The drug, developed by researchers at John Hopkins Kimmel Cancer Center, in collaboration with Danish researchers, is able to move - undetected by normal cells - through the bloodstream until activated by specific cancer proteins.
According to the researchers, a three-day course of the new drug, called G202, reduced the size of human prostate tumors grown in mice by an average of 50% in 30 days.
In addition, G202 was found to be more effective at reducing tumors than the chemotherapy drug docetaxel. They found that G202 reduced 7 out of 9 human prostate tumors in mice by more than 50% in 21 days, while docetaxel only reduced 1 out of 8 tumors by more than 50%.
Furthermore, in models of human breast cancer, bladder cancer, and kidney cancer, G202 was shown to produce at least 50% regression.
Physicians at Johns Hopkins, University of Wisconsin and the University of Texas-San Antonio then conducted a phase I clinical trial in order to evaluate the safety of G202 in 29 patients with advanced cancer. The researchers are currently planning a phase II trial to test G202 in patients suffering from liver cancer and prostate cancer.
G202 is made from a weed called Thapsia garganica that grows naturally in the Mediterranean region. The plant produces a product called thapsigargin, that has been known for thousands of years to be toxic to animals.
Samuel Denmeade, M.D., professor of oncology, urology, pharmacology and molecular sciences, explained:
"Our goal was to try to re-engineer this very toxic natural plant product into a drug we might use to treat human cancer. We achieved this by creating a format that requires modification by cells to release the active drug."
The researchers chemically modified thapsigargin and created a form that acts like a hand grenade with an intact pin. After G202 is injected, it moves through the bloodstream until it locates cancer cells and hits a protein called prostate-specific membrane antigen (PSMA). PSMA then "pulls the pin" on G202, by releasing cell-killing agents into the tumor and blood vessels that feed it.
Specifically, G202 inhibits the function of the SERCA pump, a protein that is vital for cell survival. According to the researchers, as G202 is targeted to the SERCA pump, it will be difficult for tumor cells to become resistant to the drug, as they cannot stop making the protein.
John Isaacs, Ph.D., professor of oncology, urology, chemical and biomedical engineering at Johns Hopkins said: "The exciting thing is that the cancer itself is activating its own demise."
Written by Christine Kearney