A group of researchers have announced they have discovered a new drug combination that can overcome cancer drug resistance, as well as reduce the size of cancerous tumors to a far greater degree than current treatments.
The new approach can also be applied to any type of cancer, researchers from The University of Texas at Austin and Korea University said.
Their study findings were published in the journal Chem on Aug. 23.
“The best part is that our combined drug candidate was so much more effective than one of the most powerful cancer drugs on the market,” Jonathan Sessler, a professor at UT Austin and co-lead author of the study, said in a media release.
“The difference is mind blowing,” he added.
Sessler is himself a multiple cancer survivor who has dedicated his career to seeking cancer treatments.
Sessler and his team are calling the drug they have developed C1, and have filed a patent for it.
In their study titled “Overcoming Drug Resistance by Targeting Cancer Bioenergetics with an Activatable Prodrug,” the team gave their experimental C1 drug to mice with drug resistant tumors. The study found that C1 reduced drug resistance, allowing the chemotherapy drugs to take effect.
‘Gasping for Air’
The way the drug works is related to how cancer cells grow. Cancerous tumors grow and metabolize like an “out-of-shape runner,” researchers explained in a press release.
“[The cancerous tumor] has a hard time catching its breath. It’s growing so fast and burning so much energy that it can’t get enough oxygen.”
Whereas normal cells function on aerobic, or oxygen-requiring, metabolism, early-stage tumor cells operate on a less efficient anaerobic metabolism.
“Just like an out-of-shape runner, gasping for air and experiencing cramps, in this early stage, a tutor’s metabolism is abnormal and its vulnerable, so this is also when many cancer drugs work their best,” the press release read. “But as tumors mature and shift their metabolism, like the runner getting into better shape, they often become drug resistant, a life-threatening twist for patients.”
“When it switches to a more normal metabolism, it develops resistance,” Sessler said. “But if we stop it from switching, we can keep exploiting that vulnerability.”
In the study, the researchers combined the standard chemotherapy drug Doxorubicin (D0x) with a dichloroacetic acid (DCA) subunit—an acid which reverse a cell’s metabolism from aerobic to anaerobic.
Why C1 is so effective, Sessler explained, is that it allows the two active elements reach the cancer cells simultaneously, where the DCA ensures that the cancer cells remain in an anaerobic state reducing the cells’ resistance to Dox.
The researchers found that when mice with tumors were given C1, the tumors became 75 percent smaller after two months compared to mice that were not treated.
Furthermore, the tumors treated with C1 became half the size of the tumors in mice that received the same two drugs but separately.
Tackling Drug Resistance
Drug resistance is a major hurdle cancer researchers and sufferers are currently facing, so if all goes well, the experimental drug C1 may lead the way in overcoming cancer cells’ resistance to Dox, which is sold as Adriamycin.
Another factor that contributes to C1’s efficacy lies in its ability to target the mitochondria of the cancer cells, which is the location where scientists believe the treatment will yield the highest effect, Sessler explained.
Importantly, the experimental C1 drug appeared to show “minimal whole-animal toxicity,” according to the study.
“Right now, a cancer diagnosis is often a death sentence,” Sessler said. “We’d like to see cancer become a chronic disease in our lifetime.”