ArticleBioconjugate chemistry2026
Development of a Homogeneous Trastuzumab-Triptolide Conjugate for Targeted Therapy of HER2-Overexpressing Ovarian Cancer.
Article in Bioconjugate chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Ovarian cancer remains a lethal malignancy due to chemoresistance and toxicity, which limits the dose of chemotherapy that can be used, necessitating the development of more targeted therapies such as antibody-drug conjugates (ADCs). However, conventional ADCs suffer from heterogeneity. This study aimed to develop a stable, homogeneous ADC by utilizing a bifunctional dibromomaleimide (DBM) linker to cross-link antibody cysteine residues via disulfide-bridging. A DBM linker was synthesized from 3,4-dibromofuran-2,5-dione and bound to the cytotoxic agent triptolide. This triptolide payload was then conjugated to trastuzumab via site-specific disulfide rebridging to yield a homogeneous trastuzumab-triptolide conjugate to target human epithelial growth factor receptor 2 (HER2) on ovarian cancer cells. The study evaluated the ADC's efficacy against SKOV-3 (high HER2 expression) and OVCAR-8 (low HER2 expression) cell lines. The results showed that the ADC was slightly more potent in SKOV-3 cells, yielding lower IC50 values compared to OVCAR-8. Mechanistic studies of the ADC via flow cytometry revealed that the ADC induced significant apoptosis and cell cycle arrest, characterized by a concentration-dependent increase in Caspase-3/7 expression and distinct alterations in cell population distribution. Furthermore, ADC treatment led to a concentration-dependent decrease in HER2 levels in SKOV-3 cells, confirming successful targeting. The study demonstrates that converting conventional maleimides into bifunctional DBM linkers allows the production of a homogeneous ADC via disulfide-bridging. This approach offers a promising strategy for developing potent anticancer therapeutics with improved selectivity for HER2-overexpressing ovarian cancers.
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