ML162 and Neoplasms

ML162 has been researched along with Neoplasms* in 2 studies

Other Studies

2 other study(ies) available for ML162 and Neoplasms

ArticleYear
Discovery of a Potent Glutathione Peroxidase 4 Inhibitor as a Selective Ferroptosis Inducer.
    Journal of medicinal chemistry, 2021, 09-23, Volume: 64, Issue:18

    Potent and selective ferroptosis regulators promote an intensive understanding of the regulation and mechanisms underlying ferroptosis, which is highly associated with various diseases. In this study, through a stepwise structure optimization, a potent and selective ferroptosis inducer was developed targeting to inhibit glutathione peroxidase 4 (GPX4), and the structure-activity relationship (SAR) of these compounds was uncovered. Compound

    Topics: Acetanilides; Animals; Antineoplastic Agents; Cell Line, Tumor; Enzyme Inhibitors; Ferroptosis; Lipid Peroxidation; Mice; Molecular Structure; Neoplasms; Phospholipid Hydroperoxide Glutathione Peroxidase; Structure-Activity Relationship; Tumor Burden; Xenograft Model Antitumor Assays

2021
Design and synthesis of Pictet-Spengler condensation products that exhibit oncogenic-RAS synthetic lethality and induce non-apoptotic cell death.
    Bioorganic & medicinal chemistry letters, 2012, Sep-01, Volume: 22, Issue:17

    A series of Pictet-Spengler condensation derivatives (tetrahydro-β-carbolines) was designed, synthesized and evaluated for lethality against a panel of seven cancer cell lines. Seven compounds (2a, 13, 20, 21, 27, 29 and 34) showed lethality in at least five cell lines. Among these, compound 27 showed a unique selectivity towards oncogenic-RAS expressing BJ-TERT/LT/ST/RAS(V12) tumor cells, compared to non-transformed BJ-TERT cells. Further investigation revealed that 27 induces cell death without activation of caspases. This represents a useful new probe of non-apoptotic cell death and oncogenic-RAS synthetic lethality.

    Topics: Antineoplastic Agents; Carbolines; Cell Death; Cell Line, Tumor; Cell Survival; Drug Design; Gene Expression Regulation, Neoplastic; Genes, ras; Humans; Neoplasms

2012