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News
Breast pump company secures US$8.5m in seed funding
The new breast pump promises to simulate the baby’s tongue to optimise milk output at a faster pace
An Israeli breast pump company has raised US$8.5m in seed funding to make breast pumping more accessible.
Annabella has developed a portable breast pump that claims to simulate the baby’s tongue to optimise milk output at a faster pace.
The electric device promises a more comfortable and convenient experience for mothers that could “revolutionise” the industry.
“Mothers shouldn’t have to choose between comfort and efficiency when breast pumping,” explained Masha Waldberg, co-founder of Annabella.
“Now, with the Annabella pump, they don’t have to. This investment will allow us to quicken the pace at which we bring best-in-class femtech products to market that radically improve the lived experience of mothers around the world.”
“Our mission is to empower women throughout every developmental phase of motherhood. This is only the beginning.”
The seed funding, supported by Yasmin Lukatz, founder of the Israel Collaboration Network, serial entrepreneur and investor Oren Dobronsky, Tamar Technology Ventures’ Zohar Gilon and Starry Group’s Menachem Weinfeld, will be used to help the company “fuel” product development, expand into the US market and onboard insurance providers to make breast pumping more accessible, Waldberg added.
Lukatz, founder of Israel Collaboration Network, said: “We believe that Annabella’s innovative breast pump holds the potential to revolutionise the maternal health industry, offering an unparalleled experience in comfort and efficiency.
“I am thrilled to be a part of Annabella’s journey and look forward to seeing the company’s growth and expansion into the United States.”
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.”
Insight
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