News
Femtech describes a category. Women’s health describes a life
By Ema founder and CEO, Amanda Ducach
Ema’s claim to fame is that “she” was the first agentic AI for women’s health.
That means that as the CEO, I get to spend my days speaking with women’s health founders and funders about AI for women. And… I have noticed something that I wanted to share.
There’s a growing confusion in the market: “femtech” and “women’s health” are often used interchangeably. But while they’re deeply connected, they’re not the same.
All femtech is women’s health. But not all women’s health is femtech. Both matter. But the distinction matters, too.
Femtech: A Catalyst for Innovation, Not a Catch-All
Coined in 2016 by Clue founder Ida Tin, femtech provided a language for a long-overlooked corner of healthcare and has since become one of the fastest-growing verticals in digital health.
Femtech:
- Names a market that was previously invisible.
- Unlocks funding, innovation, and legitimacy.
- Centers historically neglected needs in health tech.
Today, femtech includes everything from fertility and contraception to menopause care, pelvic health, sexual wellness, mental health, and cancer screening.
It’s a category with momentum and one that is expanding.
But categories have limits. When we frame the full breadth of women’s health needs solely through the lens of femtech, we risk both narrowing the scope and limiting its impact.
That’s not a failure of the category. It’s a signal that we must build beyond it.
Women’s Health: Bigger Than a Market. More Complex Than a Milestone
Women’s health is a lifelong, whole-body experience.

Amanda Ducach
It spans:
- Cardiovascular, metabolic, neurological, and autoimmune conditions
- Mental health across life stages
- Hormonal transitions beyond reproduction (e.g., perimenopause, PCOS)
- The interplay of biology, identity, stress, and systemic bias
And yet, women remain underdiagnosed, undertreated, and underserved, partly because mainstream healthcare systems still don’t reflect their reality.
Women’s health encompasses more than just gynaecology. It’s a biopsychosocial model of care that sees women in full, not just in episodes.
Why the Distinction Matters
Femtech is growing, but funding remains concentrated in specific stages, including fertility, pregnancy, and postpartum. These are deeply important, but they’re just a fraction of the health journey.
Most of women’s health happens outside of reproduction.
Think: PMDD in adolescence, anxiety in early adulthood, migraines and autoimmune flare-ups, perimenopause in midlife, and heart disease risk post-menopause.
When investment flows into what’s easiest to monetise in the short term, we risk reinforcing a narrow story of what women need and when.
The result? Gaps in care, missed opportunities, and underserved lives. The risk isn’t that femtech is too small. It’s that we treat women’s health as if it is.
Femtech as a Bridge, Not a Box
The future isn’t about picking sides. It’s about connecting categories with complexity.
Femtech is an essential bridge: from invisibility to visibility, from stigma to innovation. But it’s not the endpoint. To meet women where they actually are, we must:
- Design for the whole hormonal arc, not just milestones.
- Expand data models to reflect lived experience across race, gender identity, and life stage.
- Invest in long-term conditions, not just urgent ones.
- Prioritise prevention, quality of life, and self-trust, not just outcomes that are easily measurable.
As the Health Innovation Network warns, without this evolution, even well-intentioned femtech could inadvertently widen the health equity gap.
The Bottom Line
Femtech is a powerful industry. Women’s health is a lifelong mission.
All femtech is women’s health. But not all women’s health is femtech.
Recognising that is how we build products and care systems that actually fit women’s lives.
Find out more about Ema at emaapp.co
Cancer
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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