SCIENCE

Vaxeal’s unique and innovative scientific research and its improved understanding of immunological mechanisms, based on 20 years of exclusive research, are at the heart of Vaxeal’s mission to deliver cutting-edge therapies.

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Rationale of Cancer Immunotherapy targets

Vaxeal target selection was based on expression and tumour cell vital functions. Survivin and Cyclin B1 are undetectable or transiently expressed in most normal adult tissues.

They are both over-expressed in most human cancers, and play vital functions in tumor cells. Both targets are associated with a poor prognosis.

Rationale of Long Synthetic Peptides

Long peptides are vaccines able to generate strong and sustainable specific CD4+ and CD8+ T-cell responses in humans, irrespective of individual Human Leukocyte Antigen (HLA) types. In addition, Long Synthetic Peptides (LSPs) have the strong advantage to be safe and easy to manufacture compared to “biological vaccines” created from living organisms. The efficacy of the cancer immunotherapies is further increased by their formulation with new adjuvants, and fixed combination with antibodies that modulate tumour-induced immune suppression (Immune Checkpoint Blockades).

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Rationale of fixed combination with Immune Checkpoint Blockades (ICBs)

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ICBs overcome tumor-mediated immunosuppressive mechanisms: Modulate proliferation and suppressive functions of immunosuppressive cells (Regulatory CD4+ T-cells (Treg), Myeloid-derived suppressor cells or MDSCs).

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ICBs boost vaccine-induced anti-tumoral immune responses: Improve proliferation, functions and therapeutic efficacy of the anti-tumor T-cell responses induced with the cancer vaccine.

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Fixed combination of therapeutic vaccines with ICBs have the potential to reduce immune-related adverse events of ICBs: Reduction of ICB doses and treatment cycles.

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Fixed combination of therapeutic vaccines with ICBs have the potential to increase clinical efficacy of cancer: Induction of specific and long-lasting anti-tumoral CD4+ and CD8+ T-cell responses; Block immune checkpoint pathways suppressing the anti-tumoral immune response in the tumor microenvironment.

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