News
Kindbody secures US$100m to drive business growth
The company plans to open ten new fertility clinics to support growing demand
The US family-building benefits provider Kindbody has raised US$100m in capital to support company growth.
The latest financing brings Kindbody’s total equity and debt funding to more than US$290m, and its valuation to US$1.8bn, becoming the largest women-owned fertility company serving employers and consumers.
The demand for workplace fertility benefits is on the rise, with close to 90 per cent of those experiencing infertility willing to change jobs solely for the benefits.
In 2022, 61 per cent of employers with more than 500 employees provided at least some infertility coverage.
“Infertility is widespread, more common than diseases like cancer or diabetes. Yet, for far too long, high-quality fertility care has been available to only a privileged few,” said Gina Bartasi, founder and chairwoman of Kindbody.
“With the support of Perceptive Advisors, and our other investors, Kindbody is positioned to deliver on our vision to help everyone realise their dream of becoming a parent by making high-quality fertility care affordable and accessible for all.”
She added: “In 2023, Kindbody will sharpen its operations, make strategic acquisitions, and maintain our laser focus on profitable growth.”
The provider was founded in late 2018 to support the healthcare system in the US.
According to its website, Kindbody is the only family-building benefits provider that owns and operates fertility clinics saving employers 25 per cent and 30 per cent by contracting directly with them to provide virtual and in-person care to their employees.
In 2022, it added 42 new employer clients, including Walmart, and is now the fertility benefits provider for 112 companies.
“This team is unstoppable in their vision to reinvent fertility healthcare,” said Sam Chawla, portfolio manager at Perceptive.
“Kindbody’s differentiated care delivery model, focused on exceptional patient experience and outcomes at a reduced cost for employers and patients, positions it to meet the urgent need for better fertility healthcare solutions, making Kindbody an attractive opportunity for us.”
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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