94278-69-0

Upstream product

• 86111-47-9 (2,6-dichloro-4-methoxy-phenyl)-methanol 
• 124-38-9 carbon dioxide 
• 33719-74-3 3,5-dichloroanisole 

Downstream Products

• 127817-86-1 2,6-Dichlor-4-methoxybenzoesaurechlorid 
• 1438897-27-8 N-(2-bromopyridin-4-yl)-2,6-dichloro-4-methoxybenzamide 
• 1258295-70-3 2,6-dichloro-N-(2-(cyclopropanecarboxamido)pyridin-4-yl)-4-methoxybenzamide 
• 1258295-73-6 2,6-dichloro-N-(2-(cyclopropanecarboxamido)pyridin-4-yl)-4-hydroxybenzamide 
• 94294-10-7 methyl 2,4-dichloro-6-methoxybenzoate 
• 94278-65-6 methyl 2,6-dichloro-4-methoxybenzoate 
• 1186388-87-3 C₉H₇Cl₂N₃OS 
• 4641-38-7 2,6-Dichloro-4-hydroxybenzoic acid 
• 127817-91-8 N-(4-Methoxyphenyl)-N-(1,1,1-trifluor-2-propyl)-2,6-dichlor-4-methoxybenzamid 
• 127817-96-3 N-(4-Hydroxyphenyl)-N-(1,1,1-trifluor-2-propyl)-2,6-dichlor-4-hydroxybenzamid 

Relevant academic research and scientific papers

METHODS AND COMPOSITIONS FOR INHIBITING RHO/MRTF-MEDIATED DISEASES AND CONDITIONS

The present disclosure relates to methods, compositions, and kits for the inhibition of signaling by members of the Rho GTPase family. Specifically, the disclosure relates to methods, compositions and kits for the inhibition of RhoA and/or RhoC transcriptional signaling and action os the transcripton co-factors MRTF-A and/or MRTF-B. The disclosure finds use in treatment of Rho-mediated disease states (e.g., tumor metastasis and fibrosis), Rho-mediated biological conditions, and in cell signaling research.

Lead optimization of a 4-aminopyridine benzamide scaffold to identify potent, selective, and orally bioavailable TYK2 inhibitors

Herein we report our lead optimization effort to identify potent, selective, and orally bioavailable TYK2 inhibitors, starting with lead molecule 3. We used structure-based design to discover 2,6-dichloro-4-cyanophenyl and (1R,2R)-2-fluorocyclopropylamide modifications, each of which exhibited improved TYK2 potency and JAK1 and JAK2 selectivity relative to 3. Further optimization eventually led to compound 37 that showed good TYK2 enzyme and interleukin-12 (IL-12) cell potency, as well as acceptable cellular JAK1 and JAK2 selectivity and excellent oral exposure in mice. When tested in a mouse IL-12 PK/PD model, compound 37 showed statistically significant knockdown of cytokine interferon-γ (IFNγ), suggesting that selective inhibition of TYK2 kinase activity might be sufficient to block the IL-12 pathway in vivo.

2-SACCHARINYLMETHYL ARYL CARBOXYLATES USEFUL AS PROTEOLYTIC ENZYME INHIBITORS AND COMPOSITIONS AND METHOD OF USE THEREOF

A compound having the formula: STR1 wherein Ar, R 4 and R 5 are defined herein have pharmaceutical utility as proteolytic enzyme inhibitors.

PROTEOLYTIC ENZYME INHIBITION METHOD

4-R 4-R 5-2-Saccharinylmethyl aryl carboxylates, useful in the treatment of degenerative diseases, are prepared by reacting a 4-R. sup.4-R 5-2-halomethylsaccharin with an arylcarboxylic acid in the presence of an acid-acceptor.

Antiestrogenic N-(4-hydroxyphenyl)-N-(1,1,1-trifluoro-2-propyl)-4-hydroxybenzamides: Influence of hydrophobic groups substituted in the ortho-position of the benzamide-fragment on activity

Experiments are reported here to develop compounds with antiestrogenic and mammary tumor inhibiting properties. Analogues with hydrophobic groups in 2- or 2,6-position of the benzamide-fragment of N-(4-hydroxyphenyl)-N-(1,1,1-trifluoro-2-propyl)-4-hydroxy