ALLOZYNE announced positive data from preclinical studies evaluating AZ17 which is a novel bispecific Th17 antagonist that inhibits the differentiation and effector function of human Th17 cells in vivo

SEATTLE, WA, USA | November 16, 2010 | ALLOZYNE Inc. announced today positive data from preclinical studies evaluating AZ17 which is a novel bispecific Th17 antagonist that inhibits the differentiation and effector function of human Th17 cells in vivo. Results from these studies demonstrated AZ17 to have improved efficacy over individual parental antibodies in addition to high potency and affinity for each respective target. These findings are based on evaluation across two distinct disease models in psoriasis and skin graft rejection. “These results are very encouraging on many levels. First, we believe that AZ17 holds the promise of superior efficacy, safety and possibly even dosing convenience over currently marketed therapies for various autoimmune diseases. Secondly, the stability, solubility, affinity and potency of this compound are a testament to the potential of Allozyne’s antibody platform,” stated ALLOZYNE’s Chief Executive Officer, Meenu Chhabra.

In the past few years, the discovery of Th17 cells has led to a new understanding of their role in autoimmune and inflammatory diseases. AZ17 is a product of ALLOZYNE’s E. coli based CAESAR platform and is composed of two single chain variable antibody fragments (scFvs), each targeting a separate cytokine involved in the differentiation of Th17 cells. Unlike most other bispecific molecules that are constructed using genetic fusion, the two scFvs that compose AZ17 are conjugated covalently using a synthetic linker. This simultaneous inhibition of two independent Th17 cytokines represents a novel approach to treating Th17 associated diseases such as multiple sclerosis, Crohn’s and psoriasis.

About ALLOZYNE:

Headquartered in Seattle, ALLOZYNE was established in late 2005, to commercialize proprietary biociphering technology that it licensed, on an exclusive basis, from the California Institute of Technology. The biociphering platforms, CAESAR and VIGENÈRE, are able to site specifically modify any protein sequence through the substitution or addition of non-canonical amino acids, in E. coli, yeast or mammalian systems. These amino acids possess unique chemical functions and create the opportunity to site specifically modify proteins through various conjugations that will lead to an enhanced efficacy, safety and tolerability profile. In essence, these unique amino acids unlock an advanced class of chemical reactions that are superior to conventional methods available for protein modification.

ALLOZYNE has raised $36M and is supported by a top tier venture investor syndicate including MPM, Arch, OVP and Amgen Ventures. The funding has been used to rapidly progress the platforms to practice and build a significant clinical stage pipeline with distinct product opportunities that reflect the breadth of the platform and maintain the company’s focus on CNS and autoimmune diseases. ALLOZYNE’s lead program, AZ01, is a PEGylated interferon β for the treatment of multiple sclerosis (MS). Currently in Phase I trials, AZ01 offers potential advantages over existing therapies through enhanced dosing convenience and superior tolerability to existing agents. MS is a chronic disease characterized by demyelination of nerve fibers, which leads to severe nerve damage. Symptoms include fatigue as well as cognitive and visual impairment. In 2009, worldwide revenue for drugs to treat MS approached $9 billion USD with over 70% of sales coming from the interferon β class of products.

SOURCE: ALLOZYNE Inc.