July 23, 2012
* Intravenous injection of Mesenchymal Precursor Cells (MPCs) resulted in selective migration to inflamed joints and lymph nodes in a sheep model of Rheumatoid Arthritis (RA)
* A single intravenous injection of allogeneic, or "off-the-shelf", MPCs significantly reduced synovial tissue levels of TNF-alpha, IL-6, and IL-17, and reduced mononuclear cell infiltration
* Reduced cytokine and inflammatory cell levels were accompanied by significant reduction in pathology severity scores and synovial hyperplasia
* MPCs may have a mechanism of action that is unique from other biological therapies by shutting down multiple cytokine pathways simultaneously
* MPCs could be a safe, first line therapy to induce sustained improvement of joint inflammation in RA
* Phase 2 clinical trial in RA expected to commence Q4 2012
* RA is the second clinical indication, after type 2 diabetes, to be targeted using Mesoblast's intravenous product formulation
24 July 2012
: Regenerative medicine company Mesoblast Limited (ASX:MSB) today announced positive results in a large animal model of Rheumatoid Arthritis (RA) following a single intravenous injection of its proprietary allogeneic, or "off-the-shelf", immunomodulatory adult Mesenchymal Precursor Cells (MPCs).
Mesoblast Chief Executive Professor
said that the results indicated that the Company's immunomodulatory MPCs may have a mechanism of action that is unique from other biological therapies by shutting down multiple cytokine pathways simultaneously, and that this could become a first line treatment with a superior and sustained benefit on reducing inflammation and destruction of joints in people suffering from severe RA.
RA is an autoimmune disease driven and perpetuated by pro-inflammatory cytokines such as TNF-alpha, IL-6, and IL-17. Treatments targeting any of these pathways alone are only moderately effective in RA, need to be administered chronically, and may cause unacceptable infectious adverse events. A single intravenous injection of allogeneic MPCs in sheep with collagen-induced arthritis concomitantly affected T cells, monocytes/macrophages, and synoviocytes to simultaneously shut down TNF-alpha, IL-6, and IL-17 cytokine pathways, and improve joint pathology.