Our Technology

Signum is spearheading a novel, disease modifying mechanism for neurodegenerative disorders.

Research has largely focused on pathological hallmarks seen at the endpoint of disease.
Until now.

The amyloid hypothesis has dominated the field and is being tested in a number of advanced clinical trials with small molecules and biological approaches. To date these trials have not demonstrated convincing efficacy. It is likely that amyloid deposition is a late phenomenon, and additional pathways contribute to the disease, therefore amyloid modulation is not sufficiently central to affect disease course. Additional strategies are targeting other hallmarks such as the abnormally aggregated tau protein in Alzheimer's disease or alpha-synuclein in Parkinson's disease. Such approaches are still to be evaluated in the clinic. Signum targets PP2A, a master regulator of tau, acting centrally in the disease process for maximal potential efficacy.

The novelty of our approach is the target, PP2A

Signum Phosphatase technology targets specific proteins that are involved in the regulation of tau, a critical protein in Alzheimer's disease. While tau is phosphorylated by multiple protein kinases, PP2A is the major tau phosphatase accounting for ~70% of tau dephosphorylation. Reduced levels and activity of PP2A are evident in brains of patients with Alzheimer's disease – profoundly reducing the phosphatase activity by as much as half and levels of associated regulators of PP2A are also linked to manifestation of disease. Thus PP2A is linked both pathologically to the human condition and mechanistically through key proteins involved in disease pathogenesis that can act at the centre of disease processes.

By targeting PP2A we have discovered a novel approach to molecules that alleviate the threat, and halt the progression of, Alzheimer's disease