144729-44-2

Usage

Physical state

Pale yellow solid

Uses

Production of dyes, pigments, and pharmaceuticals

Toxicity

Known to be toxic if swallowed, inhaled, or in contact with skin

Respiratory system

Can cause irritation to the respiratory system

Skin contact

Can cause skin irritation

Environmental impact

Potential environmental contaminant due to harmful effects on aquatic organisms

Health effects

Exposure may lead to methemoglobinemia, a condition that interferes with the body's ability to transport oxygen in the blood

Safety precautions

Proper handling and protective measures should be followed when working with 4-Chloro-3-nitroaniline

Upstream product

• 20718-46-1 5-chloro-4-nitro-2,1,3-benzoselenadiazole 
• 95-83-0 4-Chloro-1,2-phenylenediamine 
• 89-63-4 4-Chloro-2-nitroaniline 
• 1635-61-6 5-chloro-2-nitroaniline 
• 1123-92-8 5-chloro-benzo[1,2,5]selenadiazole 

Downstream Products

• 1422955-36-9 C₁₃H₉ClFN₅O₂ 
• 1422955-34-7 C₁₃H₈ClFN₄O₂ 
• 32046-86-9 5-chloro-4-nitro-1⁽³⁾H-benzoimidazole 
• 862179-95-1 N-(1-acetyl-5-chloro-2-phenylsulfanyl-1H-benzoimidazol-4-yl)-acetamide 
• 862179-91-7 5-chloro-4-nitro-2-phenylsulfanyl-1H-benzoimidazole 
• 862179-93-9 5-chloro-2-phenylsulfanyl-1H-benzoimidazol-4-ylamine 
• 150536-36-0 6-chloro-5-nitro-2,3-diphenylquinoxaline 

Relevant academic research and scientific papers

INHIBITION OF HIF-2α HETERODIMERIZATION WITH HIF1β (ARNT)

Provided is a method of inhibiting heterodimerization of HIF-2α to HIF1β (ARNT) comprising binding certain small molecules to the HIF-2α PAS-B domain cavity but not to HIF1α and inhibiting HIF-2α heterodimerization to HIF1β (ARNT) but not inhibiting HIF1α

Development of inhibitors of the PAS-B domain of the HIF-2α transcription factor

Hypoxia inducible factors (HIFs) are heterodimeric transcription factors induced in a variety of pathophysiological settings, including cancer. We describe the first detailed structure-activity relationship study of small molecules designed to inhibit HIF-2α-ARNT heterodimerization by binding an internal cavity of the HIF-2α PAS-B domain. Through a series of biophysical characterizations of inhibitor-protein interactions (NMR and X-ray crystallography), we have established the structural requirements for artificial inhibitors of the HIF-2α-ARNT PAS-B interaction. These results may serve as a foundation for discovering therapeutic agents that function by a novel mode of action.

INDOLYLMALEIMIDE DERIVATIVES

A compound of formula (I) wherein R, R1, and R2, ring A and ring B are as defined in the specification, processes for their production, their uses, in particular in transplantation, and pharmaceutical compositions containing them.

SPIROLACTAM TRICYCLIC CGRP RECEPTOR ANTAGONISTS

Compounds of formula (I): (wherein variables A1, A2, A3, A4, A5, A6, A7, B1, B2, B3, B4, D1, D2, E1, E2, E3, E4, E5, G1, G2, J, K, T, U, V, W, X, Y and Z are as described herein) which are antagonists of CGRP receptors and which are useful in the treatment or prevention of diseases in which the CGRP is involved, such as migraine. The invention is also directed to pharmaceutical compositions comprising these compounds and the use of these compounds and compositions in the prevention or treatment of such diseases in which CGRP is involved.

TRICYCLIC ANILIDE SPIROHYDANTOIN CGRP RECEPTOR ANTAGONISTS

The present invention is directed to compounds of Formula I: I (where A1, A2, B1, B2, B3, B4, D1, D2, T, U, V, W, X, Y, Z, R4, R5a?, R5b/su

TRICYCLIC ANILIDE SPIROLACTAM CGRP RECEPTOR ANTAGONISTS

The present invention is directed to compounds of Formula I: I (where A1, A2, B1, B2, B3, B4, D1, D2, J, K, T, U, V, W, X, Y, Z, R4, R5a, R5b, R5c, m and n are defined herein) useful as antagonists of CGRP receptors and useful in the treatment or prevention of diseases in which the CGRP is involved, such as headache, migraine and cluster headache. The invention is also directed to pharmaceutical compositions comprising these compounds and the use of these compounds and compositions in the prevention or treatment of such diseases in which CGRP is involved.

Synthesis of benzimidazole based JNK inhibitors

Substituted benzimidazoles were synthesised using a number of novel reactions, including displacement of a 2-sulfone group, preparation of 4-diazo benzimidazole derivatives and lithiation of benzimidazoles in the 4-position.

Phototransformations of 6-X-5-nitroquinoxalines

Photophysical properties and photochemical activity of 6-X-5- nitroquinoxalines with electron-donor substituents (X = H, CH3, Cl, OC2H5, NH2) ortho to the nitro group were studied. The quantum yield of the formation of 5-hydroxyquinoxaline from the corresponding nitro derivative depends on the nature of the substituent and irradiation conditions. Phototransformations can go through nitro-nitrite rearrangement with the participation of two alternative T(nπ*) levels, depending on the size and electronic effects of the substituent. The latter factor is largely determined by the population on excitation of different charge-transfer states involving the nitro group.

Regiospecific Oxidative Nitration of 3,4-Dihydro-6,7-disubstituted Quinoxalin-2(1H)-ones Gives 1,4-Dihydro-5-nitro-6,7-disubstituted Quinoxaline-2,3-diones, Potent Antagonists at the NMDA/Glycine Site

The regiospecific oxidative nitration of 3,4-dihydro-6,7-disubstituted quinoxalin-2(1H)-ones (15a-h, 20) utilizing fuming nitric acid in TFA gave 1,4-dihydro-5-nitro-6,7-disubstituted quinoxaline-2,3-diones (6a-i), respectively, in good yields.Compounds 15a-h were prepared from commercially available 1-halo-3,4-disubstituted benzenes 12a-h in three steps.These were nitration, nucleophilic substitution of the halogen ortho to the nitro group with sodium glycinate, and finally, reduction of the nitro group and concomitant cyclization.Compound 20 was prepared from 16 by a different route involving alkylation of substituted o-nitroaniline 18.The final oxidative nitration yields a single, predictable nitro isomer and is a significant improvement over the direct nitration of 6,7-disubstituted quinoxaline-2,3-diones.

Synthesis and structure-activity relationships of substituted 1,4- dihydroquinoxaline-2,3-diones: Antagonists of N-methyl-D-aspartate (NMDA) receptor glycine sites and non-NMDA glutamate receptors

A series of mono-, di-, tri-, and tetrasubstituted 1,4- dihydroquinoxaline-2,3-diones (QXs) were synthesized and evaluated as antagonists at N-methyl-D-aspartate (NMDA)/glycine sites and α-amino-3- hydroxy-5-methylisoxazole-4-propionic acid-preferring non-NMDA receptors. Antagonist potencies were measured by electrical assays in Xenopus oocytes expressing rat whole brain poly(A)+ RNA. Trisubstituted QXs 17a (ACEA 1021), 17b (ACEA 1031), 24a, and 27, containing a nitro group in the 5 position and halogen in the 6 and 7 positions, displayed high potency (K(b) ~ 6-8 nM) at the glycine site, moderate potency at non-NMDA receptors (K(b) = 0.9-1.5 μM), and the highest (120-250-fold) selectivity in favor of glycine site antagonism over non-NMDA receptors. Tetrasubstituted QXs 17d,e were more than 100-fold weaker glycine site antagonists than the corresponding trisubstituted QXs with F being better tolerated than Cl as a substituent at the 8 position. Di- and monosubstituted QXs showed progressively weaker antagonism compared to trisubstituted analogues. For example, removal of the 5-nitro group of 17a results in a ~100-fold decrease in potency (10a,b,z), while removal of both halogens from 17a results in a ~3000-fold decrease in potency (10v). In terms of steady-state inhibition, most QX substitution patterns favor antagonism at NMDA/glycine sites over antagonism at non-NMDA receptors. Among the QXs tested, only 17i was slightly selective for non- NMDA receptors.