Zycan is a Disease Modifying Osteoarthritis Drug (DMOAD) for the treatment and prevention of clinical signs attributable
to degenerative and/or traumatic aseptic joint disease in horses. DMOADs are intended to prevent, retard or reverse the
morphologic cartilaginous lesions associated with degenerative joint disease (DJD).
PSGAGs, such as Zycan have been advocated for the (i) preventative treatment of joint disease (ii) chronic joint maintenance
programs and (iii) post-operative care of horses returning to training following joint surgery.

Zycan is a semi-synthetic polysulfated glycosaminoglycan (PSGAG) and is physiologically similar to the natural
mucopolysaccharides found in joint cartilage.
The low molecular weight of Zycan facilitates the distribution of the PSGAG from the bloodstream to the synovial fluid.
Distribution from the synovial fluid to the cartilage then takes place by diffusion. PSGAG is deposited in all layers of articular
cartilage and is preferentially taken up by osteoarthritic cartilage. When administered intramuscularly, synovial levels exceed
serum levels, peak in 48 hours and persist for up to 96 hours. The latter is the rationale behind every fourth day dosing.
PSGAGs exert their chondroprotective effects by inhibiting the detrimental effects of cytokines and PG’s on cartilage
and connective tissue, reducing proteoglycan breakdown, stimulating HA synthesis and enhancing the production of
glycosaminoglycan, proteoglycan and collagen.
In multiple studies, PSGAGs have been shown to:
• Inhibit various degradative proteolytic enzymes, including glycanohydrolases, glycosidases and MMPs.
• Inhibit MMP-3 more effectively than phenylbutazone, flunixin, betamethasone and HA.
• Increase collagen and GAG synthesis in articular cartilage explants and cell culture.                                                                                                                  • Stimulate synthesis of HA by synoviocytes, restoring synovial fluid viscosity.
• Inhibit PGE synthesis and the influx of leukocytes into inflammatory sites.
• Inhibit the production of superoxide radicals and pro-inflammatory IL-1.
• Increases the synthesis of proteoglycans by acting as a precursor.
• Decrease articular fibrillation and erosion.
• Decreased chondrocyte death.
• No change in partial or full thickness articular cartilage lesions has been reported.
PSGAG (250mg) has also been used intra-articularly for the treatment of acute synovitis, including post-arthroscopy (McIllwraith 2016).


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