136285-39-7

Upstream product

• 106-31-0 butanoic acid anhydride 
• 57113-91-4 methyl 3-nitroanthranilate 
• 606-18-8 3-nitroanthranilic acid 
• 134-20-3 2-carbomethoxyaniline 
• 30006-30-5 methyl 2-butyrylaminobenzoate 

Downstream Products

• 942429-41-6 C₂₄H₂₂N₄O₅ 
• 942429-58-5 C₂₅H₂₅N₃O₇ 
• 942429-46-1 C₂₄H₂₂N₄O₂ 
• 942429-51-8 C₂₄H₂₃N₇O₂ 
• 942429-62-1 C₂₅H₂₅N₃O₄ 
• 1207547-73-6 methyl 3-amino-2-butyramidobenzoate 

Relevant academic research and scientific papers

Identification and development of non-cytotoxic cell death modulators: Impact of sartans and derivatives on PPARγ activation and on growth of imatinib-resistant chronic myelogenous leukemia cells

4’-((2-Propyl-1H-benzo[d]imidazol-1-yl)methyl)-[1,1′-biphenyl]-2-carboxylic acid derived from telmisartan was identified as lead for the design of cell death modulators. In this study, we evaluated the efficacy of telmisartan itself and other sartans in combination with imatinib against K562-resistant cells. The findings were directly used to further optimize the lead structure. Telmisartan and candesartan cilexetil represented the most effective sartans, thus the influence of carboxyl/methyl carboxylate groups at positions 7 (compounds 6, 7) or 4 (compounds 12–14) at the benzimidazole core was studied. Additionally, according to the results of a former structure-activity study, telmisartan was transformed to the related amide (1). Telmisartan amide 1, as well as the esters 6 and 12 markedly sensitized the resistant CML cells to imatinib treatment. Correlation with their potency to activate PPARγ is not given. Candesartan cilexetil, telmisartan and 1 showed the profile of partial agonists at PPARγ with EC50 values of 4.2, 4.3 and 9.1 μM, respectively, while 6 and 12 caused only marginal intrinsic activation at 10 μM (Amax = 22% and 13%). However, the repression of the STAT5 phosphorylation relates with the possibility to sensitize K562-resistant CML cells to imatinib treatment. It is worth mentioning that all compounds were per se non-cytotoxic at relevant concentrations.

DIBENZOOXEPIN DERIVATIVE

A dibenzoxepin derivative represented by the following general formula (I) wherein Y is a hydrogen atom and the like, RA is a hydrogen atom and the like, X is the formula (b3) wherein RB is a hydrogen atom and the like, and the like,

TRICYCLIC COMPOUND

Provided is a tricyclic compound having a PPAR γ agonist activity, which is represented by the general formula (I) wherein Z represents a single bond or the like, Y represents a hydrogen atom, lower alkyl optionally having substituent(s) or the like, X represents a hydrogen atom or the like, A represents aryl or the like, B and C are the same or different and each represents an aromatic carbocycle or the like, R4 - R9 are the same or different and each represents hydrogen or the like, V represents a single bond or the like, R10 and R11 are the same or different and each represents hydrogen or the like, or a pharmaceutically acceptable salt thereof or the like:

Benzimidazole derivatives and their use

Novel imidazole derivatives of the formula (I): STR1 wherein R1 is an optionally substituted alkyl group, R2 and R3 are independently a group capable of forming an anion or a group which can be changed thereinto, ring A is a benzene ring optionally having, besides the group shown by R2, further substituents, and X shows linkage of phenylene group and phenyl group directly or through a spacer whose atomic length is not more than 2 and a salt thereof, show antagonistic actions to angiotensin II, thus being useful as therapeutics for cardiovascular diseases.