ArticleSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society2026
Ramucirumab induces apoptosis in Caco-2 cells via mitochondrial impairment and caspase activation.
Article in Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society, 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
Ramucirumab, a monoclonal antibody that targets vascular endothelial growth factor receptor-2 (VEGFR-2), is primarily known for its ability to inhibit angiogenesis in a variety of cancer types. Its direct cytotoxic mechanisms in colorectal cancer cells, especially those related to mitochondrial dysfunction and reactive oxygen species (ROS)-mediated apoptosis, are inadequately elucidated. This work aims to examine the involvement of mitochondrial dysfunction, oxidative stress, and caspase activation in mediating ramucirumab induced cytotoxicity in Caco-2 cells. MTT (3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide) and lactate dehydrogenase (LDH) tests were used to measure cell viability and cytotoxicity, respectively by exposing Caco-2 cells to ramucirumab for 24 h. Flow cytometry was used to analyze apoptosis and cell cycle distribution. Hoechst 33342, rhodamine 123 and carboxy-H
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