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The invention relates to compounds of formula (I), particularly for the use thereof as a medicament, especially in the treatment or prevention of neurogenerative disorders. The invention also relates to the methods for producing said compounds, and to the pharmaceutical compositions containing same.

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Reference:
Quinoxaline – Wikipedia,
Quinoxaline | C8H6N1732 | ChemSpider

 

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Chemo-enzymatic cascade processes are invaluable due to their ability to rapidly construct high-value products from available feedstock chemicals in a one-pot relay manner. Recommanded Product: 2-Chloro-7-nitroquinoxaline, In a article, mentioned the application of 55686-94-7, Name is 2-Chloro-7-nitroquinoxaline, molecular formula is C8H4ClN3O2

Parkinson’s disease (PD) is a neurodegenerative disorder of aging characterized by motor symptoms that result from the loss of midbrain dopamine neurons and the disruption of dopamine-mediated neurotransmission. There is currently no curative treatment for this disorder. To discover druggable neuroprotective compounds for dopamine neurons, we have designed and synthesized a second-generation of quinoxaline-derived molecules based on structure-activity relationship studies, which led previously to the discovery of our first neuroprotective brain penetrant hit compound MPAQ (5c). Neuroprotection assessment in PD cellular models of our newly synthesized quinoxaline-derived compounds has led to the selection of a better hit compound, PAQ (4c). Extensive in vitro characterization of 4c showed that its neuroprotective action is partially attributable to the activation of reticulum endoplasmic ryanodine receptor channels. Most interestingly, 4c was able to attenuate neurodegeneration in a mouse model of PD, making this compound an interesting drug candidate for the treatment of this disorder.

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Reference:
Quinoxaline – Wikipedia,
Quinoxaline | C8H6N1737 | ChemSpider

 

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Thirty-one quinoxalines bearing a substituted benzylamino group on position 2 and various substituents on position 3, 6, 7 and 8 of the heterocycle were prepared in order to evaluate in vitro anticancer activity. Preliminary screening performed at NCl on twenty-two compounds showed that most derivatives exhibited a moderate to strong growth inhibition activity on various tumor panel cell lines between 10-5 and 10-4 molar concentrations. Interesting selectivities were also recorded between 10-8 and 10-5 M.

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Quinoxaline – Wikipedia,
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Excess piperidine and 2-chloro-7-nitroquinoxaline 1 in diethyl ether give large amounts of the unexpected disubstitution product 6-nitro-2,3-di-piperidinoquinoxaline 3.The mechanism of this very unusual nucleophilic substitution of hydrogen is suggested to involve the oxidation of the dipiperidino-dihydroquinoxaline 10 by dissolved oxygen.

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Quinoxaline – Wikipedia,
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Thirty-five quinoxalines bearing a substituted amiline group on position 2 and various substituents on positions 3, 6, 7 and 8 were prepared in order to evaluate in vitro anticancer activity. Structural elucidation of some isomeric quinoxalinones formed by ring closure of 4-substituted-1,2-diaminobenzenes with dicarbonyl compounds was achieved by comparison with one isomer coming from an unambiguous independent route. Preliminary in vitro screening at NCI showed that many compounds exhibited a moderate to strong growth inhibition activity on various cell lines between 10-5 and 10-4 molar concentrations.

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Reference:
Quinoxaline – Wikipedia,
Quinoxaline | C8H6N1738 | ChemSpider

 

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category: quinoxaline, New Advances in Chemical Research in 2021. The transformation of simple hydrocarbons into more complex and valuable products via catalytic C–H bond functionalisation has revolutionised modern synthetic chemistry. 55686-94-7, Name is 2-Chloro-7-nitroquinoxaline, molecular formula is C8H4ClN3O2. In a article,once mentioned of 55686-94-7

2-{4-[(7-Chloro-2-quinoxalinyl)oxy]phenoxy}propionic acid (XK469) is among the most highly and broadly active antitumor agents to have been evaluated in our laboratories and is currently scheduled to enter clinical trials in 2001. The mechanism or mechanisms of action of XK469 remain to be elaborated. Accordingly, an effort was initiated to establish a pharmacophore hypothesis to delineate the requirements of the active site, via a comprehensive program of synthesis of analogues of XK469 and evaluation of the effects of structural modification(s) on solid tumor activity. The strategy formulated chose to dissect the two-dimensional parent structure into three regions – I, ring A of quinoxaline; II, the hydroquinone connector linkage; and III, the lactic acid moiety – to determine the resultant in vitro and in vivo effects of chemical alterations in each region. Neither the A-ring unsubstituted nor the B-ring 3-chloro-regioisomer of XK469 showed antitumor activity. The modulating antitumor effect(s) of substituents of differing electronegativities, located at the several sites comprising the A-ring of region I, were next ascertained. Thus, a halogen substituent, located at the 7-position of a 2-{4-[(2-quinoxalinyl)oxy]phenoxy}propionic acid, generated the most highly and broadly active antitumor agents. A methyl, methoxy, or an azido substituent at this site generated a much less active structure, whereas 5-, 6-, 8-chloro-, 6-, 7-nitro, and 7-amino derivatives all proved to be essentially inactive. When the connector linkage (region II) of 1 was changed from that of a hydroquinone to either a resorcinol or a catechol derivative, all antitumor activity was lost. Of the carboxylic acid derivatives of XK469 (region III), i.e., CONH2, CONHCH3, CON(CH3)2, CONHOH, CONHNH2, CN, or CN4H (tetrazole), only the monomethyl- and N,N-dimethylamides proved to be active.

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RhoA is a member of Rho GTPases, a subgroup of the Ras superfamily of small GTP-binding proteins. RhoA, as an important regulator of diverse cellular signaling pathways, plays significant roles in cytoskeletal organization, transcription, and cell-cycle progression. The RhoA/ROCK inhibitors have emerged as a new promising treatment for cardiovascular diseases. However, to date, RhoA inhibitors are macromolecules, and to our knowledge, small molecular-based inhibitors have not been reported. In this study, a series of first-in-class small molecular RhoA inhibitors have been discovered by using structure-based virtual screening in conjunction with chemical synthesis and bioassay. Virtual screening of ?200,000 compounds, followed by SPR-based binding affinity assays resulted in three compounds with binding affinities to RhoA at the micromolar level (compounds 1-3). Compound 1 was selected for further structure modifications in considering binding activity and synthesis ease. Fourty-one new compounds (1, 12a-v, 13a-h, and 14a-j) were designed and synthesized accordingly. It was found that eight (12a, 12j, 14a, 14b, 14d, 14e, 14 g, and 14h) showed high RhoA inhibition activities with IC50 values of 1.24 to 3.00 muM. A pharmacological assay indicated that two compounds (14g and 14 h) demonstrated noticeable vasorelaxation effects against PE-induced contraction in thoracic aorta artery rings and served as good leads for developing more potent cardiovascular agents.

Sometimes chemists are able to propose two or more mechanisms that are consistent with the available data. Quality Control of 2-Chloro-7-nitroquinoxaline, If a proposed mechanism predicts the wrong experimental rate law, however, the mechanism must be incorrect.Welcome to check out more blogs about 55686-94-7, in my other articles.

Reference:
Quinoxaline – Wikipedia,
Quinoxaline | C8H6N1733 | ChemSpider

 

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Sometimes chemists are able to propose two or more mechanisms that are consistent with the available data. Quality Control of 2-Chloro-7-nitroquinoxaline, If a proposed mechanism predicts the wrong experimental rate law, however, the mechanism must be incorrect.Welcome to check out more blogs about 55686-94-7, in my other articles.

New Advances in Chemical Research, May 2021. In heterogeneous catalysis, catalysts provide a surface to which reactants bind in a process of adsorption. Quality Control of 2-Chloro-7-nitroquinoxaline, In a article, mentioned the application of 55686-94-7, Name is 2-Chloro-7-nitroquinoxaline, molecular formula is C8H4ClN3O2

RhoA is a member of Rho GTPases, a subgroup of the Ras superfamily of small GTP-binding proteins. RhoA, as an important regulator of diverse cellular signaling pathways, plays significant roles in cytoskeletal organization, transcription, and cell-cycle progression. The RhoA/ROCK inhibitors have emerged as a new promising treatment for cardiovascular diseases. However, to date, RhoA inhibitors are macromolecules, and to our knowledge, small molecular-based inhibitors have not been reported. In this study, a series of first-in-class small molecular RhoA inhibitors have been discovered by using structure-based virtual screening in conjunction with chemical synthesis and bioassay. Virtual screening of ?200,000 compounds, followed by SPR-based binding affinity assays resulted in three compounds with binding affinities to RhoA at the micromolar level (compounds 1-3). Compound 1 was selected for further structure modifications in considering binding activity and synthesis ease. Fourty-one new compounds (1, 12a-v, 13a-h, and 14a-j) were designed and synthesized accordingly. It was found that eight (12a, 12j, 14a, 14b, 14d, 14e, 14 g, and 14h) showed high RhoA inhibition activities with IC50 values of 1.24 to 3.00 muM. A pharmacological assay indicated that two compounds (14g and 14 h) demonstrated noticeable vasorelaxation effects against PE-induced contraction in thoracic aorta artery rings and served as good leads for developing more potent cardiovascular agents.

Sometimes chemists are able to propose two or more mechanisms that are consistent with the available data. Quality Control of 2-Chloro-7-nitroquinoxaline, If a proposed mechanism predicts the wrong experimental rate law, however, the mechanism must be incorrect.Welcome to check out more blogs about 55686-94-7, in my other articles.

Reference:
Quinoxaline – Wikipedia,
Quinoxaline | C8H6N1733 | ChemSpider

 

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Note that a catalyst decreases the activation energy for both the forward and the reverse reactions and hence accelerates both the forward and the reverse reactions.Quality Control of 2-Chloro-7-nitroquinoxaline, you can also check out more blogs about55686-94-7

Quality Control of 2-Chloro-7-nitroquinoxaline, New Advances in Chemical Research in 2021. The transformation of simple hydrocarbons into more complex and valuable products via catalytic C–H bond functionalisation has revolutionised modern synthetic chemistry. 55686-94-7, Name is 2-Chloro-7-nitroquinoxaline, molecular formula is C8H4ClN3O2. In a article,once mentioned of 55686-94-7

2-{4-[(7-Chloro-2-quinoxalinyl)oxy]phenoxy}propionic acid (XK469) is among the most highly and broadly active antitumor agents to have been evaluated in our laboratories and is currently scheduled to enter clinical trials in 2001. The mechanism or mechanisms of action of XK469 remain to be elaborated. Accordingly, an effort was initiated to establish a pharmacophore hypothesis to delineate the requirements of the active site, via a comprehensive program of synthesis of analogues of XK469 and evaluation of the effects of structural modification(s) on solid tumor activity. The strategy formulated chose to dissect the two-dimensional parent structure into three regions – I, ring A of quinoxaline; II, the hydroquinone connector linkage; and III, the lactic acid moiety – to determine the resultant in vitro and in vivo effects of chemical alterations in each region. Neither the A-ring unsubstituted nor the B-ring 3-chloro-regioisomer of XK469 showed antitumor activity. The modulating antitumor effect(s) of substituents of differing electronegativities, located at the several sites comprising the A-ring of region I, were next ascertained. Thus, a halogen substituent, located at the 7-position of a 2-{4-[(2-quinoxalinyl)oxy]phenoxy}propionic acid, generated the most highly and broadly active antitumor agents. A methyl, methoxy, or an azido substituent at this site generated a much less active structure, whereas 5-, 6-, 8-chloro-, 6-, 7-nitro, and 7-amino derivatives all proved to be essentially inactive. When the connector linkage (region II) of 1 was changed from that of a hydroquinone to either a resorcinol or a catechol derivative, all antitumor activity was lost. Of the carboxylic acid derivatives of XK469 (region III), i.e., CONH2, CONHCH3, CON(CH3)2, CONHOH, CONHNH2, CN, or CN4H (tetrazole), only the monomethyl- and N,N-dimethylamides proved to be active.

Note that a catalyst decreases the activation energy for both the forward and the reverse reactions and hence accelerates both the forward and the reverse reactions.Quality Control of 2-Chloro-7-nitroquinoxaline, you can also check out more blogs about55686-94-7

Reference:
Quinoxaline – Wikipedia,
Quinoxaline | C8H6N1735 | ChemSpider

 

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The invention relates to new quinoxaline derivative compounds, to pharmaceutical compositions comprising said compounds, to processes for the preparation of said compounds and to the use of said compounds in the treatment of diseases, e.g. cancer

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Reference:
Quinoxaline – Wikipedia,
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