Use of compounds of formula (I) in the manufacture of a medicament for use in treating a disorder mediated by histone deacetylase: wherein the symbol ---- represents a single bond or a double bond or the symbol ---- R6 and R8 together represent cyclopropyl and R1 to R8 W, X and Y are as defined herein; and pharmaceutically acceptable salts thereof. Also disclosed are compounds for such uses. The compounds are useful in the treatment of cancers. They may be utilised in combination therapies with DNA methylation inhibitors and other anti cancer agents.
[EN] BIOACTIVE PRE-TUBULYSINS AND USE THEREOF<br/>[FR] PRÉ-TUBULYSINES BIOACTIVES ET LEUR UTILISATION
申请人:UNIV SAARLAND
公开号:WO2010034724A1
公开(公告)日:2010-04-01
The invention relates to bioactive pre-tubulysin derivatives, their preparation and pharmacological use.
该发明涉及生物活性的前土霉素衍生物,其制备和药理学用途。
Method of treating resistant tumors
申请人:Wyeth Holdings Corporation
公开号:US20040121965A1
公开(公告)日:2004-06-24
The invention provides a method of treating or inhibiting the growth of or eradicating a tumor in a mammal in need thereof wherein said tumor is resistant to at least one chemotherapeutic agent which method comprises providing to said mammal an effective amount of a compound of Formula II or a pharmaceutically acceptable salt thereof.
Spectral study of phosphonium salts synthesized from Michael acceptors
作者:Elleuch Haitham、Ferid Yaccoubi
DOI:10.1080/10426507.2022.2150854
日期:——
Abstract The synthesis of new phosphonium salts derived from Michael acceptors via a one-pot reaction process and the study of their NMR characteristics is described. The simple and rapid 1,4 addition of triphenylphosphine to the Michael acceptors in the presence of HBr (48%) (5 equivalents) was carried out at room temperature to give the corresponding phosphonium salts with excellent yields.
In this work, five novel phosphonium salts derived from the Michaelreaction were screened for their antiplatelet activity. Our findings revealed that compounds 2a, 2b, 2c, and 2d significantly inhibit platelet aggregation triggered by ADP or collagen (P < 0.001). Notably, compound 2c inhibited the arachidonic acid pathway (P < 0.001). Moreover, the selected compounds reduce CD62-P expression and inhibit