News
Scotland university set to study new contraceptive method after bagging US$4.4m grant
The new contraceptive method that slows down sperm will first be trialled on women, say researchers
A team of Scottish researchers have received a US$4.4m grant from the Bill & Melinda Gates Foundation to help discover a new contraceptive that would slow down sperm in the female reproductive system.
The team from the University of Dundee have discovered chemical combinations that stall sperm so that they will never be able to swim far enough to fertilise an egg.
The researchers have screened “drug libraries” to detect combinations that can disable sperm without being toxic and have so far spotted two potential candidates.
“These compounds stop the sperm swimming fast,” explained Professor Chris Barratt of the School of Medicine.
“The sperm will move, it will still twitch, but it will not make any headway. It is a car that is moving in the slow lane. It will never get anywhere, it is almost too slow to see — but it is not dead so [the compound] is not toxic to the cell.”
But although the compounds would affect the sperm, the Bill & Melinda Gates Foundation grant is intended to help turn the chemicals into treatments that could be given to women in the form of a pill, patch or gel.
“My understanding is the Gates foundation wants this contraceptive approach to be taken by the female not the male,” Barratt told the Times.
“Obviously if we find something interesting that affects the sperm you can see if that can be taken by the male but our focus is on the female tract.”
He added: “Our ultimate aim is to produce a non-hormonal contraceptive for women, improving contraceptive choice, particularly for those in low and middle income countries.
“If we find products that affect sperm cells, it may be they could be developed for the man.”
Data suggest that between 2015-19, there were 121 million unintended pregnancies, with women living in the world’s poorest regions nearly three times as likely to fall pregnant unintentionally, in comparison to those in the wealthiest regions.
However, the need to develop further forms of contraception have previously been hampered by the relatively poor understanding of human sperm biology and the absence of an efficient system to screen the effects of potential drug compounds on sperm activity.
Jason Swedlow, Professor of Molecular Cell and Developmental Biology, said: “We really know very little about how sperm cells work.
“It is technically very challenging to develop potential new drugs which affect sperm. To do this we have had to develop new ways to measure the effects of compounds on sperm.”
The University of Dundee aims to study this matter by bringing together experts in reproductive medicine, drug discovery, mechanism of action and cell biology.
Ian Gilbert, head of the drug discovery unit, said: “A project of this complexity can’t be undertaken without the extensive, collaborative capability that exists here at Dundee.
“We all contribute our unique skillsets, and all of the key decisions are decided between us. This is hugely complex work, and to have such a broad range of input is hugely advantageous.”
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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