13675-94-0

Basic information

• Product Name: 4-CHLORO-6-NITROQUINOLINE
• Synonyms: 4-CHLORO-6-NITROQUINOLINE;NSC 146766
• CAS NO: 13675-94-0
• Molecular Formula: C₉H₅ClN₂O₂
• Molecular Weight: 208.6
• EINECS: -0
• Mol File: 13675-94-0.mol

Chemical Properties

• Melting Point: 142.5 °C
• Boiling Point: 351.397 °C at 760 mmHg
• Flash Point: 166.319 °C
• Appearance: /
• Density: 1.484
• Vapor Pressure: 8.35E-05mmHg at 25°C
• Refractive Index: 1.688
• Storage Temp.: under inert gas (nitrogen or Argon) at 2-8°C
• PKA: 1.82±0.16(Predicted)
• CAS DataBase Reference: 4-CHLORO-6-NITROQUINOLINE(CAS DataBase Reference)
• NIST Chemistry Reference: 4-CHLORO-6-NITROQUINOLINE(13675-94-0)
• EPA Substance Registry System: 4-CHLORO-6-NITROQUINOLINE(13675-94-0)

Safety Data

• Hazardous Substances Data: 13675-94-0(Hazardous Substances Data)

Usage

Uses

Used in Pharmaceutical Industry:
4-Chloro-6-nitroquinoline is used as a reactant for the preparation of arylaminoquinoline derivatives. These derivatives have been identified as potent inhibitors of the epidermal growth factor receptor (EGFR), which plays a crucial role in cell signaling and is often overexpressed in various types of cancer. By inhibiting EGFR, these derivatives can potentially help in the treatment of cancer and other diseases associated with abnormal cell growth.
Used in Chemical Synthesis:
In addition to its pharmaceutical applications, 4-chloro-6-nitroquinoline can also be utilized as an intermediate in the synthesis of various other organic compounds. Its unique structure and functional groups make it a valuable building block for the development of new molecules with diverse applications in different industries, such as agrochemicals, dyes, and materials science.

InChI:InChI=1/C9H5ClN2O2/c10-8-3-4-11-9-2-1-6(12(13)14)5-7(8)9/h1-5H

Upstream product

• 13675-92-8 6-nitroquinoline-N-oxide 
• 23432-42-0 4-hydroxy-6-nitro-quinoline 
• 21873-49-4 6-nitroquinoline-4(1H)-one 
• 529-37-3 4(1H)-quinolinone 
• 613-50-3 6-nitroquinoline 
• 611-36-9 quinolin-4-ol 
• 6943-17-5 6-nitroquinazolone 
• 100-01-6 4-nitro-aniline 
• 78596-42-6 ethyl α-ethoxycarbonyl-β-(4-nitroanilino)acrylate 
• 103514-53-0 ethyl 6-nitro-4-oxo-1,4-dihydroquinoline-3-carboxylate 
• 15568-92-0 5-(N-phenyl)-aminomethylene-2,2-dimethyl-1,3-dioxane-4,6-dione 

Downstream Products

• 124496-62-4 6-nitro-4-phenoxy-quinoline 
• 1085192-91-1 4-chloroquinolin-6-amine 
• 116632-55-4 6-nitro-[4]quinolylamine 
• 338797-21-0 4-((R)-3-Methyl-piperazin-1-yl)-6-nitro-quinoline 
• 658710-29-3 N-(6-nitroquinolin-4-yl)-N-[2-(N,N-dimethylamino)ethyl]-2-iodo-4,5-dimethoxybenzamide 
• 1020086-26-3 4-[4-({3-[(1-methyl-4-pyridiniumyl)amino]benzoyl}amino)anilino]-6-nitroquinolinium dichloride 
• 1163730-96-8 1-(3-tert-butyl-1-m-tolyl-1H-pyrazol-5-yl)-3-(4-(6-nitroquinolin-4-ylamino)phenyl)urea 
• 1163730-95-7 1-(3-tert-butyl-1-p-tolyl-1H-pyrazol-5-yl)-3-(3-(6-nitroquinolin-4-ylamino)phenyl)urea 
• 1219717-61-9 N-(3-bromophenyl)-6-nitroquinolin-4-amine 

Relevant articles and documents

Molecular Docking Studies and Synthesis of Amino-oxy-diarylquinoline Derivatives as Potent Non-nucleoside HIV-1 Reverse Transcriptase Inhibitors

In this study, amino-oxy-diarylquinolines were designed using structure-guided molecular hybridization strategy and fusing of the pharmacophore templates of nevirapine (NVP), efavirenz (EFV), etravirine (ETV, TMC125) and rilpivirine (RPV, TMC278). The anti-HIV-1 reverse transcriptase (RT) activity was evaluated using standard ELISA method, and the cytotoxic activity was performed using MTT and XTT assays. The primary bioassay results indicated that 2-amino-4-oxy-diarylquinolines possess moderate inhibitory properties against HIV-1 RT. Molecular docking results showed that 2-amino-4-oxy-diarylquinolines 8(a-d) interacted with the Lys101 and His235 residue though hydrogen bonding and interacted with Tyr318 residue though π-π stacking in HIV-1 RT. Furthermore, 8a and 8d were the most potent anti-HIV agents among the designed and synthesized compounds, and their inhibition rates were 34.0% and 39.7% at 1 μM concentration. Interestingly, 8a was highly cytotoxicity against MOLT-3 (acute lymphoblastic leukemia), with an IC 50 of 4.63±0.62 μg/mL, which was similar with that in EFV and TMC278 (IC 50 7.76±0.37 and 1.57±0.20 μg/ml, respectively). Therefore, these analogs of the synthesized compounds can serve as excellent bases for the development of new anti-HIV-1 agents in the near future.

A Selective and Orally Bioavailable Quinoline-6-Carbonitrile-Based Inhibitor of CDK8/19 Mediator Kinase with Tumor-Enriched Pharmacokinetics

Senexins are potent and selective quinazoline inhibitors of CDK8/19 Mediator kinases. To improve their potency and metabolic stability, quinoline-based derivatives were designed through a structure-guided strategy based on the simulated drug–target dockin

AKT3 MODULATORS

Compounds of Formula la, lb, or Ic, (Ia); (Ib); or (Ic), are described, where the various substituents are defined herein. The compounds can modulate a property or effect of Akt3 in vitro or in vivo, and can also be used, individually or in combination with other agents, in the prevention or treatment of a variety of conditions. Methods for synthesizing the compounds are described. Pharmaceutical compositions and methods of using these compounds or compositions, individually or in combination with other agents or compositions, in the prevention or treatment of a variety of conditions are also described.

AKT3 MODULATORS

Compounds of Formula la, lb, or Ic, are described, where the various substituents are defined herein. The compounds can modulate a property or effect of Akt3 in vitro or in vivo, and can also be used, individually or in combination with other agents, in the prevention or treatment of a variety of conditions. Methods for synthesizing the compounds are described. Pharmaceutical compositions and methods of using these compounds or compositions, individually or in combination with other agents or compositions, in the prevention or treatment of a variety of conditions are also described.

QUINOLINE-BASED COMPOUNDS AND METHODS OF INHIBITING CDK8/19

Disclosed herein are quinoline-based compounds and method for inhibiting CDK8 or CDK19 for the intervention in diseases, disorders, and conditions. The quinoline-based composition comprise substituents at quinoline ring positions 4 and 6, wherein the substituent at position 4 is selected from a substituted or unsubstituted arylalkylamine or a substituted or unsubstituted arylhetrocyclylamine. Pharmaceutical compositions comprising the substituted qunioline compositions, methods of inhibiting CDK8 or CDK19, and methods of treating CDK8/19-associated diseases, disorders, or conditions are also disclosed.

Visible-Light-Photocatalyzed Reductions of N-Heterocyclic Nitroaryls to Anilines Utilizing Ascorbic Acid Reductant

A photoreductive protocol utilizing [Ru(bpy)3]2+ photocatalyst, blue light LEDs, and ascorbic acid (AscH2) has been developed to reduce nitro N-heteroaryls to the corresponding anilines. Based on experimental and computational results and previous studies, we propose that the reaction proceeds via proton-coupled electron transfer between AscH2, photocatalyst, and the nitro N-heteroaryl. The method offers a green catalytic procedure to reduce, e.g., 4-/8-nitroquinolines to the corresponding aminoquinolines, substructures present in important antimalarial drugs.

2, 6-Di-Nitrogen-Containing Substituted Purine Derivative, And Preparation Method, Pharmaceutical Composition And Use Thereof

The present invention provides a 2, 6-di-nitrogen-containing substituted purine derivative having a formula (I) structure, or pharmaceutical salt or hydrate thereof, and preparation method and use thereof. The compound is broad spectrum anticancer, low to

Further studies on bis-charged tetraazacyclophanes as potent inhibitors of small conductance Ca2+-activated K+ channels

Previously, quinolinium-based tetraazacyclophanes, such as UCL 1684 and UCL 1848, have been shown to be extraordinarily sensitive to changes in chemical structure (especially to the size of the cyclophane system) with respect to activity as potent non-peptidic blockers of the small conductance Ca 2+-activated K+ ion channels (SKCa). The present work has sought to optimize the structure of the linking chains in UCL 1848. We report the synthesis and SKCa channel-blocking activity of 29 analogues of UCL 1848 in which the central CH2 of UCL 1848 is replaced by other groups X or Y = O, S, CF2, CO, CHOH, CC, CHCH, CHMe to explore whether subtle changes in bond length or flexibility can improve potency still further. The possibility of improving potency by introducing ring substituents has also been explored by synthesizing and testing 25 analogues of UCL 1684 and UCL 1848 with substituents (NO2, NH2, CF 3, F, Cl, CH3, OCH3, OCF3, OH) in the 5, 6 or 7 positions of the aminoquinolinium rings. As in our earlier work, each compound was assayed for inhibition of the afterhyperpolarization (AHP) in rat sympathetic neurons, an action mediated by the SK3 subtype of the SK Ca channel. One of the new compounds (39, R7 = Cl, UCL 2053) is twice as potent as UCL 1848 and UCL 1684: seven are comparable in activity.

Synthesis and biological evaluation of 4-anilinoquinolines as potent inhibitors of epidermal growth factor receptor

The mutant receptor tyrosine kinase EGFR is a validated and therapeutically amenable target for genotypically selected lung cancer patients. Here we present the synthesis and biological evaluation of a series of 6- and 7-substituted 4-anilinoquinolines as potent type I inhibitors of clinically relevant mutant variants of EGFR. Quinolines 3a and 3e were found to be highly active kinase inhibitors in biochemical assays and were further investigated for their biological effect on EGFR-dependent Ba/F3 cells and non-small cell lung cancer (NSCLC) cell lines.

Development of a fluorescent-tagged kinase assay system for the detection and characterization of allosteric kinase inhibitors

Kinase disregulation disrupts the intricate network of intracellular signaling pathways and contributes to the onset of diseases such as cancer. Although several kinase inhibitors are on the market, inhibitor selectivity and drug resistance mutations persist as fundamental challenges in the development of effective long-term treatments. Chemical entities binding to less conserved allosteric sites would be expected to offer new opportunities for scaffold development. Because no high-throughput method was previously available, we developed a fluorescence-based kinase binding assay for identifying and characterizing ligands which stabilize the inactive kinase conformation. Here, we present a description of the development and validation of this assay using the serine/threonine kinase p38R. By covalently attaching fluorophores to the activation loop of the kinase, we were able to detect conformational changes and measure the Kd, kon, and koff associated with the binding and dissociation of ligands to the allosteric pocket. We report the SAR of a synthesized focused library of pyrazolourea derivatives, a scaffold known to bind with high affinity to the allosteric pocket of p38R. Additionally, we used protein X-ray crystallography together with our assay to examine the binding and dissociation kinetics to characterize potent quinazoline- and quinoline-based type II inhibitors, which also utilize this binding pocket in p38α. Last, we identified the b-Raf inhibitor sorafenib as a potent low nanomolar inhibitor of p38α and used protein X-ray crystallography to confirm a unique binding mode to the inactive kinase conformation.