320590-29-2Relevant articles and documents
Transition Metal Salts-Catalyzed Aza-Michael Reactions of Enones with Carbamates
Kobayashi, Shu,Kakumoto, Kentaro,Sugiura, Masaharu
, p. 1319 - 1322 (2002)
(Matrix Presented) Several transition metal salts were found to catalyze aza-Michael reactions of enones with carbamates efficiently. The catalytic activity was strongly dependent on the nature of the metal salts. While conventional Lewis acids such as BF
Highly efficient phosphine-catalyzed aza-Michael reactions of α,β-unsaturated compounds with carbamates in the presence of TMSCl
Xu, Li-Wen,Xia, Chun-Gu
, p. 4507 - 4510 (2004)
Aza-Michael reactions of enones with carbamates took place efficiently in the presence of a catalytic amount of phosphine and TMSCl to afford the total products in high yields. The new catalytic system was also efficient in the aza-Michael reaction of chalcone, which was difficult to react with carbamates by transition metal salts catalysts.
Discovery of the c-Jun N-Terminal Kinase Inhibitor CC-90001
Apuy, Julius,Bahmanyar, Sogole,Benish, Brent,Bennett, Brydon L.,Blease, Kate,Canan, Stacie S.,Condroski, Kevin,Delgado, Mercedes,Elsner, Jan,Erdman, Paul,Haelewyn, Jason,Hilgraf, Robert,Khambatta, Godrej,Lebrun, Laurie,McCarrick, Meg,Moghaddam, Mehran F.,Mortensen, Deborah S.,Nagy, Mark A.,Norris, Stephen,Paisner, David,Romanow, William J.,Satoh, Yoshitaka,Tikhe, Jayashree,Xu, Li,Yoon, Won
, p. 18193 - 18208 (2021/12/27)
As a result of emerging biological data suggesting that within the c-Jun N-terminal kinase (JNK) family, JNK1 and not JNK2 or JNK3 may be primarily responsible for fibrosis pathology, we sought to identify JNK inhibitors with an increased JNK1 bias relative to our previous clinical compound tanzisertib (CC-930). This manuscript reports the synthesis and structure-activity relationship (SAR) studies for a novel series of JNK inhibitors demonstrating an increased JNK1 bias. SAR optimization on a series of 2,4-dialkylamino-pyrimidine-5-carboxamides resulted in the identification of compounds possessing low nanomolar JNK inhibitory potency, overall kinome selectivity, and the ability to inhibit cellular phosphorylation of the direct JNK substrate c-Jun. Optimization of physicochemical properties in this series resulted in compounds that demonstrated excellent systemic exposure following oral dosing, enabling in vivo efficacy studies and the selection of a candidate for clinical development, CC-90001, which is currently in clinical trials (Phase II) in patients with idiopathic pulmonary fibrosis (NCT03142191).
THIOPHENE DERIVATIVES FOR THE TREATMENT OF DISORDERS CAUSED BY IGE
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Page/Page column 376; 377, (2020/01/11)
Thiophene derivatives of formula (I) and a pharmaceutically acceptable salt thereof are provided. These compounds have utility for the treatment or prevention of disorders caused by IgE, such as allergy, type 1 hypersensitivity or familiar sinus inflammation.
THERAPEUTICALLY ACTIVE COMPOUNDS AND THEIR METHODS OF USE
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Page/Page column, (2015/03/31)
Provided are methods of treating a cancer characterized by the presence of a mutant allele of IDH1/2 comprising administering to a subject in need thereof a compound described here.
