The Problem

Cancer cells produce a small peptide called VIP that suppresses the function of cytotoxic T-cells and prevents them from attacking tumor cells.

VIP binds to the VPAC1 receptors on cytotoxic T-cells thereby inhibiting a tumor-killing activation signal.

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Our Solution

• Cancer cells over-express VIP creating immunosuppression that limits anti-cancer immunity.
• Activated T cells up-regulate VIP receptors.
• VIP is a conserved pathway in evolution, and Cambium's VIP receptor antagonists activate human T cells and mouse T cells, facilitating clinical translation.
• Cambium’s VIP-receptor antagonist drug enhances immunological attack on cancer in multiple mouse cancer model systems.
• No toxicity signal of the VIP receptor antagonists in mice.

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A pharmacological dose of ANT308 potentiates the activation of human T cells

Predicted binding affinities of novel VIP-R antagonists to human VIP receptors correlate with the survival of leukemic mice treated with these drugs.