| June 28, 2020
Capivasertib, cancer drug discovered through collaborative work between the Institute of Cancer Research, London, and partners, has entered a major Phase III trial for breast cancer. The CAPItello-291 trial will recruit around 830 patients from 20 countries and will examine the effects of the drug in pre- or post-menopausal women, and men, with an advanced form of estrogen receptor (ER) positive, human epidermal growth factor receptor 2 (HER2) negative breast cancer. The trial, which is doing sponsored by AstraZeneca, the pharmaceutical giant, will measure the effectiveness of capivasertib, in combination with fulvestrant, an existing hormone treatment, against a placebo with fulvestrant.
If the trial is successful, it could establish the combination of these two drugs as a new breast cancer treatment regimen, also indicating potential for regulatory approval. Capivasertib is a major targeted inhibitor for AKT, the cancel driving protein, also called PKB. This protein is a vital node in a signaling network that is dysregulated in several types of cancers and aids in driving the disease. ICR researchers had revealed the 3D structure of AKT before ICR scientists from the Cancer Research UK Therapeutics Unit collaborated with Astex to identify precursors to the drug. The launch of the CAPItello-291 trial comes after the announcement of the initial results of Phase II trial FAKTION, which was led by researchers from Cardiff University, the Christie NHS Foundation Trust, the Velindre Cancer Centre, and the University of Manchester. These results were published in February in the journal the Lancet Oncology. The research findings suggested that the drug capivasertib might provide a 6-month survival benefit to women diagnosed with advanced ER-positive breast cancer when used in combination with fulvestrant.
The ER-positive, HER2-negative breast cancer cells consist of copies of the estrogen receptor, which allows them to grow but inhibits them from over-producing copies of the human epidermal growth factor (HER2). This breast cancer is typically driven by the activation of AKT, and when the disease relapses or spreads, treatment options become limited.
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