Modulating the Alternative Pathway of the Complement System to Treat Inflammatory Diseases

Product Development

Taligen’s lead products are monoclonal antibodies and recombinant fusion proteins which target key factors in the alternative complement pathway. These products are in preclinical stages of development to treat systemic as well as local inflammatory conditions.

TA106

TA106 is a Fab fragment of a monoclonal antibody which inhibits complement factor B. The initial clinical applications for TA106 will be for local therapy of inflammatory diseases including asthma and macular degeneration.

TA106 is being developed as an inhaled product candidate for the treatment of asthma. Asthma is a chronic inflammatory disease of the small airways of the lungs that is estimated to affect over 10 million individuals in the US and 30 million worldwide. Although current therapies control the disease in most individuals, 10-15% of patients (1-2 million individuals in US) have severe asthma which is inadequately controlled with maximum doses of current therapies. If approved for marketing, TA106 would be a novel therapeutic for asthma with broad anti-inflammatory activity.

Taligen is also developing TA106 as a potential intraocular therapy for the treatment of age-related macular degeneration (AMD).  Recent data have indicated that complement activation plays a critical role in the inflammation that leads to both dry and wet macular degeneration.  Abnormalities of factor B, the target of TA106, and of complement factor H, a critical regulator of the amplification of complement activation, have been strongly associated with AMD.  Taligen has data which indicate that intraocular injection of TA106 reduces retinal damage in an animal model of dry AMD. 

TT30 (Targeted Factor H)

Taligen is developing novel compounds which are intended to selectively deliver complement inhibitors such as Factor H to sites where complement activation is occurring and driving inflammation. Taligen scientists have demonstrated that targeted delivery of complement inhibitors is more efficacious, requires a lower dose of product and is safer than untargeted inhibitors.

The Company has proof-of-concept data using this technology in animal models of choroidal neovascularization, inflammatory arthritis, ischemia-reperfusion injury, stroke and spinal cord injury. Taligen has data which demonstrate that targeted delivery of the complement inhibitory portion of factor H to sites of complement activation with TT30 (CR2~factor H) is equally efficacious in animal models of choroidal neovascularization when given by systemic or by intraocular injection.

This targeting technology is designed to provide local regulation of complement activation without triggering systemic complement inhibition, potentially allowing application to a broad range of autoimmune and inflammatory diseases.