Skip to main content
DN

Developing New Drugs for AML and PDAC

The startup develops small-molecule peptide drugs that activate the immune system to enhance anti-tumor activity in cancer patients. Their therapeutics include checkpoint inhibitor peptides that have demonstrated improved efficacy in treating pancreatic cancer, melanoma, and leukemia across multiple preclinical models.

Atlanta, United StatesFounded 20182100+ followers
Updated 3 months ago

Funding

$400K raised to dateRaised to date based on public sources. This may differ from the amount the company actually raised and is based only on what is publicly available on the internet.

Funding rounds are not available yet.

Founders

Product

Problem

In many cancers, tumor cells suppress the immune system by overproducing vasoactive intestinal peptide (VIP), which binds to VPAC1 receptors on cytotoxic T-cells, inhibiting their ability to attack the tumor. Current cancer treatments often fail to fully restore T-cell function in these immunosuppressive environments.

Solution

Cambium Oncology develops first-in-class immunotherapies that target the VIP/VPAC1 signaling axis to re-establish immune surveillance and enhance anti-tumor activity. Their small-molecule VIP-receptor antagonists, such as ANT308 and CAMV-01, block VIP signaling, preventing the suppression of cytotoxic T-cells and allowing them to effectively target and kill cancer cells. This approach aims to improve patient outcomes by restoring the body's natural ability to fight cancer, particularly in tumors with high VIP or VPAC1 expression. Cambium's therapeutics can be used as standalone treatments or in combination with PD-1 blockers for a synergistic effect. Preclinical studies have demonstrated efficacy and safety in animal models of acute myeloid leukemia (AML), pancreatic ductal adenocarcinoma (PDAC), and melanoma.

Target Audience

The primary target audience includes cancer patients with tumors that overexpress VIP, as well as oncologists and researchers seeking novel immunotherapeutic approaches to enhance anti-tumor immunity.

Features

  • Small-molecule antagonists targeting the VIP/VPAC1 signaling pathway
  • Selective blockade of VIP binding to VPAC1 receptors on cytotoxic T-cells
  • Enhanced activation and tumor-killing ability of T-cells
  • Demonstrated efficacy in preclinical models of AML, PDAC, and melanoma
  • Potential for synergistic effects when combined with PD-1 inhibitors
  • Biomarker-driven patient selection based on VIP or VPAC1 expression levels
This profile is AI-generated and may contain inaccuracies.