ProtAffin AG announced preclinical data on its MCP-1 decoy programme in a model of multiple sclerosis at the ECTRIMS/ACTRIMS conference, the largest conference in the world focussed on Multiple Sclerosis.
The company presented a poster on its MCP-1 decoy program at the Immunomodulation session at the ECTRIMS/ACTRIMS conference, which is the 5th Joint Triennial Congress of the European and Americas Committees for Treatment and Research in Multiple Sclerosis. The Company presented in vivo efficacy data of the glycan-binding MCP-1 decoy protein PA508 in a model of experimental autoimmune encephalomyelitis (EAE), a gold-standard preclinical model of Multiple Sclerosis. PA508 showed a significant improvement in the clinical score over 28 days, as well as histology in the CNS, with PA508 showing a reduction in inflammatory infiltrates and preservation of myelin structures in the spinal cord and cerebellum.
Prof. Andreas Kungl, CSO of ProtAffin commented: “We are excited by these data which indicates that Multiple Sclerosis is an additional therapeutic opportunity for this second program at ProtAffin, in addition to previously published data of PA508 in murine models of myocardial infarction, restenosis and autoimmune uveitis. It furthermore underlines the ability to efficiently generate multiple product candidates from ProtAffin’s proprietary CellJammer discovery technology. As we move our lead programme, the IL-8 decoy PA401 into Phase 1 Q2 2012, we aim to establish the innovative therapeutic concept of biopharmaceuticals targeting glycans as a novel modality to optimally down-regulate proteins that bind glycans.”
The MCP-1 decoy programme is the second pipeline programme at ProtAffin. The current lead compound, PA508, is based on the human protein MCP-1/CCL2 which has been modified by the CellJammer discovery technology, to reduce its binding to the GPCR receptor CCR2, while significantly increasing the affinity for its heparan sulphate co-receptor. The decoy MCP-1 proteins exert a strong anti-inflammatory effect by displacing inflammatory wildtype MCP-1 from glycan structures involved in the inflammatory process. This novel method of downregulating the MCP-1/CCR2 axis in inflammatory and neuro-inflammatory diseases has multiple benefits vs. small molecule CCR2 antagonists and mAb approaches which have been previously investigated by Pharma and Biotech companies.
PA508 is in preclinical research at ProtAffin and the Company expects to initiate preclinical development of this programme later in 2012. Patents encompassing PA508 and other MCP-1 variants have been filed in the EU, US and all other major territories.