (I) which is described in the specification, a preparation method for the compounds, and application of the compounds as IDO inhibitors. The compounds provided by the invention can be used for preventing and/or treating a plurality of diseases, such as Alzheimer's disease, cataract, infections related to cellular immune activation, autoimmune diseases, AIDS, cancers, depression, the metabolic disorder of tryptophan or the like.

A Concise Total Synthesis of Breitfussin A and B

(Chemical Equation Presented). The first total synthesis of breitfussin A and B is described. The approach features two palladium-catalyzed cross-couplings installing the indole and pyrrole onto the oxazole core and selective lithiation/iodination of a common indole-oxazole fragment providing 2,4-diiodinated or 2-iodinated oxazoles as potential precursors for breitfussin A and B, respectively. An unexpected acid promoted deiodination was utilized in the synthesis of breitfussin B. Comparison of the synthetic material with previously reported spectral data of isolated breitfussin A and B verified the structure of the breitfussin framework.

INHIBITORS OF KRAS G12C

Compounds having activity as inhibitors of G12C mutant KRAS protein are provided. The compounds have the following structure (I): or a pharmaceutically acceptable salt, tautomer, prodrug or stereoisomer thereof, wherein R1, R2a, R3a, R3b, R4a, R4b, G1, G2, L1, L2, m1, m2, A, B, W, X, Y, Z and E are as defined herein. Methods associated with preparation and use of such compounds, pharmaceutical compositions comprising such compounds and methods to modulate the activity of G12C mutant KRAS protein for treatment of disorders, such as cancer, are also provided.

Substituted 2-nitrobenzyltrichloroacetate esters for photodirected oligonucleotide detritylation in solid films

Oligonucleotide microarray fabrication by chemical synthesis using photoacid generators in solid films could have advantages over existing methods, but has not matched the accuracy of conventional synthesis where detritylation is performed with acid solut

Pyranouidole Derivatives and the Use Thereof for the Treatment of Hepatitis C Virus Infection or Disease

The invention is directed to novel pyranoindole derivatives and analogs as well as compositions containing the same and to the use thereof for the treatment, prevention or inhibition of viral infections and associated diseases caused by the Hepatitis C vi

5-HT6 receptor antagonists: lead optimisation and biological evaluation of N-aryl and N-heteroaryl 4-amino-benzene sulfonamides

RO-04-6790 (6a) has been identified in a random screen for 5-HT6 receptor antagonists. In a medicinal chemistry optimisation program a series of analogs comprising N-heteroaryl- and N-arylbenzenesulfonamides have been synthesised and investigated for their binding affinity. Compounds with a log D profile indicative of brain penetration have been subjected to in vivo testing for reversal of a scopolamine-induced retention deficit in a passive avoidance paradigm.