Informace o publikaci
SYNTHESIS AND BIOLOGICAL EVALUATION OF BASIC AMINOACETOPHENONE-DERIVED KETIMINES
| Autoři | |
|---|---|
| Rok publikování | 2025 |
| Druh | Další prezentace na konferencích |
| Fakulta / Pracoviště MU | |
| Citace | |
| Popis | Schiff bases are versatile ligands widely used in metal coordination chemistry, capable of forming stable complexes with a wide variety of metal ions. These metal-ligand complexes exhibit extensive therapeutic potential, including antibacterial, antifungal, antiviral, antimalarial, anti-inflammatory, cytotoxic, enzyme-inhibitory, and anticancer properties. Due to their ability to form such complexes, many Schiff bases also play a crucial role in a number of enzymatic reactions. One potential target enzyme is aminopeptidase N (AP-N), a neutral zinc-binding metalloenzyme. Inhibitors of this ubiquitous enzyme may offer effective and broad-spectrum therapeutic applications. Both AP-N and the nuclear factor kappa-B (NF-?B) are critical components involved in various cellular processes, including immune regulation and inflammation. AP-N, which plays a role in peptide metabolism, and NF-?B, a key transcription factor in inflammatory pathways, appear to be functionally connected in the regulation of inflammation and immune response. AP-N may influence NF-?B activation through the metabolism of peptides involved in inflammatory pathways. These two factors may also cooperate in the context of cancer biology and metastasis. The series of basic thiosemicarbazone, semicarbazone, and oxime derivatives of acetophenone with diverse substitution of various symmetrical secondary amines and heterocyclic amines, were synthesized. Compounds showing the most potent inhibitory activity against AP-N (based on IC50 values) were further tested for their ability to inhibit cell proliferation in three different cell lines. These lead compounds are now also being tested for their potential to inhibit the pro-inflammatory transcription factor NF-?B, in an effort to uncover deeper connections between AP-N inhibition and inflammation-related signaling pathways. |
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