Mechanism of Action - Part 1

PTS disrupts lipid rafts in cancer cells, blocking survival pathways and inducing apoptosis.

 

【Left - cancer cells without PTS treatment】：Cancer cells (such as lung cancer, liver cancer, breast cancer, head and neck cancer, prostate cancer, etc.) have more lipid raft structures on the cell membrane than normal cells, resulting in an active AKT-mTOR-p70S6K mechanism, causing cancer cell proliferation.

【Right - cancer cells with PTS treatment】：When PTS enters cancer cells, PTS causes abnormal cholesterol metabolism pathways in cancer cells, which interfere with the stability of the lipid raft structure, resulting in the blockage of downstream cancer cell survival, proliferation, and metastasis pathways (AKT-mTOR-p70S6K) and eventually leads to apoptosis. Therefore, when PTS enters cells, it has a greater impact on cancer cells than normal cells.

Paper publish: https://pubmed.ncbi.nlm.nih.gov/30555320/

   

Part 2

 

PTS disrupts cholesterol recycling in cancer cells, blocking survival pathways, and activating autophagy, ultimately leading to apoptosis.

   

     In the 2021 study, it was further confirmed that PTS interferes with cholesterol recycling to the cell membrane, resulting in a decrease in the cholesterol content of the cell membrane of lung cancer cells, which in turn interferes with the stability of the lipid raft structure, resulting in the blockage of downstream cancer cell survival, proliferation, and metastasis. At the same time, it also activates autophagy, which eventually leads to apoptosis of cancer cells.

Paper publish: https://www.mdpi.com/1420-3049/26/19/5967

    

Part 3

   

PTS downregulates CA9 and HIF-1α, modulates the tumor microenvironment, and enhances the efficacy of PD-1 therapy by disrupting cancer cell survival pathways.

    

     Cancer cells have more abundant CA9 on the cell membrane than normal cells, such as lung cancer, liver cancer, H&N cancer, breast cancer, and melanoma, resulting in an active PI3K-AKT-HIFα mechanism, causing cancer cell proliferation and acidification of the tumor microenvironment. PTS upregulated the expression of apoptosis-related proteins and downregulated CA9, HIF-1α, and VEGF proteins, possibly through modulation of p38 MAPK and ERK1/2 phosphorylated proteins. PTS can bind to CA9 directly to modulate the tumor microenvironment, exhibiting synergistic effects when combined with immune-checkpoint inhibitor αPD-1 therapy.

Paper publish: https://www.sciencedirect.com/science/article/pii/S0753332223013318

    

Part 4

    

Through intratumoral injection, PTS selectively targets tumor cells, leading to apoptosis and necrosis while sparing normal cells.

   

     Through the intratumoral injection route, PTS greatly reduces the impact on surrounding normal cells, and eventually destroys tumor cell lysosomes and mitochondria, resulting in apoptosis and necrosis of tumor cells.

Paper publish: https://pubmed.ncbi.nlm.nih.gov/26302210/