A novel cancer treatment that uses a weakened herpes virus to attack tumors cured a test patient’s cancer during an experimental trial. The drug, called RP2, completely obliterated the oral cancer of a man who signed up for a speculative treatment as a last resort.
The 39-year-old told British news media that he had suffered from cancer of the salivary glands, which continued to grow despite attempts at treatment. He was preparing for end of life when he decided to try a last-ditch effort at the Institute of Cancer Research in the UK.
Since receiving the drug in 2020, Krzysztof Wojkowski of west London has been cancer-free; but researchers aren’t fully convinced that they have found a “miracle” drug just yet.
Other patients in Wojkowski’s trial saw their tumors shrink, but the majority did not experience a significant change. Thirty percent of patients who took the trial drug alone saw some benefit, and about 23 percent of patients who took the drug as part of a combined treatment plan appeared to benefit, as well. Promising, but not groundbreaking.
One significant “positive” of the trial, though, was the lack of side effects RP2 produced. Traditional cancer therapies like chemo or radiation wreak havoc on the body, but RP2’s primary side effect was a bit of tiredness.
“We’ll see some more studies done in the very near future, and I’m excited — certainly not disheartened or skeptical,” Jonathan Zager of the Moffitt Cancer Center told Insider.
Other herpes drugs have been used to help cure skin cancer since 2015
So how does RP2 work exactly? It is a modified herpes virus (you know, the virus that causes cold sores) that supposedly only targets tumors. It is also injected directly into tumors, rather than working systemically like most therapies.
Once it has infiltrated, the virus “replicates itself until the cancer cell explodes.” What’s especially unique about RP2 is the “one-two punch” it brings against tumors — not only destroying the cells, but also rallying the immune system to attack what’s left, lead researcher Kevin Harrington said in a news release.
The results are even more important considering that the patients recruited for clinical trials typically faced very low odds of survival. Many trial recipients, like Wojkowski, had already exhausted traditional therapies and surgeries when they heard about RP2.
“When we have tumors that are heavily pretreated and they respond favorably — to RP2 or [similar therapies]— that’s even more food for thought, in the sense that now we have tumors that were resistant to treatment and are responding,” said Zager, who has treated hundreds of skin cancer patients with a herpes variant similar to RP2 since 2015.
According to Harrington, RP2 may work even better than prior drugs, based on early indicators.
“[RP2] had other modifications to the virus so that when it gets into cancer cells it effectively signs their death warrant,” Harrington proclaimed.