ATL1101 is a 2nd generation antisense inhibitor of IGF-Ir which has shown potent activity in laboratory studies, including in human cancer cells.
ATL1101 is an antisense inhibitor of insulin like growth factor 1 receptor (IGF-Ir). IGF-Ir is one of the best known of a family of cell signalling molecules that are referred to as “anti-apoptotic”. These molecules prolong cell survival by inhibiting programmed cell death (apoptosis). Inhibition of cell survival molecules like IGF-Ir can render tumour cells more susceptible to cell death with cytotoxic (cell death inducing) drugs. Similar “chemosensitiser” therapeutic approaches targeting the IGF-Ir are under investigation in several large pharmaceutical companies, lending support to ATL’s antisense-based strategy against the same target.
In animal studies ATL1101 demonstrated its effectiveness in suppressing human prostate cancer tumour growth in mouse models of human prostate cancer. ATL1101 targets the insulin-like growth factor-1 receptor (IGF-Ir) which is a high interest therapeutic target in oncology. Drugs targeting IGF-Ir are being developed by a number of major pharmaceutical companies for a variety of cancer indications. Of significance, ATL1101 is the only gene-silencing or RNA-targeting drug to this target known by the Company to be in development.
A publication describing ATL1101 pharmacology in prostate cancer cells and tumours entitled ‘Antisense Oligonucleotide Targeting of Insulin-Like Growth Factor-1 Receptor (IGF-1R) in Prostate Cancer’ was published in the February 2010 edition of the highly regarded international scientific journal ‘The Prostate’.
The Company is continuing to assess possible development paths and partnering options for the drug.
Prostate cancer is the second most frequently diagnosed cancer in men after skin cancer. Metastatic disease invariably progresses to hormone refractory or castrate-resistant prostate cancer (CRPC) if given enough time. Prostate tumours are initially androgen (male sex hormone) dependent, and can be treated with androgen ablation therapy (the term “castration” can be used to describe removal of the source of androgen), however once the disease progresses to its most dangerous and aggressive form, CRPC, treatment options are limited and prognosis is poor. Treatment options depend on disease severity and include radiation and chemotherapy, which are designed to induce programmed cell death (apoptosis) of tumour cells. There is a pressing need for the development of new treatment options.