What does the science say? Alpha-2 Macroglobulin (α2M) is a powerful inhibitor of cartilage catabolic factors and slows the progression of osteoarthritis by preventing cartilage breakdown and loss.

Astaria Global has been advancing its proprietary line of α2M plasma technologies to introduce Alpha2EQ for inflammation/degeneration of joints in horses. Alpha2EQ is powered by the advanced, patented AlphaActive Concentrate Process. AlphaActive is a highly improved process leveraging PRP methodology derivative of Platelet Poor Plasma (PPP) that concentrates plasma proteins from the equine patient’s own blood. This process isolates the α2M molecule, which is a powerful inhibitor of cartilage catabolic factors and slows the progression of osteoarthritis by preventing cartilage breakdown and loss. The patented, proprietary filtration process removes the harmful proteins that can remain in other autologous plasma products to allow for a pure α2M product with no inflammatory cytokines. It is the only autologous process to concentrate α2M for mammals to obtain a U.S. patent.
Alpha-2 Macroglobulin (α2M) is a large glycoprotein, which is part of the innate immune system (Buresova 2009). The α2M molecule has proven success in decreasing inflammation, relieving pain and modulating cartilage degeneration that is the result of osteoarthritis. With Alpha2EQ, veterinarians can process and treat in just one hour with an uncomplicated three-step, minimally invasive procedure. The multi-dose kit allows veterinarians to inject multiple sites in the same treatment and excess α2M from the injectate bag can be frozen for future treatments. Alpha2EQ is drug free and has no competition restrictions. It has no banned substances. Always follow your organization’s rules for general joint injections.
The means of α2M protease inhibition has been referred to as the “trapping” mechanism. A short, unique segment of amino acids near the middle of the polypeptide chain acts as a “bait” region, which is vulnerable to cleavage by most proteases. After a protease cleaves the “bait” region, conformational changes in the α2M molecule are triggered— springing the “trap” — resulting in entrapment of the protease molecule (Barrett, 1973). Trapping the protease molecule produces two important results: the protease molecule is sterically hindered from accessing its substrate and the receptor binding site on each α2M monomer is exposed, enabling those molecules containing protease to be bound and cleared via phagocytosis— unbound α2M is not cleared from the site (Rehman 2013).

The mechanism of action suggests that — in addition to inhibiting protease activity — α2M supplementation beyond endogenous levels may inhibit osteoarthritic cartilage degradation in vivo by decreasing cartilage catabolic and inflammatory factors (Wang 2014). α2M may offer a useful therapeutic approach to the management of osteoarthritis by reducing gene expression of specific classes of proteases involved in cartilage matrix degradation and favoring its repair (Kobayashi 2005). α2M is a negative regulator of the catabolic factors associated with joint trauma and osteoarthritis. However, it is not present at sufficient levels to suppress all of the catabolic factors in an inflamed joint (Wang 2014).

For best results, blood processing should be performed prior to anesthesia. Do not administer non-steroidal anti-inflammatory drugs (NSAIDs) or sedatives within 72 hours before drawing blood. NSAIDs or sedatives may affect the concentration of α2M in the blood.

Excess α2M from the injectate bag can be frozen for future treatments.

  • Barrett AJ and Starkey PM. The interaction of Alpha2-Macroglobulin with proteinases. Biochem J 1973;133:709-724.
  • Buresova V, Hajdusek O, Franta Z, et al. IrAM—An Alpha2-mMcroglobulin from the hard tick Ixodes ricinus: Characterization and function in phagocytosis of a potential pathogen Chryseobacterium indologenes. Dev Comp Immunol. 2009;33:489-498.
  • Kobayashi M, Squires GR, Mousa A, et al. Role of interleukin-1 and tumor necrosis factor ­in matrix degradation of human osteoarthritic cartilage. Arthritis Rheum. 2005;52(1):128-135.
  • Rehman A, Ahsan H, Khan F. Alpha2-Macroglobulin: a physiological guardian. J Cell Physiol 2013;228:1665-1675.
  • Wang S, Wei X, Zhou J, et al. Identification of Alpha2-Macroglobulin as a master inhibitor of cartilage-degrading factors that attenuates the progression of posttraumatic osteoarthritis. Arthritis Rheumatol 2014;66:1843-1853.