Flightless I

OUR TECHNOLOGES

Flightless I

Flightless I is a novel drug target that regulates important cellular behaviours including mobility, contraction, adhesion, proliferation and cytokine production.  The activity of Flightless I is mediated through interaction with components of the cell’s cytoskeleton, modulation of intracellular signalling pathways and regulation of cellular transcription events. 

 The flightless I gene was originally identified in Drosophila melanogaster, where mutations in the flightless I locus were found to cause flightlessness due to disordered indirect flight muscles (Campbell et al., (1993) PNAS 90 11386-11390). 

Flightless I is a negative regulator of the migratory and proliferative events of tissue repair.  Inhibition of Flightless I using antibodies has been shown to improve wound repair in murine and porcine models of normal and compromised would healing [reference publication link], and a murine model of Epidermolysis Bullosa (see figure below) [reference the publication list link]. 

In addition, anti-flightless antibodies have been shown to reduce the incidence and growth of skin tumours in a mouse model of squamous cell carcinoma (see below). 

Treatment of early stage blisters with anti-flightless antibodies improve healing in a mouse model of Epidermolysis Bullosa

Reference:   Kopecki et al., 2012 Topically Applied Flightless I Neutralizing Antibodies Improve Healing of Blistered Skin in a Murine Model of Epidermolysis Bullosa Acquisita J Invest Dermatol  133:1008-16

Anti-flightless antibodies formulated in a cream vehicle were applied onto the skin of EB mice for three consecutive days at the start of blister formation.  EB mice treated with anti-flightless antibodies were observed to have significantly fewer blisters and reduced number of lesions compared with EB mice treated with control IgG antibody.

Treatment of skin tumours with anti-flightless I reduces their incidence and severity.