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36 NAD + -dependent cancer cell proliferation and metastasis Given the massive demand for NAD + to support the metabolism reprogramming, the genome integrity and gene transcription in tumorigenesis, cancer cells enhance the capacity of NAD + production through various pathways

In pre-clinical in-vitro and animal model studies, PNC-27 has demonstrated a range of significant oncological findings: Broad cancer cell selectivity demonstrated cytotoxicity against human metastatic colon adenocarcinoma, transformed rat brain capillary endothelial cells, cervical carcinoma, metastatic breast carcinoma, non-small cell lung carcinoma, osteosarcoma, pancreatic carcinoma, ovarian cancer, and multiple haematological malignancies while showing no effect on untransformed normal cell lines or human haematopoietic stem cells from cord blood p53-independent activity PNC-27 kills both MCF-7 breast cancer cells (expressing wild-type p53) and MDA-MB-157 cells (homozygously p53-deficient), as well as K562 leukaemia cells (p53-null) confirming its mechanism does not require functional p53 signalling Mitochondrial disruption beyond plasma membrane pore formation, PNC-27 enters cancer cells and disrupts mitochondrial membranes, confirmed by IEM with gold-labelled anti-PNC-27 antibody on cancer cell mitochondria