348-20-9

Usage

Category

Organic compound

Common uses

Intermediate in the production of pharmaceuticals, agrochemicals, and specialty chemicals

Physical properties

Colorless liquid, faint sweet aroma, insoluble in water, soluble in organic solvents

Reactivity

Useful as a building block in the synthesis of various organic compounds due to its unique reactivity and functional groups

Safety precautions

Potential health hazards and flammability, handle with care and follow proper safety precautions.

Upstream product

• 367-27-1 2,4-difluorophenol 
• 75-03-6 ethyl iodide 

Downstream Products

• 651734-62-2 3-ethoxy-2,6-difluoro-benzoic acid 
• 1026845-54-4 1-Ethoxy-2,4-difluoro-3-((E)-2-nitro-vinyl)-benzene 
• 1026053-70-2 2,6-difluoro-3-ethoxyphenethylamine 
• 1026813-86-4 1-ethoxy-2,4-difluoro-3-vinyl-benzene 
• 1028263-18-4 3-Ethoxy-2,6-difluoro-benzaldehyde 

Relevant academic research and scientific papers

USE OF KINASE INHIBITORS TO PROMOTE NEOCHONDROGENESIS

This invention provides methods for utilizing compounds that inhibit cyclin-dependent kinase and tyrosine kinase enzymes in the promotion of neochondrogenesis and the enhancement, protection and repair of cartilage. In certain embodiments the invention relates to methods of using compounds of formula (I): and pharmaceutically acceptable salts thereof, to promote neochondrogenesis, wherein, R1,R2, R3, R4, R5, R6, A, B, D, and E have any of the values defined therefor in the specification.

Kinase inhibitors

This invention provides phenyl-substituted pyrimidopyrimidines, dihydropyrimido-pyrimidines, pyridopyrimidines, naphthyridines, and pyridopyrazines of the general formula: that inhibit cyclin-dependent kinase and tyrosine kinase enzymes, methods and intermediate compounds for their synthesis, as well as pharmaceutical compositions and methods for their use in treating, inhibiting or preventing maladies associated with cell proliferative disorders, including angiogenesis, atherosclerosis, restenosis, and cancer.

Urea-PETT compounds as a new class of HIV-1 reverse transcriptase inhibitors. 3. Synthesis and further structure-activity relationship studies of PETT analogues

The further development of allosteric HIV-1 RT inhibitors in the urea analogue series of PETT (phenylethylthiazolylthiourea) derivatives is described here. The series includes derivatives with an ethyl linker (1-5) and racemic (6-16) and enantiomeric (17-

Phenethylthiazolylthiourea (PETT) compounds as a new class of HIV-1 reverse transcriptase inhibitors. 2. Synthesis and further structure-activity relationship studies of PETT analogs

Phenylethylthiazolylthiourea (PETT) derivatives have been identified as a new series of nonnucleoside inhibitors of HIV-1 RT. Structure-activity relationship studies of this class of compounds resulted in the identification of N-[2-(2-pyridyl)ethyl]-N'-[2-(5-bromopyridyl)]-thiourea hydrochloride (trovirdine; LY300046.HCl) as a highly potent anti-HIV-1 agent. Trovirdine is currently in phase one clinical trials for potential use in the treatment of AIDS. Extension of these structure-activity relationship studies to identify additional compounds in this series with improved properties is ongoing. A part of this work is described here. Replacement of the two aromatic moleties of the PETT compounds by various substituted or unsubstituted heteroaromatic rings was investigated. In addition, the effects of multiple substitution in the phenyl ring were also studied. The antiviral activities were determined on wild-type and constructed mutants of HIV-1 RT and on wild-type HIV-1 and mutant viruses derived thereof, Ile100 and Cys181, in cell culture assays. Some selected compounds were determined on double- mutant viruses, HIV-1 (Ile100/Asn103) and HIV-1 (Ile100/Cys181). A number of highly potent analogs were synthesized. These compounds displayed IC50's against wild-type RT between 0.6 and 5 nM. In cell culture, these agents inhibited wild-type HIV-1 with ED50's between I and 5 nM in MT-4 cells. In addition, these derivatives inhibited mutant HIV-1 RT (Ile 100) with IC50's between 20 and 50 nM and mutant HIV-1 RT (Cys 181) with IC50's between 4 and 10 nM, and in cell culture they inhibited mutant HIV-1 (Ile100) with ED50's between 9 and 100 nM and mutant HIV-1 (Cys181) with ED50's between 3 and 20 nM.