implications Cardiac therapeutic implications Since AP is known to have an excitatory effect on cardiac muscle contractility at very low concentrations, without interfering with heart rate and blood pressure, it has been suggested to be useful as a possible treatment for patients with heart failure. Digoxin (purified cardiac glycoside) has more side-effects and is less potent than AP (which is 200 times more potent in the case of AP-A and AP-C, while AP-B is even more potent). AP-Q is quite similar to vesnarinone, a quinolinone derivative, a medicine that can be given to patients with chronic heart failure. Only lower doses of both AP-Q and vesnarinone have beneficial effects without raising blood pressure or heart rhythm. There is a narrow dose range in which the contractility is improved but also arrhythmias could be induced. AP itself cannot be used for therapeutic admission, because the stability of the molecule after oral transmission is too low and an immunological reaction might occur since the molecule is unfamiliar to the body. However, it may be possible to modify its structure using biological engineering. Studies have also been performed to investigate the effects of AP-Q in acute liver injury. Given in low doses (3.5–7 microgram/kg) AST and ALT are decreased, whereas high doses of AP-Q (14 microgram) increase these liver enzyme values. AP-Q also increases the delayed outward potassium current thereby increasing the outflow of potassium ions from hepatocytes. This causes a hyperpolarization of its membrane potential. This hyperpolarizing effect could lead to increased uptake of substrates that help in restoring the cellular ATP levels. References Neurotoxins Ion channel toxins Sea anemone toxins Protein toxins