170282-53-8

Upstream product

• 1711-10-0 3-iodobenzoyl chloride 
• 1117-97-1 N,0-dimethylhydroxylamine 
• 6638-79-5 N,O-dimethylhydroxylamine*hydrochloride 
• 618-51-9 3-Iodobenzoic acid 

Downstream Products

• 406162-36-5 [4-(3-chlorophenyl)-2-methoxy-6-quinolinyl](3-iodophenyl)-methanone 
• 717900-62-4 (4-chloro-7-cyclopentyl-7H-pyrrolo[2,3-d]pyrimidin-5-yl)-(3-iodo-phenyl)-methanone 
• 1602731-56-5 C₂₂H₂₅N₅O 
• 1602732-13-7 C₂₂H₁₉N₅O₃S 
• 1602732-15-9 C₂₅H₂₂N₆O 
• 1602732-17-1 C₂₁H₂₀N₆OS 
• 1602732-20-6 C₂₁H₁₇N₅O 
• 1602732-22-8 C₂₂H₁₉N₅O₂ 
• 1602732-24-0 C₂₂H₁₉N₅O 
• 1602732-27-3 C₂₁H₁₆FN₅O 
• 1602732-29-5 C₂₁H₁₆BrN₅O 
• 1602732-31-9 C₂₁H₁₆IN₅O 
• 1602732-33-1 C₂₁H₁₈N₆O 
• 1602732-35-3 C₂₁H₁₆N₆O₃ 

Relevant academic research and scientific papers

Development of a p38α-selective radioactive probe for qualitative diagnosis of cancer using SPECT

Objective: p38 mitogen-activated protein (MAP) kinase (p38α) has drawn attention as a new target molecule for the treatment and diagnosis of cancer, and its overexpression and activation have been reported in various types of cancer. In this study, a single photon emission computed tomography (SPECT) imaging probe of p38α was developed to noninvasively image p38α activity for effective qualitative diagnosis of cancer. Methods: Pyrrolepyridine derivatives, m-YTM and p-YTM, were designed and synthesized based on the structure of the p38α-selective inhibitor. Radioactive iodine-labeled m-YTM, [125I]m-YTM, was synthesized because m-YTM greatly inhibited the phosphorylation of p38α upon examining the inhibitory effects of the compounds. After investigating the binding affinity of [125I]m-YTM to the recombinant p38α, a saturation binding experiment using activated p38α and inactive p38α was performed to determine the binding site. Uptake of [125I]m-YTM into various cancer cell lines was investigated, and the pharmacokinetics was evaluated using tumor-bearing mice. Results: The inhibitory activity of m-YTM was approximately 13 times higher than that of SB203580, a p38α-selective inhibitor. The binding site of [125I]m-YTM was estimated to be the p38α activating site, similar to that of SB203580, because the [125I]m-YTM bound strongly to both activated p38α and inactive p38α. Various different cancer cells incorporated [125I]m-YTM; however, its accumulation was significantly reduced by treatment with SB203580. Pharmacokinetics study of [125I]m-YTM in B-16 tumor-bearing mice was examined which revealed high accumulation of radioactivity in tumor tissues. The ratios of radioactivity in the B-16 tumor to that in blood were 3.1 and 50 after 1 and 24?h, respectively. The ratio of radioactivity in the tumor to that in blood in the tumor-bearing mice generated using other cancer cell lines was also ≥ 1 at 1?h after the administration of the probe. Conclusions: This study suggests that [123I]m-YTM has potential as a p38α imaging probe effective for various cancer types.

Synthesis of Perfluoroalkyl-Substituted Vinylcyclopropanes by Way of Enhanced Neighboring Group Participation

A simple, high yielding, two-step, one-pot protocol for the preparation of trifluoromethyl-substituted vinylcyclopropanes from α-CF3 homoallyl alcohols is disclosed. Destabilization of the cationic intermediate by the electron-withdrawing CF3 group greatly enhances neighboring group participation of the alkene, allowing ring closure to predominate. The reaction can be extended to the difluoromethyl and pentafluoroethyl group, enabling the preparation of a diverse array of fluoroalkyl-substituted vinylcyclopropanes. A diverse array of fluoroalkyl-substituted vinylcyclopropanes are prepared in a simple, high-yielding, two-step, one-pot protocol by means of cationic ring-closure.

Identification of novel SIRT2-selective inhibitors using a click chemistry approach

A series of 114 SIRT inhibitor candidates was assembled using 'click chemistry', by reacting two alkynes bearing 2-anilinobenzamide pharmacophore with 57 azide building blocks in the presence of Cu(I) catalyst. Screening identified two SIRT2-selective inhibitors, which were more SIRT2-selective than AGK2, a known SIRT2 inhibitor. These findings will be useful for further development of SIRT2-selective inhibitors.

IMIDAZOLE DERIVATIVE

A CB2 receptor modulator comprising an imidazole derivative represented by the general formula (I): [wherein, R1 represents optionally substituted lower alkyl or the like; R2 represents optionally substituted cycloalkyl or the like; R3 represents optionally substituted aryl or the like; and n represents an integer of 0 to 3] or a pharmaceutically acceptable salt thereof as an active ingredient, and the like are provided.

NOVEL IMIDAZOLE DERIVATIVES AND THEIR USE AS PHARMACEUTICAL AGENTS

Compounds of the general formula (I) are valuable therapeutics for the treatment of cancer and cancer related diseases.

PYRROLOPYRIMIDINE DERIVATIVES

The invention relates to compounds of the formula 1or a pharmaceutically acceptable salt, prodrug or hydrates thereof, wherein Q, A, L, R1, R2 and R3 are as defined herein. The invention also relates to pharmaceutical compositions containing the compounds of formula 1 and to methods of treating hyperproliferative disorders in a mammal by administering the compounds of formula 1.

2-(2,6-dichlorophenyl)-diarylimidazoles

The invention is directed to compounds of formula (I), which are valuable therapeutics for the treatment of cancer and related diseases.

Substituted phenyl compounds

Compounds of formula (I) are described wherein R1is hydrogen, -(lower alkyl)q(CO2R6or OH), —CN, —C(R7)═NOR8, NO2, —O(lower alkyl)R9, —C≡C—R10, —CR11═C(R12)(R13), —C(═O)CH2C(═O)CO2H, —CO(R14), alkylthio, alkylsulphinyl, alkylsulphonyl, carbamoyl, thiocarbamoyl, substituted carbamoyl, substituted thiocarbamoyl, sulphamoyl or an optionally substituted nitrogen-containing ring, m, n, o and p are independently zero or 1 and R2, R3, R4and R5are various groups; and physiologically acceptable salts, N-oxides and prodrugs thereof. The compounds have endothelin antagonist activity and are useful as pharmaceuticals.