On March 1, 2021 Cancer Research UK and Teon Therapeutics, Inc. (Teon) today (Monday 1 March) reported that they have signed a collaboration agreement to progress the early phase clinical development of Teon’s first-in-class small molecule adenosine A2B receptor antagonist, TT-702 (Press release, Teon Therapeutics, MAR 1, 2021, View Source [SID1234575900]).
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Cancer Research UK is the world’s leading cancer charity dedicated to saving lives. Teon is a biopharmaceutical company that is developing a focused portfolio of small molecules that modulate metabolic signalling pathways in the tumour microenvironment.
Under the terms of the clinical development partnership, Cancer Research UK will sponsor the first-in-human Phase I/II clinical trial of TT-702, which will be led by a team at The Institute of Cancer Research, London, and The Royal Marsden NHS Foundation Trust.
TT-702 targets cancer’s ability to evade the human immune response, enabling the immune system to expose and then destroy cancer cells. The hope is that TT-702 could be used to treat patients with advanced hard-to-treat solid tumours, including metastatic castrate-resistant prostate cancer, which is an aggressive form of cancer which has progressed despite surgery and hormone therapy.
Cancer Research UK’s Centre for Drug Development will work closely with Teon throughout the collaboration and share clinical insights as they emerge to help guide TT-702’s future development strategy.
Teon retains the rights to further develop and commercialise TT-702 and will receive the results of the clinical trial from Cancer Research UK in return for undisclosed success-based milestone and royalty payments.
TT-702 is an adenosine receptor antagonist and specifically targets the A2B receptor, which is over expressed on various types of tumour cells and immune cells*.
High levels of adenosine in the tumour microenvironment activate the A2B receptor, triggering tumour cells to grow and suppress T-cells, allowing the cancer cells to avoid immune detection.
TT-702 prevents the A2B receptor being activated by high levels of adenosine, which prevents cancer cell growth and enhances the anti-tumour immune response.
The Centre for Drug Development, Teon, and a team of clinical investigators led by Professor Johann de Bono are currently preparing to open a first-in-human clinical trial in the second half of 2021.
The researchers will test the safety and efficacy of TT-702 in multiple cancer indications, including hard-to-treat prostate cancer and triple negative breast cancer. TT-702 will be evaluated as both a monotherapy and in combination with anti-PD1 immunotherapy or hormonal therapy.
Dr Nigel Blackburn, Cancer Research UK’s director of drug development, said: "We are delighted to be working with Teon to advance TT-702 into human trials, and the drug makes an exciting addition to our growing portfolio of innovative anti-cancer agents. Finding new ways to target difficult-to-treat cancers remains a research priority for Cancer Research UK, and despite the challenges from the COVID-19 pandemic, we are continuing to leverage new partnerships like Teon, so we can bring potentially life-saving treatments closer to patients who need them."
Ken Horne, president and chief operating officer at Teon Therapeutics, said: "The partnership with the Centre for Drug Development provides an ideal route for Teon to pursue early-phase clinical development of TT-702, and leverage the incredible resources that Cancer Research UK brings. We are very excited to collaborate with a world-class investigator like Professor de Bono, thanks to the Centre for Drug Development".
Professor Johann de Bono, Professor of Experimental Cancer Medicine at The Institute of Cancer Research, London, and Consultant Medical Oncologist at The Royal Marsden NHS Foundation Trust, said: "We are excited to begin clinical trials of this new anti-cancer drug in several types of cancer. This new agent targets the evasive strategies cancer takes against the human immune response, exposing cancer cells to the immune system for destruction."