Researchers at Dartmouth College have found that adding the common blood pressure drug telmisartan to a widely used cancer treatment boosted its effectiveness.

The medication enhanced the cancer-fighting power of olaparib, a targeted therapy known as a PARP inhibitor, according to the laboratory and mouse studies. Olaparib works by blocking the PARP enzyme, which helps repair damaged DNA in cells. By inhibiting this enzyme, the drug makes it harder for cancer cells to fix themselves, leading to cell death — especially in cancers with genetic mutations such as BRCA1 or BRCA2.

The combination of telmisartan and olaparib was effective even in cancers that do not carry these classic BRCA mutations, according to Study Finds. Researchers discovered the drug pairing activates an entirely different pathway, using the immune system’s own alarm signals to help destroy cancer cells.

The inexpensive blood pressure drug appears to strip away a protective protein known as PD-L1 from the surface of cancer cells, allowing olaparib to enter more easily and attack tumors. Telmisartan also improved olaparib’s effectiveness even when PD-L1 was not present, potentially expanding the benefits of the combination.

Scientists believe telmisartan works by triggering a molecular alarm system inside tumor cells called STING, or Stimulator of Interferon Genes. The STING pathway plays a key role in the body’s innate immune response.

When activated, STING helps the immune system detect abnormal or damaged DNA within cells and triggers the production of signaling proteins known as interferons. These interferons alert and mobilize immune cells to attack cancer or fight infections. In cancer therapy, activating this pathway may enhance the immune system’s ability to target and eliminate tumors.

When telmisartan and olaparib were used together, production of type 1 interferons increased significantly compared to either drug alone. However, the researchers found the treatment depends on a fully functioning immune system. In mice lacking T cells and B cells, the drug combination was not effective.

The researchers hope future human trials will confirm these findings, potentially offering a new way to treat cancer using medications that are already widely available and FDA-approved.