Siponimod (BAF312) is a dual agonist at the sphingosine-1 phosphate receptors, S1PR1 and S1PR5. The S1P receptor is commonly found on the surface of specific cells residing in the central nervous system (CNS), that are responsible for causing CNS damage that drives loss of function in secondary progressive multiple sclerosis (SPMS). Siponimod (BAF312) enters the brain and by binding to these specific receptors, may prevent the activation of these harmful cells, helping to reduce the loss of physical and cognitive function associated with SPMS.

Tedizolid (also known as TR-700, DA-7157) as is an active compound, which is produced by plasma or intestinal phosphatases, after administration of the drug, tedizolid phosphate either orally or intravenously. The mechanism of action of tedizolid occurs through inhibition of bacterial protein synthesis by binding to the 23S ribosomal RNA of the 50S subunit, thereby preventing the formation of the 70S initiation complex and inhibiting protein synthesis.

Mannose 6-phosphate (M6P) has type-I integral membrane receptors. M6P-receptors bind and transport M6P-enzymes to lysosomes, but it can also modulate the activity of a variety of extracellular M6P-glycoproteins (i.e., latent TGFbeta precursor, urokinase-type plasminogen activator receptor, Granzyme B, growth factors, Herpes virus). M6P has been demonstrated to reduce active TGF-β1 expression on cultured tendon fibroblasts and improved range of movement in a rabbit flexor tendon injury model. Studies of M6P in relation to skin scarring demonstrate improvement in scar cosmesis and accelerated return of normal dermal architecture. Juvidex, a formulation of M6P, inhibits the activation of TGF-beta1 and TGF-beta2, which are present at high levels in adult wounds that scar. On the other hands, M6P in a 600 mM hypertonic solution (Adaprev) potentially acts via a physical, non-chemical, hyperosmotic effect.

Glucose-6-phosphate belongs to the class of organic compounds known as monosaccharide phosphates. It lies at the start of two major metabolic pathways: glycolysis and the pentose phosphate pathway. It is a glucose-6-phosphatase substrate. Hexokinase is inhibited by its product, glucose 6-phosphate. The non-enzymatic glycation of myosin by glucose 6-phosphate is probably the primary cause for the observed loss of the ATPase activity of myosin.