in largest part excreted unchanged by the kidneys (60-80%), with the remaining mostly metabolised by the liver. The half-life for digoxin is 36–48 hours for people with a normal renal function and up to 6 days for people with a compromised renal function. This makes the renal function an important factor in the toxicity of digoxin and perhaps for cerberin as well. Mechanism of action There is very little formal, modern published information on the mechanism of action of cerberin. Cerberin, as a cardiac glycoside, is seen as binding to and inhibiting the cellular Na+/K+ -ATPase, because it binds to the alpha-subunit of the enzyme. This is the catalytic moiety. There are also a beta- and FXYD subunits. These two subunits influence the affinity of cerberin to Na+/K+ -ATPase. The expression of the beta- and FXYD-subunit is tissue-specific. Because of this, cerberin will have different effects in different tissues. When cerberin binds to the Na+/K+-ATPase the conformation of the enzyme changes. This will lead to the activation of signal transduction pathways in the cell. A detailed description of the effects of cerberin in the cell is given below. Na+/K+-ATPase pump Na+/K+-ATPase is an ion transport system of sodium and potassium ions and requires energy. It is often used in many types of cellular systems. Sodium ions move out of the cell and potassium ions enter the cell (3:2) with the aid of this pump. During the transport of these ions, the enzyme undergoes several changes in conformation. Including a phosphorylation and dephosphorylation step. The transport of Na+ and K+ is important for cell survival. Cardiac glycosides, such as cerberin, alter the transport of ions against their gradient. Cerberin is able to bind to the extracellular part of the Na+/K+-ATPase pump and can block the dephosphorylation step. Due to this inhibition it is impossible to transport sodium and potassium across the membrane and results in raising intracellular concentration of Na+. Na+/Ca2+-exchanger Accumulation of intracellular sodium ions cause an increase of intracellular calcium. This is because the calcium-sodium exchange pump’s activity decreases. The calcium-sodium exchange pump exchanges Ca2+ and Na+ without the use of energy. This exchanger is essential for maintaining sodium and calcium homeostasis. The exact mechanism by which this exchanger works is unclear. It is known that calcium and sodium can move in either direction across the membrane of muscle cells. It is also known that three sodium ions are