Propanc Biopharma’s CSO Predicts PRP Could Solve Problem That Impacts Response Rate of Immune Checkpoint Inhibitors Treating Solid Tumors

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British Journal of Cancer Concludes Tumor cell-intrinsic PD-L1 function promotes EMT

MELBOURNE, Australia, July 17, 2024--(BUSINESS WIRE)--Propanc Biopharma, Inc. (OTC Pink: PPCB) ("Propanc" or the "Company"), a biopharmaceutical company developing novel cancer treatments for patients suffering from recurring and metastatic cancer, today announced that the Company’s lead asset, PRP, could solve the problem that impacts the response rate of immune checkpoint inhibitors treating PD-L1-High (Programmed Death-Ligand 1) solid tumors, such as lung cancer. Propanc’s Chief Scientific Officer and Co-Founder Dr Julian Kenyon, MD, MB, ChB, predicts that pretreatment of PD-L1-high solid tumors with PRP as a combinatorial approach could reverse the promotion of epithelial to mesenchymal transition (EMT) pathways induced by PD-L1, a fundamental process by which malignant cells promote tumor growth and metastasis. Tumor cells that undergo the EMT are motile and invasive, spreading and seeding new tumors, as well as become immortal, no longer dying off naturally. They are also non-dividing, which means they are resistant to standard treatment approaches.

Use of immune therapy, such as checkpoint inhibitors, have become increasingly widespread for treating solid tumors as an effective method to stop the immune system from turning off before cancer is eliminated completely. The immune system relies on T cells to fight cancer. These specialized cells are extremely powerful and have the potential to damage healthy cells. The Immune Checkpoint Inhibitors Market is US$47.22 Billion in 2023, and expected to reach US$158.26 Billion by 2031 according to FutureWise Research. Despite growing popularity, response rates range between 15 to 30% in most solid tumors. As a result, scientific research is being conducted to consider how to improve response rates.

A recent study published in the British Journal of Cancer (May, 2024), highlights that EMT induced by tumor cell-intrinsic (i.e., belonging naturally) PD-L1 signaling predicts a poor response to immune checkpoint inhibitors in PD-L1-High lung cancer. PD-L1 is a protein that acts as a kind of "brake" to keep the body’s immune system under control. PD-L1 may be found on some normal cells and in higher-than-normal amounts on some types of cancer cells. When PD-L1 binds to another protein called PD-1 (Programmed Death protein, found on T cells), it keeps T cells from killing the PD-L1-containing cells, including cancer cells. Anticancer drugs called immune checkpoint inhibitors bind to PD-L1 and block its binding to PD-1. This releases the ‘brakes’ on the immune system and leaves T cells free to kill cancer cells. "The implication is that PRP will enable PD-L1 non responders to become responders," according to Dr Kenyon.