Vidac Pharma publishes results of next-generation drug candidate tests in human and murine tumor models

London (UK), July 25, 2024 (07:30 CET) – Vidac Pharma Holdings Plc. (Hamburg and Stuttgart: T9G; ISIN:GB00BM9XQ619; WKN: A3DTUQ), a clinical-stage oncology biopharmaceutical company pioneering a novel class of cancer treatments, today announces that promising results of its study with VDA-1275 in multiple mouse cancer and human cellular organoid models of solid tumors are now available online, as a preprint submitted to peer review. The study showed that VDA-1275 showed statistically significant efficacy as a monotherapy, as well as synergistic effects in combination with two standard-of-care cancer treatments, and that it moreover induced an immunologic response.

The main findings of the study were that VDA-1275:

• reinstates apoptosis (programmed cell death),
• halts rapid proliferation of cancer cells,
• reduces the hyper-glycolytic metabolism typical of tumors, a process that produces the main fuel for the rapid proliferation of cancer cells,
• triggers an immunologic response by inducing anti-tumor macrophages and inhibits tumor-promoting macrophages and promoting anti-tumor memory cells,
• increases survival in a murine colorectal cancer model in a statistically significant way,
• demonstrates a synergistic effect in combination with widely used anti-cancer drugs in a 3D organoid model of human liver cancer.

“These results provide evidence that VDA-1275 might in the future be used as a standalone drug, or in combination therapy that might allow more effective and safer treatment of patients with solid tumors. Vidac’s small molecules target the abnormal positioning of the HK2 enzyme, which is a central cause in cancer, but not its everyday benign use in the cellular metabolism. This means our drugs might have fewer side-effects,” said Max Herzberg, CEO at Vidac Pharma.

VDA-1275 as well as the more advanced VDA-1102, now in Phase 2b clinical studies to treat advanced actinic keratosis and Phase 2 testing in cutaneous T-cell lymphoma, disrupt the interaction between hexokinase 2 (HK2) and the voltage-dependent anion channels (VDACs) in mitochondria. Cancer cells overexpress HK2, which catalyzes the first step of the glucose metabolism necessary to fuel tumor growth. HK2 blocks the channels, which prevents apoptosis, supports cancer cell proliferation, and suppresses immune responses. The resulting high concentrations of lactate lead to an acidic and low-oxygen micro-environment in the cancer cells and the nearby tumor microenvironment which fosters cancer growth. Clinical data for Vidac’s first-generation metabolic checkpoint modulator candidates have shown effects in halting cancer cell proliferation and restoring immune-sensitivity and apoptosis.