A new drug which blocks cancer repairing its DNA halted the growth of tumours in more than half of patients in a clinical trial.
The 21 people treated had a range of advanced cancers including breast, bowel and prostate tumours and had already been treated with other medicienes.
The drug, which is currently known by the code BAY1895344, stopped tumour growth in eight patients and shrunk the tumours of another four, according to results published in journal Cancer Discovery on Tuesday.
Researchers said the early-stage trial, led by the Institute of Cancer Research (ICR) and the Royal Marsden NHS Foundation Trust, highlights the potential of a new class of drugs, known as ATR inhibitors, which work by blocking a key molecule involved in repairing DNA.
Professor Paul Workman, chief executive of the ICR, said: “It is exciting to see a new class of precision medicine showing such promise in early trials.
“At the ICR, we have pioneered ways of treating cancer by exploiting the weaknesses that tumours often have in repairing their DNA. I am hopeful that later-stage trials will show that this new class of ATR inhibitors can prove effective against cancers with defective systems for DNA repair.
“And we are keen to investigate whether they could prevent tumours from developing resistance to another important class of medicine called PARP inhibitors, which work in a similar way.”
Further trials are now under way with the hope the drug could be developed into a new targeted treatment for patients with cancers with certain defects in DNA repair.
Study leader Professor Johann de Bono, a professor of experimental cancer medicine at ICR and consultant medical oncologist at the Royal Marsden trust, said: “Our new trial shows that this promising new treatment is safe and can benefit some patients even with very advanced cancers.
“The new drug, which is currently known only by the code BAY1895344, works by blocking a molecule called ATR which is involved in repairing DNA.
“It seems to be especially effective in patients whose tumours have defects in a gene called ATM which mean their ability to repair DNA is already weakened – suggesting that this could become a new form of targeted treatment.
“It is very promising to see patients responding in an early-stage trial like this, and we are looking forward to further clinical trials to test the drug’s efficacy.”