A patented approach to restoring chemotherapy effectiveness in colorectal and other cancers where treatment resistance is driven not by tumor genetics, but by bacteria. DnaK Therapeutics targets the bacterial protein that shields cancer cells from apoptosis.
DnaK inhibitors block the bacterial protein that suppresses p53, restoring the tumor's natural apoptosis pathway and allowing standard chemotherapy to work as intended.
Most colorectal cancer research focuses on the tumor itself. DnaK Therapeutics starts with a different question: what if the bacteria living inside the tumor are the reason standard chemotherapy stops working?
Certain bacteria found within colorectal tumors produce the DnaK heat shock protein in large quantities. These Cancer Associated Bacteria (CAB) create a microenvironment that protects tumor cells from both the immune system and cytotoxic agents.
The bacterial DnaK protein interferes directly with p53, the body's primary tumor suppression pathway. When p53 is blocked, cancer cells are unable to initiate apoptosis, meaning standard chemotherapy drugs like 5-FU and oxaliplatin lose their effectiveness.
DnaK Therapeutics has developed patented inhibitors that block the DnaK protein before it can suppress p53. When combined with established chemotherapy agents, the inhibitors restore the cancer cell's apoptosis pathway, making treatment-resistant tumors responsive again.
DnaK Therapeutics is advancing three parallel development tracks. Each addresses a distinct aspect of the CAB-driven chemotherapy resistance problem, with the goal of bringing both a therapeutic and a companion diagnostic to clinical validation.
Identifying, refining, and patenting small molecule inhibitors that specifically target the bacterial DnaK protein. Current focus: optimizing binding affinity and minimizing off-target effects in colorectal cancer models.
Preclinical studies combining DnaK inhibitors with 5-FU and oxaliplatin, the standard-of-care agents for colorectal cancer. Primary outcome: demonstrating restored tumor cell apoptosis and reduced treatment resistance.
Developing a diagnostic test to measure DnaK concentration in tumor samples. This test would stratify patients by CAB burden, enabling oncologists to identify who is most likely to benefit from DnaK inhibitor therapy before treatment begins.