News
Ovarian cancer drug to launch in UK at US price
AbbVie said on Monday that it will launch ovarian cancer drug Elahere in the UK at the same list price as in the US.
The announcement follows President Donald Trump’s push for drugmakers to align domestic prices with the lowest levels paid by comparable high-income countries under his “most-favoured-nation” policy.
The US currently pays nearly three times more for prescription medicines than other developed nations.
AbbVie is in talks with the National Institute for Health and Care Excellence, the UK’s cost-effectiveness watchdog, to ensure the drug is valued fairly.
The company said these discussions will determine when Elahere is launched in the UK. AbbVie did not immediately respond to a request on pricing.
The move comes after Bristol Myers Squibb said last week it plans to introduce its schizophrenia drug Cobenfy in the UK next year at a price matching its US list price.
AbbVie was one of 17 drugmakers to receive letters from President Trump in July outlining how they should cut prices to match those paid overseas.
Unlike in the US, where market forces determine drug prices, European governments typically negotiate directly with companies to set prices for their health systems.
Elahere, available in the US since 2022, belongs to a new class of therapies called antibody-drug conjugates, sometimes referred to as “guided missile” drugs.
These treatments use antibodies to deliver chemotherapy directly to cancer cells with a specific protein on their surface, allowing for more precise treatment while reducing harm to healthy tissue.
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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