New treatment for cisplatin-resistant cancer with OGG1 inhibitors

Unique molecule opens up potential new cancer treatment

Cisplatin has been used since the late 1970s in chemotherapy for many types of cancer. The treatment causes DNA damage in the cancer cells and is often effective.

“In many cases, however, the patient responds progressively worse to the treatment over time. This is due to the tumour developing resistance to cisplatin and leads to the death of many patients”, says Thomas Helleday.

A new molecule inhibits an enzyme, OGG1, that repairs the damage caused to the cancer cells by cisplatin and thus reduces the effectiveness of the treatment.

“A major part of our project has been to develop more pharmacologically effective variants of the molecule”, says Thomas Helleday.

A sufficiently strong molecule

Now Helleday and his team have a molecule they want to take through to animal experimentation and clinical trial.

“Our first molecule worked on cell cultures but was not sufficiently effective to take into clinical trials. Now we have one which is just over 1 000 times as potent and the aim is shortly to select a clinical candidate and start testing on mice as well as larger animals. This will take two to three years, after which we can seriously begin clinical trials.”

New interesting lead

The team has also discovered that the OGG1 inhibitor they have developed has very good anti-inflammatory properties, which potentially opens up a new research path on severe inflammatory diseases such as chronic obstructive pulmonary disease (COPD).

Several investments

The financial support and coaching from Swelife has been very important to the project’s success. Along the way, follow-up investments have been added by stakeholders including Almi Företagspartner and the Novo Nordisk foundation.

“There could be a great need for a new drug against cancer and inflammation. For investors, it is interesting that other drugs of this type sell for between two and five million USD per year, says Thomas Helleday.

Text: Jörgen Olsson

Updated: 18 January 2018

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