Cancer Research UK and Hummingbird Bioscience have teamed up to develop the latter’s anti-HER3 antibody drug, HMBD-001, for the treatment of people with HER3 driven cancer.
The antibody works by targeting the HER3 receptor, which when activated through binding to other cancer-associated proteins, turns on a strong signal that causes cancer cells to grow and divide.
This activation is common in multiple solid tumours, including breast, gastric, pancreatic, ovarian and lung cancers, and is also seen when cancers develop resistance to existing cancer therapies. HMBD-001 is the only anti-HER3 antibody in development that binds to the most critical region involved in HER3 activation, turning off this signal completely.
Because of this, if successful, HMBD-001 could be used in the treatment of multiple cancers and be effective against drug resistant cancers.
Under the terms of the partnership, Cancer Research UK’s Centre for Drug Development will fund the programme, manufacture the clinical grade antibody and conduct a Phase I clinical trial to evaluate drug safety, toxicity and efficacy.
Also, Hummingbird will retain the rights to further advance the HMBD-001 programme and following completion of the trial, will have the option to acquire the rights to the clinical trial results to support further development of the antibody.
Dr Nigel Blackburn, Cancer Research UK’s director of drug development, said that the company are “thrilled to be working with Hummingbird to fast track such a promising new antibody, through one of the most difficult stages of drug development.
“For many people with cancer, targeted treatments can work in the short term, but drug resistance sometimes leads to the eventual return of their tumour. We hope this antibody may be able to overcome a key mechanism of drug resistance and help us find new lasting ways to tackle the disease.”
Hummingbird’s antibody is distinct from other anti-HER3 agents currently in development because it blocks all mechanisms through which HER3 can be activated, overcoming an intrinsic mechanism that has prevented previous HER3 therapeutics from working effectively.
