By Deena Beasley
(Reuters) – AstraZeneca and Daiichi Sankyo’s Enhertu was shown in a large trial to delay the growth of hormone-sensitive breast cancer by about five months for people with low levels of HER2 protein whose cancer progressed following endocrine therapy, according to research presented on Sunday.
The findings, presented in Chicago at the annual meeting of the American Society of Clinical Oncology, could significantly broaden the range of breast cancer patients that might benefit from Enhertu, an antibody-drug conjugate designed to deliver toxic chemotherapy directly to tumors.
The data show an “unprecedented” improvement in progression-free survival, supporting the thesis that antibody-drug conjugates can deliver their payloads more specifically to cancer cells, ASCO President Dr. Lynn Schuchter said in a briefing with Reuters.
Study participants given Enhertu lived for a median of 13.2 months before their cancer worsened, compared with 8.1 months for those given chemotherapy. Results were similar for patients with low and “ultra-low” levels of HER2.
About 70% of breast cancer cases are hormone-receptor positive, and are initially treated with drugs that interfere with hormones like estrogen. If their cancer worsens, the only current option for those patients is chemotherapy. Another 20-25% of breast cancers are HER2 positive, or HER2 “high,” and can be treated with drugs like Roche’s Herceptin.
Enhertu is currently approved as a second-line treatment for HER2 positive breast cancer. Sales of the drug totaled about $2.6 billion last year.
If approved for HER2 low and ultra-low breast cancers, eight out of out 10 women with metastatic breast cancer could be treated with Enhertu, AstraZeneca oncology research chief Susan Galbraith told Reuters.
She said the company is working with global regulatory agencies to submit the latest Enhertu breast cancer data.
A number of other trials are underway aimed at moving the drug into earlier lines of therapy.
Galbraith said Enhertu is effective at reaching tumors with low levels of HER2 due to the mechanism linking the antibody to the drug. “Our linker is stable in the blood. When it gets to the tumor it gets cleaved and then it can go across the cell membrane,” she said.
(Reporting by Deena Beasley, Editing by Nick Zieminski)
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