Some scientific research about 3,6-Dichloropyridazine

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Antirhinoviral heteroamine-substituted pyridazines

Novel pyridazinamines having antirhinoviral activity, compositions containing these compounds as active ingredient, and a method of inhibiting combating or preventing the growth of viruses in warm-blooded animals suffering from diseases caused by these viruses.

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Pyridazine – Wikipedia,
Pyridazine | C4H4N1526 – PubChem

 

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Discovery of 1,2,3-triazole-based fibroblast growth factor receptor modulators

To avoid production of a phospholipidosis-inducing metabolite, we replaced the amide structure of SUN13837 (1) with a 1,2,3-triazole. The resulting 1,2,3-triazole analog of 1 (compound 2) displayed greater neuroprotective activity than 1. Structural modification of 2 yielded compound 10, which showed improved neuroprotective activity and negligible mechanism-based inactivation against CYP3A4. In addition, installation of a methyl group at the 5-position of 1,2,3-triazole of 10 significantly boosted the neuroprotective activity. These 1,2,3-triazole derivatives displayed reduced phospholipidosis risk, sufficient systemic exposure, and high central nervous system penetration, and therefore may be potentially useful agents for the treatment of neurodegenerative diseases.

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Pyridazine – Wikipedia,
Pyridazine | C4H4N692 – PubChem

 

Some scientific research about 6-Chloropyridazine-3-carbonitrile

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Studies on a series of milnacipran analogs containing a heteroaromatic group as potent norepinephrine and serotonin transporter inhibitors

A series of milnacipran analogs containing a heteroaromatic group were synthesized and studied as monoamine transporter inhibitors. Many compounds exhibited higher potency than milnacipran at NET and NET/SERT with no significant change in lipophilicity. For example, compound R-26f was about 10-fold more potent than milnacipran with IC50 values of 8.7 and 26 nM at NET and SERT, respectively.

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Pyridazine – Wikipedia,
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The important role of 6-Chloropyridazine-3-carboxylic acid

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Palladium-catalyzed C-2 selective arylation of quinolines

An efficient method for the Pd-catalyzed regioselective C-2 arylation of quinolines is presented. Reactions of various substituted quinolines and unactivated arenes have been conducted under mild conditions. The result shows good product yields of 2-arylquinolines, which are highly useful building blocks for the synthesis of bioactive alkaloid natural products and drug molecules.

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Some scientific research about 141-30-0

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One of the major reasons for studying chemical kinetics is to use measurements of the macroscopic properties of a system, Safety of 3,6-Dichloropyridazine, such as the rate of change in the concentration of reactants or products with time.In a article, mentioned the application of 141-30-0, Name is 3,6-Dichloropyridazine, molecular formula is C4H2Cl2N2

PYRIDAZINONE DERIVATIVE AND PDE INHIBITOR CONTAINING THE SAME AS ACTIVE INGREDIENT

It is to provide a novel pyridazinone derivative represented by the following general formula (1), which is useful as a pharmaceutical and has a phosphodiesterase inhibitory action: wherein R1 represents H or C1-6 alkyl, each of R2 and R3 represents H, X, C1-6 alkoxy, Z represents O or S, and A represents AA or BB, wherein AA represents: and BB represents: wherein R4 represents H or C1-6 alkyl, and each of R5 and R6 represents C1-6 alkyl.

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Pyridazine | C4H4N1400 – PubChem

 

The Absolute Best Science Experiment for 1121-79-5

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METHODS FOR TREATING HCV

This invention relates to combinations of therapeutic molecules useful for treating hepatitis C virus infection. The present invention relates to methods, uses, dosing regimens, and compositions.

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Archives for Chemistry Experiments of 141-30-0

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New pyridazine-bridged NHC/pyrazole ligands and their sequential silver(I) coordination

A family of new pyridazine-bridged NHC/pyrazole ligand precursors HL 1-5 were prepared and fully characterized including analysis by XRD {HL1 = 3-[3-(2,6-diisopropylphenyl)-3H-imidazolium-1-yl]-6-(3- pyridin-2-yl-pyrazol-1-yl)-pyridazine, HL2 = 3-[3-(2,4,6- trimethylphenyl)-3H-imidazolium-1-yl]-6-(3-pyridin-2-yl-pyrazol-1-yl) -pyridazine, HL3 = 3-[3-(2,4,6-trimethylphenyl)-3H-imidazolium-1-yl]- 6-(3,5-dimethylpyrazol-1-yl)-pyridazine, HL4 = 3-(3-tert-butyl-3H- imidazolium-1-yl)-6-(3,5-dimethylpyrazol-1-yl)-pyridazine, HL5 = 3-[3-(2,4,6-trimethylphenyl)-3H-imidazolium-1-yl]-6-(3-methyl-5-phenylpyrazol-1- yl)-pyridazine, X = PF6- or BF4-}. Reaction of the ligand precursors with Ag2O yielded various silver(I) complexes whose structures have been elucidated crystallographically. In complexes [(L3)2Ag](PF6) (4) and[(L 4)2Ag](PF6) (4?) the single silver(I) ion is coordinated in a linear fashion by the NHC moieties of the two ligand strands. An NMR titration with AgBF4 reveals that 4 can bind two more silver(I) ions. The complex [(L5)2Ag2](PF 6)2 (5?) features an additional silver(I) centre bound to the two pyrazole rings, whereas in [(L3)2Ag 2](BF4)2 (6) ligand reshuffling has occurred to give antiparallel ligand strands with {CNHCNpyrazole} coordination of each metal ion. Secondary interactions with the pyridazine N-atom are observed in some cases. An additional third silver(I) ion can be accommodated between the central pyridazine bridges, as shown in [(L 3)2Ag3](PF6)2(BF 4) (7). The sequence of binding events and the identity of the species in solution have been investigated by NMR spectroscopy and ESI mass spectrometry. A family of new pyridazine-bridged ditopic ligands has been prepared, which provide both an organometallic NHC and a classic N-donor compartment. Two opposing strands of these ligands sequentially bind up to three silver(I) ions. Complexation starts at the NHC subunit and involves some ligand reshuffling to form a trisilver arrangement, which has been elucidated by NMR spectroscopy and X-ray crystallography. Copyright

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Pyridazine – Wikipedia,
Pyridazine | C4H4N1957 – PubChem

 

Awesome and Easy Science Experiments about 3-Phenyl-6-chloropyridazine

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Papain-catalyzed peptide bond formation: Enzyme-specific activation with guanidinophenyl esters

The substrate mimetics approach is a versatile method for small-scale enzymatic peptide-bond synthesis in aqueous systems. The protease-recognized amino acid side chain is incorporated in an ester leaving group, the substrate mimetic. This shift of the specific moiety enables the acceptance of amino acids and peptide sequences that are normally not recognized by the enzyme. The guanidinophenyl group (OGp), a known substrate mimetic for the serine proteases trypsin and chymotrypsin, has now been applied for the first time in combination with papain, a cheap and commercially available cysteine protease. To provide insight in the binding mode of various Z-XAA-OGp esters, computational docking studies were performed. The results strongly point at enzyme-specific activation of the OGp esters in papain through a novel mode of action, rather than their functioning as mimetics. Furthermore, the scope of a model dipeptide synthesis was investigated with respect to both the amino acid donor and the nucleophile. Molecular dynamics simulations were carried out to prioritize 22 natural and unnatural amino acid donors for synthesis. Experimental results correlate well with the predicted ranking and show that nearly all amino acids are accepted by papain.

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Pyridazine | C4H4N2612 – PubChem

 

Archives for Chemistry Experiments of 6-Chloropyridazine-3-carbonitrile

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Discovery and optimization of a novel series of liver X receptor-alpha agonists

A novel series of hexafluorocarbinols were discovered as potent activators of the liver X receptor-alpha using a fluorescence polarization assay. Structure-activity relationship study led to the identification of compounds that are more potent agonists than the endogenous ligand, 24(S), 25-epoxycholesterol, with similar efficacy. Several compounds, including T0901317, were shown to have desirable pharmacokinetic profiles suitable for in vivo studies.

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N-phenyl-4-pyrazolo[1,5-6]pyridazin-3-ylpyrimidin-2-amines as potent and selective inhibitors of glycogen synthase kinase 3 with good cellular efficacy

Glycogen synthase kinase 3 regulates glycogen synthase, the rate-determining enzyme for glycogen synthesis. Liver and muscle glycogen synthesis is defective in type 2 diabetics, resulting in elevated plasma glucose levels. Inhibition of GSK-3 could potentially be an effective method to control plasma glucose levels in type 2 diabetics. Structure-activity studies on a N-phenyl-4-pyrazolo[1,5-b]pyridazin-3-ylpyrimidin-2-amine series have led to the identification of potent and selective compounds with good cellular efficacy. Molecular modeling studies have given insights into the mode of binding of these inhibitors. Since the initial leads were also potent inhibitors of CDK-2/CDK-4, an extensive SAR was performed at various positions of the pyrazolo[1,5-b] pyridazin core to afford potent GSK-3 inhibitors that were highly selective over CDK-2. In addition, these inhibitors also exhibited very good cell efficacy and functional response. A representative example was shown to have good oral exposure levels, extending their utility in an in vivo setting. These inhibitors provide a viable lead series in the discovery of new therapies for the treatment of type 2 diabetes.

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