News
Kitazato and IVF2.0 forge groundbreaking collaboration to revolutionise IVF with AI solutions
The collaboration aims to advance real-time sperm selection for intracytoplasmic sperm injection (ICSI) and embryo ranking
Kitazato, a trailblazing Japanese corporation specialising in assisted reproduction products, and IVF2.0, a leader in AI software for assisted reproductive technology (ART), have joined forces in a strategic collaboration.
The partnership aims to advance real-time sperm selection for intracytoplasmic sperm injection (ICSI), and embryo ranking based on ploidy prediction, ushering in a new era for the IVF market.
Under this agreement, Kitazato will leverage its multi-national distribution network to introduce standardised reproducible data-driven decision-making to IVF laboratories in many regions of the world through IVF2.0’s software.
IVF2.0’s suite of AI tools, including sperm selection (SiD) and embryo selection (ERiCA), assists embryologists in making critical choices to optimize fertility outcomes.
Mr Futoshi Inoue, president and CEO of Kitazato, expresses enthusiasm, stating: “Partnering with IVF2.0 demonstrates our commitment to innovation. We embrace technologies that aim to boost success rates, standardize procedures, and democratize fertility treatment for all.”
Professor Andrew Drakeley, co-founder and board chair of IVF2.0, emphasises the significance of the collaboration.
He said: “Our bond with Kitazato, a prestigious company with world-class products, underscores the growing need for implementing AI tools in IVF clinics globally. This marks a substantial step in the right direction.”
Kitazato, Kitazato – Quality Results for Life (kitazato-ivf.com), renowned for delivering quality products in assisted reproduction, aligns with IVF2.0’s mission to enhance IVF outcomes through AI.
IVF2.0’s innovative software platform employs AI and computer vision technology to elevate key steps in the IVF process.
Learn more at IVF 2.0 (ivf20.ai)

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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