Tocainide is a primary amine analog of lidocaine with antiarrhythmic properties useful in the treatment of ventricular arrhythmias. Tocainide, like lidocaine, produces dose-dependent decreases in sodium and potassium conductance, thereby decreasing the excitability of myocardial cells. In experimental animal models, the dose-related depression of sodium current is more pronounced in ischemic tissue than in normal tissue. Tocainide is a Class I antiarrhythmic compound with electrophysiologic properties in man similar to those of lidocaine, but dissimilar from quinidine, procainamide, and disopyramide. The recommended initial dosage is 400 mg every 8 hours. The usual adult dosage is between 1200 and 1800 mg/day in a three-dose daily divided regimen. Doses beyond 2400 mg per day have been administered infrequently. Patients who tolerate the t.i.d. the regimen may be tried on a twice-daily regimen with careful monitoring. Tocainide commonly produces minor, transient, nervous system and gastrointestinal adverse reactions, but is otherwise generally well tolerated.

Deslanoside is a cardiotonic glycoside from the leaves of Digitalis lanata. It is used to treat congestive heart failure and supraventricular arrhythmias due to reentry mechanisms, and to control ventricular rate in the treatment of chronic atrial fibrillation. Deslanoside inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium and calcium concentrations. Increased intracellular concentrations of calcium may promote activation of contractile proteins (e.g., actin, myosin). It also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential.

Digoxin is a cardiac glycoside derived from the purple foxglove flower. In 1785, the English chemist, botanist, and physician Sir William Withering published his findings that Digitalis purpurea could be used to treat cardiac dropsy (congestive heart failure; CHF). Digoxin has been in use for many years, but was not approved by the FDA for treatment of heart failure (HF) until the late 1990s. Another FDA indication for digoxin is atrial fibrillation (AF). Digoxin also has numerous off-label uses, such as in fetal tachycardia, supra-ventricular tachycardia, cor pulmonale, and pulmonary hypertension. Digitoxin inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium and calcium concentrations. Increased intracellular concentrations of calcium may promote activation of contractile proteins (e.g., actin, myosin). Digoxin also has Para sympathomimetic properties. By increasing vagal tone in the sinoatrial and atrioventricular (AV) nodes, it slows the heart rate and AV nodal conduction.

Methoxamine is an alpha-adrenergic agonist that induces prolonged peripheral vasoconstriction, and can also stimulate the release of arginine vasopressin in humans. In clinical trials, methoxamine was found to improve fecal incontinence. It had been marketed by Glaxo-Smith-Kline under the brand name Vasoxyl but has been discontinued. Methoxamine was also found to stimulate the induction of hiPSC-derived hepatoblasts to ALBUMIN+ cells.

Mephentermine, an amphetamine-derived phenethylamine, is an alpha 1 adrenergic receptor agonist and a hypertensive drug. Mephentermine is mainly used as a vasopressor agent with a sympathomimetic action, primarily causing release of noradrenaline and increasing cardiac output due to positive inotropic effect on the myocardium. The injectable preparation of mephentermine is commonly used for the short-term treatment of various hypotensive states such as shock or hypotension accompanying myocardial infarction or spinal anesthesia or surgical procedures like cesarean section. There is evidence on the fetal metabolic effect and placental transfer of mephentermine. However, a few studies have shown that mephentermine is as effective as phenylephrine in preventing maternal hypotension after spinal anesthesia and has similar effect on neonatal outcome. It is being widely used in developing countries like India as it is much more economical than phenylephrine and offers ease of use as it does not necessitate multiple dilutions as injectable. It is also available in India as 10 mg oral tablets. Despite it was thought earlier to have a little stimulant effect its abuse potential has increased, especially in sports due to its stimulant properties. Like amphetamines, it has shown to increase athletic performance in strength exercises and endurance in a dose of 14 mg/70 kg body weight. It has been proposed that phentermine, which is the main metabolite of mephentermine, acts by inhibiting monoaminoxidases A and B. Mephentermine adverse effects has been related to CNS simulation, excessive rises in blood pressure, and arrhythmias. Wyamine Sulfate (brand name of mephentermine sulfate) approved by FDA in 1951 was discontinued in USA.

Oxedrine (Sympatol, p-synephrine) is a naturally occurring alkaloid molecule first appeared in Europe towards the end of the 1920s being sold as a drug under the brand name Sympatol. Oxedrine was then being prescribed as a remedy for a number of respiratory conditions, which include asthma, whooping cough, colds, and hay fever. More recently, synephrine gained popularity as a weight loss aid and it has become a favored component in the more popular brands of weight loss supplement stacks. This popularity can be attributed in part to the ban imposed on ephedra, to which it shares similar mechanisms of action. Most, if not all of the synephrine being sold as a dietary supplement is extracted and synthesized from the Citrus aurantium plant, more commonly known as bitter orange. Just like ephedrine, synephrine has vasoconstrictive abilities, although at a lesser potency compared to ephedrine. There is no mention of synephrine in editions of Drill's Pharmacology in Medicine later than the 3rd, nor is there any reference to synephrine in the 2012 Physicians' Desk Reference, nor in the current FDA "Orange Book". One current reference source describes synephrine as a vasoconstrictor that has been given to hypotensive patients, orally or by injection, in doses of 20–100 mg.

Sparteine is a class 1a antiarrhythmic agent; a sodium channel blocker. It is the predominant alkaloid in Lupinus mutabilis, and is thought to chelate the bivalents calcium and magnesium. It is not FDA approved for human use as an antiarrhythmic agent. It is also used as a chiral base in organic chemistry, and as a ligand in organic chemical synthesis. Marketed under the brand name Spal in Taiwan and Sparteine in Brazil.

Fosfructose is a cytoprotective natural sugar phosphate under development by Questcor (formerly Cypros) for the potential treatment of cardiovascular ischemia, sickle cell anemia and asthma. Fosfructose acts by stimulating anaerobic glycolysis which generates adenosine triphosphate under ischemic conditions and improve the cellular energy metabolism in ischemic and hypoperfused tissues. Hypoxia forces ischemic tissue to anaerobic glycolysis for energy, which yields two molecules of ATP per glucose in contrast to 36 molecules of ATP generated during oxidative phosphorylation . Addition of exogenous Fosfructose can produce two more molecules of ATP in an uncompensated anaerobic environment and hence facilitate the recovery of ischemia tissue. Fosfructose breaks down into glyceraldehyde-3-phosphate and dihydroxyacetone phosphate, which will further break down into two molecules of pyruvate and finally produce two molecules of ATP. Other mechanisms include inhibition of the generation of oxygen free radicals by neutrophils, stabilization of cell membranes, and maintainance of the correct xanthine dehydrogenase/oxidase ratio by preventing the depletion of phosphorylated compounds in ischemic tissues. In myocardial infarction patients, FDP can improve the hemodynamic parameters, attenuate ECG proven ischemic injury and arrhythmia, prevent ATP and creatine phosphate depletion from ischemic myocardium, reduce infarct size, and increase survival rate. Exogenously administered Fosfructose has also been proven beneficial for a variety of other ischemic organs, such as liver, kidney, bowel and even brain as a consequence of its ability to penetrate to the blood brain barrier. Fosfructose trisodium had been in phase I clinical trials for the treatment of heart transplant rejection. Fosfructose trisodium had been in phase II clinical trials for the treatment of heart failure, perioperativ eischaemia and reperfusion injury. Fosfructose trisodium had been in phase III clinical trials for the treatment of sickle cell anaemia. However, all these research has been discontinued. In China, FDP has been approved and marketed as a commercial drug.

Coenzyme Q10, also known as ubiquinone, ubidecarenone, coenzyme Q, and abbreviated at times to CoQ10 or Q10 is a coenzyme that is ubiquitous in the bodies of most animals. It is a 1,4-benzoquinone, where Q refers to the quinone chemical group and 10 refers to the number of isoprenyl chemical subunits in its tail. This fat-soluble substance, which resembles a vitamin, is present in most eukaryotic cells, primarily in the mitochondria. It is a component of the electron transport chain and participates in aerobic cellular respiration, which generates energy in the form of ATP. Ninety-five percent of the human body’s energy is generated this way. Therefore, those organs with the highest energy requirements—such as the heart, liver, and kidney—have the highest CoQ10 concentrations. There are three redox states of CoQ10: fully oxidized (ubiquinone), semiquinone (ubisemiquinone), and fully reduced (ubiquinol). The capacity of this molecule to act as a 2 electron carrier (moving between the quinone and quinol form) and 1 electron carrier (moving between the semiquinone and one of these other forms) is central to its role in the electron transport chain, and as radical-scavenging antioxidant. Coenzyme Q10 works foremost in every cell of your body to synthesize energy. In cells' mitochondria, CoQ10 helps generate adenosine triphosphate (ATP), your body's energy currency. It makes sense that organs with the highest energy needs - including the heart, liver, and kidneys - contain large amounts of CoQ10. Among its roles, ubiquinol protects fats, protein, low-density lipoprotein (LDL, a cholesterol transporter), and DNA from oxidative damage. It also regenerates vitamin E, another powerful antioxidant. Even though Coenzyme Q10 is a supplement and occurs naturally in your body, it doesn't mean that it's side effect free. However, most CoQ10 side effects are mild. Some people may experience allergies to increased Coenzyme Q10. There have been some reports of rashes and itching. Other side effects include a lowering of blood sugar within the body. CoQ10 is not approved by the U.S. Food and Drug Administration (FDA) for the treatment of any medical condition. It is sold as a dietary supplement. In the U.S., supplements are not regulated as drugs, but as foods. How CoQ10 is manufactured is not regulated and different batches and brands may vary significantly. As an over-the-counter nutritional supplement, CoQ10 has been used to treat many things, from heart disease, high blood pressure and high cholesterol to diabetes, breast cancer and gum disease. CoQ10 supposedly can help with immune deficiencies, increase fertility, treat Alzheimer's and Parkinson's, reduce ringing in the ears, delay aging and improve skin, and increase athleticism The key benefits of coenzyme Q10 are summarized as below. A 2014 Cochrane Collaboration meta-analysis found "no convincing evidence to support or refute" the use of CoQ10 for the treatment of heart failure. Evidence with respect to preventing heart disease in those who are otherwise healthy is also poor. A 2009 Cochrane review concluded that studies looking at the effects of CoQ10 on blood pressure were unreliable, and therefore no conclusions could be made regarding its effectiveness in lowering blood pressure. Available evidence suggests that "CoQ10 is likely ineffective in moderately improving" the chorea associated with Huntington's disease. No large well-designed clinical trials of CoQ10 in cancer treatment have been done. The National Cancer Institute identified issues with the few, small studies that have been done stating, "the way the studies were done and the amount of information reported made it unclear if benefits were caused by the CoQ10 or by something else". The American Cancer Society has concluded, "CoQ10 may reduce the effectiveness of chemo and radiation therapy, so most oncologists would recommend avoiding it during cancer treatment. Lower levels of CoQ10 have also been observed in people with Parkinson's disease. Preliminary research has found that increasing CoQ10 may increase levels of the neurotransmitter dopamine, which is thought to be lowered in people with Parkinson's disease. It has also been suggested that CoQ10 might protect brain cells from damage by free radicals. A small, randomized controlled trial examined the use of 360 mg CoQ10 or a placebo in 28 treated and stable Parkinson's disease patients. After 4 weeks, CoQ10 provided a mild but significant significant mild improvement in early Parkinson's symptoms and significantly improved performance in visual function. As an antioxidant, Coenzyme Q10 helps protect your body against the harmful effects of toxins and also aids the absorption of beneficial vitamins and minerals. Antioxidants are sometimes credited with boosting weight loss, possibly due to their energising effect on the body helping increase the fat-burning benefits of exercise.

Enoximone is an inhibitor of PDE3, which is used for the treatment of congestive heart failure. Also enoximone was shown to inhibit PDH in cardiac myocytes. The inhibition was shown to occur secondary to stimulating fatty acid oxidation