121845-92-9

Usage

Uses

Used in Organic Synthesis:
Benzoic acid, 2-[(2-nitroethylidene)amino](9CI) is used as a synthetic intermediate in the chemical industry for the preparation of various organic compounds. Its unique structure allows it to participate in a range of chemical reactions, making it a valuable building block for the synthesis of pharmaceuticals, agrochemicals, and other specialty chemicals.
Used in Pharmaceutical Industry:
In the pharmaceutical industry, Benzoic acid, 2-[(2-nitroethylidene)amino](9CI) is utilized as a key component in the development of new drugs. Its chemical properties enable it to form stable derivatives and complexes with other molecules, which can be further explored for their therapeutic potential.
Used in Agrochemical Industry:
Benzoic acid, 2-[(2-nitroethylidene)amino](9CI) also finds applications in the agrochemical industry, where it is employed as a precursor for the synthesis of various agrochemicals, such as pesticides and herbicides. Its ability to form stable compounds with other molecules makes it a promising candidate for the development of new and effective agrochemical products.

Synthesis Reference(s)

Journal of the American Chemical Society, 69, p. 365, 1947 DOI: 10.1021/ja01194a060

Upstream product

• 5653-21-4 metazonic acid 
• 118-92-3 anthranilic acid 
• 99584-53-9 1,1-dibromo-2-nitro-ethane 
• 552-37-4 sodium o-aminobenzoate 
• 2099-63-0 anthranilic acid hydrochloride 
• 75-52-5 nitromethane 
• 56813-76-4 1,1-dichloro-2-nitroethane 

Downstream Products

• 125836-07-9 3-nitro-4-(1H)-quinolone 
• 890086-92-7 2-cyclohexyl-1H-imidazo[4,5-c]quinoline 
• 890086-97-2 2-cyclohexyl-1H-imidazo[4,5-c]quinoline 5-oxide 
• 890087-03-3 4-chloro-2-cyclohexyl-1H-imidazo[4,5-c]quinoline 
• 42606-33-7 3-nitro-4-aminoquinoline 
• 39061-97-7 4-chloro-3-nitroquinoline 
• 132206-92-9 4-chloro-1H-imidazo[4,5-c]-quinoline 
• 132206-99-6 N-phenyl-2-cyclopentyl-1H-imidazo[4,5-c]quinolin-4-amine 
• 39862-58-3 as-Triazino<5,6-c>chinolin 
• 121845-94-1 3,4-dihydro-3,3-dimethyl-1,2,4-triazino[5,6-c]quinoline 

Relevant academic research and scientific papers

Regioisomerism-dependent TLR7 agonism and antagonism in an imidazoquinoline

Chronic immune activation is a hallmark of progressive HIV infection. Recent reports point to the engagement of toll-like receptor 7 (TLR7) and -9 by viral RNA as contributing to the activation of innate immune responses, which drive viral replication leading to immune exhaustion. The only known class of TLR7 antagonists is single-stranded phosphorothioate oligonucleotides, which has been demonstrated to inhibit immune activation in human and Rhesus macaque in vitro models. The availability of a selective and potent small-molecule TLR7 antagonist should allow the evaluation of potential benefits of suppression of TLR7-mediated immune activation in HIV/AIDS. Gardiquimod is a known N1-substituted 1H-imidazoquinoline TLR7 agonist, the synthesis of which has not been published. We show that the 3H regioisomer is completely inactive as a TLR7 agonist and is weakly antagonistic. A des-amino precursor of the 3H regioisomer is more potent as a TLR7 antagonist, with an IC50 value of 7.5 μM. This class of compound may serve as a starting point for the development of small-molecule inhibitors of TLR7.

IMIDAZOQUINOLINE-TYPE COMPOUNDS AND USES THEREOF

Provided in the present disclosure are imidazoquinoline-type compounds, methods for their preparation, pharmaceutical compositions thereof and their use, wherein the imidazoquinoline-type compounds, upon local administration, form depots inducing cell mediated immune response while mitigating a systemic proinflammatory immune response.

LOCALLY ACTING TOLL-LIKE RECEPTOR 7 (TLR7) AND/OR TLR8 AGONIST IMMUNOTHERAPY COMPOUNDS AND THEIR USES

Provided in the present disclosure are immunotherapy compounds, pharmaceutical compositions thereof and their use, wherein the immunotherapy compounds, upon local administration, form depots inducing cell mediated immune response while mitigating a systemic proinflammatory immune response.

Toll-like receptor-8 agonistic activities in C2, C4, and C8 modified thiazolo[4,5-c]quinolines

Toll-like receptor (TLR)-8 agonists typified by the 2-alkylthiazolo[4,5-c] quinolin-4-amine (CL075) chemotype are uniquely potent in activating adaptive immune responses by inducing robust production of T helper 1-polarizing cytokines, suggesting that TLR8-active compounds could be promising candidate vaccine adjuvants, especially for neonatal vaccines. Alkylthiazoloquinolines with methyl, ethyl, propyl and butyl groups at C2 displayed comparable TLR8-agonistic potencies; activity diminished precipitously in the C2-pentyl compound, and higher homologues were inactive. The C2-butyl compound was unique in possessing substantial TLR7-agonistic activity. Analogues with branched alkyl groups at C2 displayed poor tolerance of terminal steric bulk. Virtually all modifications at C8 led to abrogation of agonistic activity. Alkylation on the C4-amine was not tolerated, whereas N-acyl analogues with short acyl groups (other than acetyl) retained TLR8 agonistic activity, but were substantially less water-soluble. Immunization in rabbits with a model subunit antigen adjuvanted with the lead C2-butyl thiazoloquinoline showed enhancements of antigen-specific antibody titers.

A3 ADENOSINE RECEPTOR ALLOSTERIC MODULATORS

The present invention relates to allosteric modulation of A3 adenosine receptor (A3AR) and provides for the use of an A3 adenosine receptor modulator (A3RM),for the preparation of pharmaceutical compositions for

Structure-activity relationships of new 1H-imidazo[4,5-c]quinolin-4-amine derivatives as allosteric enhancers of the A3 adenosine receptor

1H-Imidazo[4,5-c]quinolin-4-amine derivatives have been synthesized as allosteric modulators of the human A3 adenosine receptor (AR). Structural modifications were made at the 4-amino and 2 positions. The compounds were tested in both binding and functional assays, and many were found to be allosteric enhancers of the action of A3AR agonists by several different criteria. First, a potentiation of the maximum efficacy of the agonist C1-IB-MECA was observed for numerous derivatives. Also, a number of these compounds decreased the rate of dissociation of the agonist [ 125I]I-AB-MECA from the A3AR. Most prominently, compound 43 (LUF6000) was found to enhance agonist efficacy in a functional assay by 45% and decrease dissociation rate similarly without influencing agonist potency. The structural requirements for allosteric enhancement at the A3AR were distinct from the requirements to inhibit equilibrium binding. Thus, we have prepared allosteric enhancers of the human A3AR that have an improved allosteric effect in comparison to the inhibition of equilibrium binding at the orthosteric site.

CYCLOADDITION REACTIONS OF N-ALKOXYCARBONYL-4-QUINOLONES

3-Ethoxycarbonyl-4-1(H)-quinolone (2) and 3-nitro-4-1(H)-quinolone (3) reacted with a variety of chloroformates to give the N-acyl-3-ethoxycarbonyl-4-1(H)-quinolones (4a-d) and N-acyl-3-nitro-4-1(H)-quinolones (5a,b) respectively.Reaction of (4a,b,d) with 1-methoxy-3-(trimethylsilyloxy)-1,3-butadiene (6) gave the respective cycloadduct, 5,10a-diethoxycarbonyl-3,10-dioxo-1-methoxy-octahydroacridine (7a) and the analogues (7b,d).Treatment of (5a,b) with the above diene gave rise to two cycloadducts 3,10-dioxo-5-ethoxycarbonyl-1-methoxy-10a-nitro-octahydroacridines which had arisen from addition from the exo and endo transition states.The quinolones (4a,b) on reaction with Gesson's diene (12) and the ketene acetals (15) and (16), afforded Michael adducts 2--methyl-1-carboethoxy-4-methoxycyclohexa-1,3-diene (14a), and (14b), (17), (18) respectively.Base treatment of (14a,b) gave the aminoketone 7-(2'-aminobenzoyl)-8-hydroxy-3-methoxy-1,2-dihydronaphthalene (19) which was acetylated to afford (20).The latter could be selectively O-deacetylated to give 7-(2'-acetamidobenzoyl)-8-hydroxy-3-methoxy-1,2-dihydronaphthalene (21).