The scientific basis of high-dose intravenous vitamin C (IVC) therapy in cancer treatment involves several interconnected mechanisms. Vitamin C, known for its antioxidant properties, reaches significantly higher blood levels when administered intravenously. Studies have shown that when administered at supraphysiologic concentrations, ascorbic acid can significantly decrease cell proliferation in a variety of cancer cell lines, including those from prostate, pancreatic, hepatocellular, and colon cancers. This effect is primarily mediated through a chemical reaction that generates hydrogen peroxide, which is cytotoxic to cancer cells. This reaction can lead to the downregulation of specific transcription factors, disruption of iron metabolism, and induction of oxidative DNA damage, leading to cancer cell death​

Another important aspect of high-dose IVC therapy is its potential to enhance the effects of certain chemotherapy drugs. Research has indicated that pharmacological doses of ascorbic acid can improve the efficacy of drugs like arsenic trioxide in ovarian cancer cells and gemcitabine in pancreatic cancer cells. Additionally, high-dose ascorbate has been reported to increase radio sensitivity in cells of glioblastoma multiforme, resulting in greater cell death than from radiation treatment alone.

Animal model studies further support these findings. Tumor growth inhibition has been observed in animal models of pancreatic, liver, prostate, mesothelioma, and ovarian cancers following treatment with pharmacological ascorbate. In some models, the combination of ascorbate with standard cancer treatments, such as gemcitabine or radiation therapy, resulted in greater decreases in tumor volume and weight compared to standard treatments alone, suggesting a synergistic effect.