14123-79-6

Upstream product

• 1529-41-5 3-chloro-benzeneacetonitrile 
• 141-78-6 ethyl acetate 
• 75-36-5 acetyl chloride 

Downstream Products

• 14123-60-5 3-chlorophenylacetone 
• 66154-45-8 (E)-3-amino-2-(3-chlorophenyl)but-2-enenitrile 
• 1346260-42-1 (E)-1-(3-chlorophenyl)-2-(methoxyimino)propan-1-one 
• 10557-17-2 1-(3-chlorophenyl)propane-1,2-dione 
• 62538-18-5 4-(3-chlorophenyl)-5-methyl-1H-pyrazol-3-amine 
• 921620-90-8 4-bromo-2-(3-chloro-phenyl)-3-oxo-butyronitrile 
• 113494-31-8 2,4-diamino-5-(3-chlorophenyl)-6-methylpyrimidine 

Relevant academic research and scientific papers

N -Acetyl-3-aminopyrazoles block the non-canonical NF-kB cascade by selectively inhibiting NIK

NF-κB-inducing kinase (NIK), an oncogenic drug target that is associated with various cancers, is a central signalling component of the non-canonical pathway. A blind screening process, which established that amino pyrazole related scaffolds have an effect on IKKbeta, led to a hit-to-lead optimization process that identified the aminopyrazole 3a as a low μM selective NIK inhibitor. Compound 3a effectively inhibited the NIK-dependent activation of the NF-κB pathway in tumour cells, confirming its selective inhibitory profile.

Use of Pyrazolo(1,5A)Pyrimidin-7-YL Amine Derivatives in the Treatment of Neurological Disorders

The invention relates to methods of using the compounds of the invention, including pyrazolo[1,5a]pyrimidin-7-yl amine compounds and salts thereof, as well as pharmaceutical compositions comprising the same, in the treatment of Eph receptor-related (e.g., neurological) injuries and disorders. The invention also relates to modulating the activity of an Eph receptor in a cell, stimulating neural regeneration, and reversing neuronal degeneration, by administering a compound of the invention to a cell or subject in an effective amount.

PYRAZOLO[1.5-A]PYRIMIDIN-7-YL AMINE DERIVATIVES AS PROTEIN KINASE INHIBITORS

The invention relates to pyrazolo[1,5a]pyrimidin-7-yl amine derivatives of formula (I) and salts thereof, their use in the treatment of protein kinase dependent diseases.

Synthesis of N-substituted indole derivatives via PIFA-mediated intramolecular cyclization

(Chemical Equation Presented) A variety of N-arylated and N-alkylated indole derivatives were synthesized by way of a phenyliodine bis(trifluoroacetate) (PIFA)-mediated intramolecular cyclization. This novel method allows for the construction of an indole skeleton by joining the N-atom on the side chain to the benzene ring at the last synthetic step. Other novel pyrrole-fused aromatic compounds can also be achieved by this method.

Organic compounds

The invention relates to the use of pyrazolo[1,5a]pyrimidin-7-yl amine compounds and salts thereof in the treatment of kinase dependent diseases and for the manufacture of pharmaceutical preparations for the treatment of said diseases, novel pyrazolo[1,5a]pyrimidin-7-yl amine compounds, and a process for the preparation of the novel pyrazolo[1,5a]pyrimidin-7-yl amine compounds.

PYRAZOLO[1,5-A]PYRIMIDIN-7-YL-AMINE DERIVATIVES FOR USE IN THE TREATMENT OF PROTEIN KINASE DEPENDENT DISEASES

The invention relates to the use of pyrazolo[1,5a]pyrimidin-7-yl amine compounds and salts thereof in the treatment of kinase dependent diseases and for the manufacture of pharmaceutical preparations for the treatment of said diseases, novel pyrazolo[1,5a]pyrimidin-7-yl amine compounds, and a process for the preparation of the novel pyrazolo[1,5a]pyrimidin-7-yl amine compounds.

Development of 2,4-diaminopyrimidines as antimalarials based on inhibition of the S108N and C59R+S108N mutants of dihydrofolate reductase from pyrimethamine resistant Plasmodium falciparum

The reduced binding of pyrimethamine to Serl08Asn (S108N) mutants of parasite dihydrofolate reductase (DHFR), which forms the basis of resistance of Plasmodium falciparum to pyrimethamine, is largely due to steric constraint imposed by the bulky side chain of N108 on Cl of the 5-p-Cl-phenyl group. This and other S108 mutants with bulky side chains all showed reduced binding to pyrimethamine and cycloguanil. Less effect on binding to some bulky mutants was observed for trimethoprim, with greater flexibility for the 5-substituent. S108N DHFR also binds poorly with other pyrimethamine derivatives with bulky groups in place of the p-Cl, and the binding was generally progressively poorer for the double (C59R+S108N) mutant. Removal of the p-Cl or replacement with m-Cl led to better binding with the mutant DHFRs. Pyrimethamine analogues with unbranched hydrophobic 6-substituents showed generally good binding with the mutant DHFRs. A number of compounds were identified with high affinities for both wild-type and mutant DHFRs, with very low to no affinity to human DHFR. Some of these compounds show good antimalarial activities against pyrimethamine-resistant P. falciparum containing the mutant DHFRs with low cytotoxicity to three mammalian cell lines.