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Synthesis of sinomenine derivatives with potential anti-leukemia activity.

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Title: Synthesis of sinomenine derivatives with potential anti-leukemia activity.
Authors: Gao, Xiang1 (AUTHOR), Li, Hao-Nan1 (AUTHOR), Liu, Peng-Ju1 (AUTHOR), Long, Xiao-Kang2 (AUTHOR), Guo, Xue-Hai3 (AUTHOR), Hua, Hui-Ming1 (AUTHOR) huimhua@163.com, Li, Da-Hong1 (AUTHOR) lidahong0203@163.com
Source: Journal of Asian Natural Products Research. Dec2025, Vol. 27 Issue 12, p1819-1835. 17p.
Subject Terms: *IN vitro studies, *CLINICAL drug trials, *ALKALOIDS, *MITOCHONDRIA, *RESEARCH funding, *ANTINEOPLASTIC agents, *APOPTOSIS, *CELL proliferation, *BIOLOGICAL products, *IN vivo studies, *CELL cycle, *DESCRIPTIVE statistics, *LEUKEMIA, *PLANT extracts, *CELL lines, *DRUG design, *COMBINED modality therapy, *MOLECULAR structure, *COMPARATIVE studies, *CHROMATOGRAPHIC analysis, *PHARMACODYNAMICS
Abstract: In recent years, with sinomenine hydrochloride as the main ingredient, Qingfengteng had been formulated as various dosage forms for clinical treatment. Subsequent findings confirmed a variety of biological roles for sinomenine. Here, 15 H2S-donating sinomenine derivatives were synthesized. Target hybrids a11 displayed substantial cytotoxic effects on cancer cell lines, particularly against K562 cells, with an IC50 value of 1.36 μM. In-depth studies demonstrated that a11 arrested cell cycle at G1 phase, induced apoptosis via both morphological changes in nucleus and membrane potential collapse in mitochondria. These results indicated a11 exerted an antiproliferative effect through apoptosis induction via mitochondrial pathway. [ABSTRACT FROM AUTHOR]
Database: Academic Search Index
Description
Abstract:In recent years, with sinomenine hydrochloride as the main ingredient, Qingfengteng had been formulated as various dosage forms for clinical treatment. Subsequent findings confirmed a variety of biological roles for sinomenine. Here, 15 H2S-donating sinomenine derivatives were synthesized. Target hybrids a11 displayed substantial cytotoxic effects on cancer cell lines, particularly against K562 cells, with an IC50 value of 1.36 μM. In-depth studies demonstrated that a11 arrested cell cycle at G1 phase, induced apoptosis via both morphological changes in nucleus and membrane potential collapse in mitochondria. These results indicated a11 exerted an antiproliferative effect through apoptosis induction via mitochondrial pathway. [ABSTRACT FROM AUTHOR]
ISSN:10286020
DOI:10.1080/10286020.2024.2327524