News
FDA approves ‘novel’ formulation to treat breast and ovarian cancer
The US Food and Drug Administration (FDA) has approved Shorla Oncology’s new drug application for TEPYLUTE, a new formulation to treat breast and ovarian cancer.
The American Cancer Society estimates that more than 300,000 women will be diagnosed with breast cancer in the US in 2024. About 19,680 US women will be diagnosed with ovarian cancer.
TEPYLUTE is the third drug in the Shorla portfolio to obtain FDA approval, with several other cancer drugs awaiting approval for the US market.
Previously known as SH-105, the asset is a ready-to-dilute, injectable product that simplifies preparation and ensures dosing accuracy for breast and ovarian cancer treatments.
According to Shorla, this new liquid formulation of thiotepa, a standard oncology product, removes the requirement for complex reconstitution and supports “just in time” preparation, providing “consistent” dosing accuracy.
“This approval fulfils an unmet need by addressing the shortcomings and handling complexities of the current lyophilised powder formulation,” said Sharon Cunningham, chief executive officer and co-founder of Shorla Oncology.
“We have taken a vital oncology drug and made it easier for oncology clinics and hospitals to use, while also reducing medical personnel exposure to a hazardous drug.”
Rayna Herman, chief commercial officer of Shorla Oncology, said: “Among TEPYLUTE’s many benefits, it removes the necessity to reconstitute which can introduce additional risks of drug preparation errors. We look forward to providing an update on our launch plans for TEPYLUTE in the near future.”
Orlaith Ryan, chief technical officer and co-founder of Shorla Oncology, added: “The approval of TEPYLUTE represents an important milestone for Shorla as our first in-house developed NDA.”
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Diagnosis
Lung cancer drug shows breast cancer potential
Ovarian cancer cells quickly activate survival responses after PARP inhibitor treatment, and a lung cancer drug could help block this, research suggests.
PARP inhibitors are a common treatment for ovarian cancer, particularly in tumours with faulty DNA repair. They stop cancer cells fixing DNA damage, which leads to cell death, but many tumours later stop responding.
Researchers identified a way cancer cells may survive PARP inhibitor treatment from the outset, pointing to a potential way to block that response. A Mayo Clinic team found ovarian cancer cells rapidly switch on a pro-survival programme after exposure to PARP inhibitors. A key driver is FRA1, a transcription factor (a protein that turns genes on and off) that helps cancer cells adapt and avoid death.
The team then tested whether brigatinib, a drug approved for certain lung cancers, could block this response and boost the effect of PARP inhibitors. Brigatinib was chosen because it inhibits multiple signalling pathways involved in cancer cell survival.
In laboratory studies, combining brigatinib with a PARP inhibitor was more effective than either treatment alone. Notably, the effect was seen in cancer cells but not normal cells, suggesting a more targeted approach.
Brigatinib also appeared to act in an unexpected way. Rather than working through the usual DNA repair routes, it shut down two signalling molecules, FAK and EPHA2, that aggressive ovarian cancer cells rely on. FAK and EPHA2 are proteins that relay survival signals inside cells. Blocking both at once weakened the cells’ ability to adapt and resist treatment, making them more vulnerable to PARP inhibitors.
Tumours with higher levels of FAK and EPHA2 responded better to the drug combination. Other data link high levels of these molecules to more aggressive disease, pointing to potential benefit in harder-to-treat cases.
Arun Kanakkanthara, an oncology investigator at Mayo Clinic and a senior author of the study, said: “This work shows that drug resistance does not always emerge slowly over time; cancer cells can activate survival programmes very early after treatment begins.”
John Weroha, a medical oncologist at Mayo Clinic and a senior author of the study, said: “From a clinical perspective, resistance remains one of the biggest challenges in treating ovarian cancer. By combining mechanistic insights from Dr Kanakkanthara’s laboratory with my clinical experience, this preclinical work supports the strategy of targeting resistance early, before it has a chance to take hold. This strategy could improve patient outcomes.”
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