Vidac Pharma Holdings Plc., a clinical-stage oncology biopharmaceutical company, today announced promising results for its drug candidate VDA-1275 in multiple mouse cancer and human cellular organoid models of solid tumours.
VDA-1275 showed statistically significant efficacy as a monotherapy, as well as synergistic effects in combination with two standard-of-care cancer treatments: sorafenib, a kinase inhibitor and cisplatin, a widely used chemotherapy drug.
The study also showed that VDA-1275 induced an immunologic response, inducing anti-tumour macrophages and memory T-cells, and inhibiting tumour-promoting macrophages.
The company will present these findings on 28 February, at the Sachs 17th Annual European Life Sciences CEO Forum.
“It is an exciting moment for me to share the results for VDA-1275, which is up to a hundred times more potent than our other drug candidate, VDA-1102,” Vidac Pharma Chief Executive Officer Max Herzberg said.
“VDA-1275 is showing all the signs of being a potent inhibitor of cancer cell proliferation and being capable of reinstating programmed cell death, or apoptosis. The massive synergistic effect in combination with widely used cancer drugs offers hope that this selective therapy might become a routine part of combination treatments and reduce side effects of traditional chemotherapy.”
As a stand-alone treatment, VDA-1275 significantly increased survival in a murine colorectal cancer model, with a survival benefit similar to Opdivo in a head-to-head comparison.
Human and murine 2D and 3D cell culture models showed statistically significant survival in lung, prostate and colon cancer.
In a 3-D organoid model of human liver cancer, VDA-1275 reduced the concentrations of sorafenib and cisplatin needed to achieve IC50 cancer cell viability by 50% and 95%, respectively.
Finally, VDA-1275 triggered an immune response by inducing anti-tumour M1 macrophages and inhibiting tumour-promoting M2 macrophages. The molecule also induced a shift of mouse CD8+ effector T-cells to memory cells without a negative effect on T Cells survival.
The company is planning to published the results in a peer-reviewed publication.
Both VDA-1275 and the more advanced VDA-1102, now in Phase 2b testing of advanced actinic keratosis and Phase 2 testing of cutaneous T cell lymphoma, disrupt the interaction between hexokinase 2 (HK2) and the voltage-dependent anion channels (VDACs) in mitochondria.
Cancer cells over express HK2, which catalyses the first step of the glucose metabolism necessary to fuel tumour growth.
HK2 blocks VDACs, which prevents apoptosis, supports cancer cell proliferation and suppresses immune responses. Clinical data for Vidac’s first-generation metabolic checkpoint modulator candidates have shown powerful effects in halting cancer cell proliferation and restoring immune-sensitivity and apoptosis.
