News
Sage Therapeutics appoints investor Jessica Federer to board of directors
Federer’s work focuses on addressing the gender gap in healthcare and innovation
The US biotech company Sage Therapeutics has announced the appointment of investor Jessica Federer to the company’s board of directors.
Federer, a managing partner at Supernode Ventures, aims to address a critical gap in innovation by accelerating change through investment in early-stage femtech and health technology companies.
She was the first chief digital officer for the Bayer AG group, as well as the first woman to hold that role in the industry.
During her tenure, Federer united the company’s global digital strategy and investments to accelerate growth and held leadership positions in regulatory affairs, market access, communications, and public affairs.
“I’m honoured to join the Sage Board of Directors at such an incredibly exciting time,” the investor said in a statement.
“Sage has led the way in maternal mental health care, an area of great need and one that is particularly important to me.
“I’m looking forward to supporting the company’s goal of redefining how we think about and treat a wide range of brain health conditions. I see the vast potential for data and digital strategies in the brain health area.”
Sage Therapeutics is a Massachusetts-based biotech developing brain health medicines.
The company aims to improve brain health and change how brain disorders are thought about and treated.
Barry Greene, Sage Therapeutics CEO, said: “We are thrilled to have Jessica join our board of directors.
“She is a champion for patients and has a track record of innovation in data and digital transformation which will be a key future growth driver for the industry.
“Jessica’s innate curiosity, commitment to challenging convention, and patient-first mindset are consistent with the critical values that define our leaders.
“Her unique expertise in data and digitalisation at the intersection of policy and science will help us continue to scale our commercial growth ambitions.”
Federer began her public health career as an analyst at the Agency for Healthcare Research and Quality in the U.S. Department of Health and Human Services.
She has served on the United Nations International Telecommunications Union (UN-ITU) advisory board, as well as participated in engagements with the World Economic Forum, and is considered a thought leader in digital health.
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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