News
Female-led biotech start-up raises £1.27m to develop drug delivery technology for cancer therapy
The London-based company aims to help combat late-stage cancers using proprietary technology
The preclinical biotech start-up Vitarka Therapeutics has secured £1.27m to “revolutionise” intracellular drug delivery through tumour-targeted technology.
Founded in 2021 by Dr Vineeta Tripathi, the company is developing combination medicines using RNAi therapies and a non-viral drug delivery platform to help combat late-stage cancers.
Its “tumour-targeted” platform technology, called EndoPore, aims to target solid tumours and deliver therapeutics for intracellular targets.
The new funds will be used to accelerate the the company’s technology for pre-clinical validation. The development plan will also progress towards pharmacokinetics studies and improving technical processes for large-scale manufacturing.
“It has just been a year since we defined our product so to raise such a substantial amount within this timeframe is remarkable,” said Tripathi.
“Our new investors bring a range of complementary expertise to Vitarka and we are delighted to be working with them. We thank them, together with Innovate UK, for all their support.”
Stephen Chambers, partner and managing director of IndiBio New York, part of SOSV, said: “At IndieBio, we look for companies that want to make a difference in the world and have the passion and skills to deliver on their dreams, and we found that in abundance with Vitarka.
“We are excited about this investment as it represents a unique opportunity to contribute to the advancement of medical treatments and improve patient outcomes.”
He added: “The RNAi and non-viral drug delivery space is full of untapped potential, and we are confident that Vitarka’s unique approach will unleash the full power of this emerging class of therapeutics.
“We are thrilled to continue supporting Vitarka and look forward to being a part of their growth and success.”
Hassan Mahmudul, investor, UKI2S and Future Planet Capital added: “Delivering RNA therapeutics into the right tissues without off-target toxicity is a major problem faced by the pharma industry.
“That is why we are excited to back Vitarka and their unique approach to drug delivery.
“Their development of a novel platform technology has the potential to provide a solution which safely combats tumours and we look forward to continuing our partnership with them”.
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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