54006-63-2

Usage

Chemical Properties

White solid

InChI:InChI=1/C10H7ClN2O2/c11-7-3-1-6(2-4-7)8-5-9(10(14)15)13-12-8/h1-5H,(H,12,13)(H,14,15)/p-1

Upstream product

• 108-90-7 chlorobenzene 
• 39757-35-2 methyl 4-(4-chlorophenyl)-2,4-dioxobutanoate 
• 79508-09-1 methyl 3‐(4‐chlorophenyl)‐1H‐pyrazole‐5‐carboxylate 
• 99-91-2 para-chloroacetophenone 
• 88330-75-0 4-(4-chlorophenyl)-2,4-dioxobutyric acid ethyl ester sodium salt 
• 938182-43-5 5-(4-chlorophenyl)-1H-pyrazole-3-carboxylic acid ethyl ester 
• 5814-38-0 ethyl 4-chlorobenzoylpyruvate 

Downstream Products

• 1239470-62-2 (3-(4-chlorophenyl)-1H-pyrazol-5-yl)(morpholino)methanone 
• 1135147-90-8 (3-(4-chlorophenyl)-1H-pyrazol-5-yl)(piperidin-1-yl)methanone 
• 1277167-57-3 C₂₂H₂₃ClN₄O₂ 
• 1277167-59-5 C₂₀H₂₀ClN₅O 
• 1277167-58-4 C₂₀H₂₀ClN₅O 
• 1277167-60-8 C₂₀H₂₀ClN₅O 
• 1277167-61-9 C₂₁H₂₇ClN₄O 
• 1277167-73-3 C₂₂H₂₂ClN₅O₃ 
• 1277167-72-2 C₂₇H₂₄ClFN₄O₂ 
• 1024611-60-6 C₁₂H₁₂ClN₃O₂ 

Relevant academic research and scientific papers

Design, synthesis, biological evaluation and in silico studies of pyrazole‐based nh2‐acyl oseltamivir analogues as potent neuraminidase inhibitors

Oseltamivir represents one of the most successful neuraminidase (NA) inhibitors in the current anti‐influenza therapy. The 150‐cavity of NA was identified as an additional binding pocket, and novel NA inhibitors have been designed to occupy the 150‐cavity

Fragment-based lead generation of 5-phenyl-1H-pyrazole-3-carboxamide derivatives as leads for potent factor xia inhibitors

FXIa is suggested as a major target for anticoagulant drug discovery because of reduced risk of bleeding. In this paper, we defined 5-phenyl-1H-pyrazole-3-carboxylic acid derivatives as privileged fragments for FXIa inhibitors' lead discovery. After repla

5-Aryl-1H-pyrazole-3-carboxylic acids as selective inhibitors of human carbonic anhydrases IX and XII

Inhibitory activity of a congeneric set of 23 phenyl-substituted 5-phenyl-pyrazole-3-carboxylic acids toward human carbonic anhydrase (hCA, EC 4.2.1.1) isoforms I, II, IX and XII was evaluated by a stopped-flow CO2 hydrase assay. These compounds exerted a clear, selective inhibition of hCA IX and XII over hCAI and II, with Ki in two to one digit micromolar concentrations (4-50 μM). Derivatives bearing bulkier substituents in para-position of the phenyl ring inhibited hCA XII at one-digit micromolar concentrations, while derivatives having alkyl substituents in both ortho- and meta-positions inhibited hCA IX with Kis ranging between 5 and 25 μM. Results of docking experiments offered a rational explanation on the selectivity of these compounds toward CA IX and XII, as well as on the substitution patterns leading to best CA IX or CA XII inhibitors. By examining the active sites of these four isoforms with GRID generated molecular-interaction fields, striking differences between hCA XII and the other three isoforms were observed. The field of hydrophobic probe (DRY) appeared significantly different in CA XII active site, comparing to other three isoforms studied. To the best of our knowledge such an observation was not reported in literature so far. Considering the selectivity of these carboxylates towards membrane-associated over cytosolic CA isoforms, the title compounds could be useful for the development of isoform-specific non-sulfonamide CA inhibitors.

Pyrazole derivatives as inhibitors of arachidonic acid-induced platelet aggregation

Antiplatelet drugs are promising therapeutics to intervene with platelet aggregation in arterial thrombosis, most prominently in myocardial infarction and ischemic stroke. Here, we describe the synthesis and structure-activity relationships of potent inhibitors of platelet aggregation based on the 1,5-diarylpyrazol-3-carboxamide scaffold. Analogs from this series demonstrated potent anti-aggregatory activities against arachidonic acid-induced platelet aggregation, as measured by turbidimetric method of Born. 1,5-Diarylpyrazole-3- carboxamides obtained with small-basic amines (7, 8, 50, 51, 61, 62) displayed the strongest activity with IC50 values in low nanomolar range (5.7-83 nM). On the basis of their high potency in cellular environment, these straightforward pyrazole derivatives may possess potential in the design of more potent compounds for intervention with cardiovascular diseases.

NOVEL NK-3 RECEPTOR SELECTIVE ANTAGONIST COMPOUNDS, PHARMACEUTICAL COMPOSITION AND METHODS FOR USE IN NK-3 RECEPTORS MEDIATED DISORDERS

The present invention is directed to novel compounds of formula I and their use as therapeutic compounds.

Pyrazole derivatives as partial agonists for the nicotinic acid receptor

Nicotinic acid as a hypolipidemic agent appears unique due to its potential to increase HDL cholesterol levels to a greater extent than other drugs. However, it has some side effects, among which severe skin flushing is the most frequent and often limits patients' compliance. In a search for novel agonists for the recently identified and cloned G protein-coupled nicotinic acid receptor, we synthesized a series of substituted pyrazole-3-carboxylic acids that proved to have substantial affinity for this receptor. The affinities were measured by inhibition of [3H] nicotinic acid binding to rat spleen membranes. Potencies and intrinsic activities relative to nicotinic acid were determined by their effects on [35S]GTPγS binding to rat adipocyte and spleen membranes. Interestingly, most compounds were partial agonists. In particular, 2-diazabicyclo-[3,3,O 4,8]octa-3,8-diene-3-carboxylic acid (4c) and 5-propylpyrazole-3-carboxylic acid (4f) proved active with Ki values of approximately 0.15 μM and EC50 values of approximately 6 μM, while their intrinsic activity was only ～50% when compared to nicotinic acid. Even slightly more active was 5-butylpyrazole-3-carboxylic acid (4g) with a Ki value of 0.072 μM, an EC50 value of 4.12 μM, and a relative intrinsic activity of 75%. Of the aralkyl derivatives, 4q (5-(3-chlorobenzyl)pyrazole-3-carboxylic acid) was the most active with a relatively low intrinsic activity of 39%. Partial agonism of the pyrazole derivatives was confirmed by inhibition of G protein activation in response to nicotinic acid by these compounds. The pyrazoles both inhibited the maximum effect elicited by 100 μM nicotinic acid and concentration dependently shifted nicotinic acid concentration-response curves to the right, pointing to a competive mechanism of action.