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.

Troxerutin (TXN) is a flavonoid present in tea, coffee, cereal grains, and a variety of fruits and vegetables. It inhibits the agglomeration of blood platelets and red blood cells; prevents thrombogenesis; protects endothelial cells; and enhances microcirculation. It possess anti-inflammatory and anti-apoptotic properties. Troxerutin protected different cell types (epithelial cells, fibroblasts and lymphocytes) against peroxyl radical-induced apoptosis, necrosis and mitotic death. It scavenged intracellular basal and inducible ROS levels and also restored depletion of intracellular GSH levels. Troxerutin might provide a safe and effective treatment for rhinorrhea in the common cold deserves systematic evaluation. The use of a mixture of troxerutin, diosmin and hesperidin is a safe and effective mean of managing symptoms of acute hemorrhoidal disease. Troxerutin is used for the treatment of chronic venous insufficiency.

Diosmin is a flavone indicated for the treatment of venous disease i.e., chronic venous insufficiency (CVI) including spider and varicose veins, leg swelling (edema), stasis dermatitis and venous ulcers. Diosmin is also used as a stand-alone or surgical adjunctive therapy in hemorrhoidal disease. There are extensive clinical trials that show diosmin improves all stages of venous disease including venous ulcers and improves quality of life. Diosmin prolongs the vasoconstrictor effect of norepinephrine on the vein wall, increasing venous tone, and therefore reducing venous capacitance, distensibility, and stasis. This increases the venous return and reduces venous hyperpressure present in patients suffering from CVI. Diosmin improves lymphatic drainage by increasing the frequency and intensity of lymphatic contractions, and by increasing the total number of functional lymphatic capillaries. Furthermore, diosmin with hesperidine decreases the diameter of lymphatic capillaries and the intralymphatic pressure. Diosmin reduces the expression of endothelial adhesion molecules (ICAM1, VCAM1), and inhibits the adhesion, migration, and activation of leukocytes at the capillary level. This leads to a reduction in the release of inflammatory mediators, principally oxygen free radicals, and prostaglandins (PGE2, PGF2a). Diosmin is currently a prescription medication in some European countries (under the Dio-PP, Venotec, Daflon etc. tradenames), and is sold as a nutritional supplement in the United States.

Pyridoxal phosphate (PLP, pyridoxal 5'-phosphate, P5P) is a coenzyme, the active form of vitamin B6. Pyridoxal 5′-phosphate (PLP) is used as a cofactor for a wide range of enzymes including mitochondrial cysteine desulfurase, cystathionine γ-synthase (CGS), ornithine 4,5-aminomutase (OAM), and d-serine dehydratase. The versatility of PLP arises from its ability to covalently bind the substrate, and then to act as an electrophilic catalyst, thereby stabilizing different types of carbanionic reaction intermediates. PLP acts as a coenzyme in all transamination reactions, in various beta-elimination reactions, in the condensation reaction in heme synthesis.

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.

Alprenolol is a beta adrenoreceptor blocking agent and 5HT1A antagonist, developed by AstraZeneca and now available as generic drug. It is used for treatment of hypertension, angina pectoris due to coronary atherosclerosis and acute myocardial infarction.

Cloranolol is a specific beta-adrenergic antagonist. It is used as an antiarrhythmic agent. Its antiarrhythmic effectiveness stronger than propranol and equal or surpass the effectivity of pindolol. It has a negligible cardiodepressant activity as compared to other beta-adrenergic antagonists. Cloranolol has mainly cardiorespiratory side effects judging from the beta-blocker characteristics

Ketanserin is a selective 5HT2A receptor antagonist which was initially developed as an anti-hypertensive medicine. However, now the drug is available as a topical gel formulation for the treatment of wounds, burns, ulcers and anal fissure (Sufrexal brand name). The drug action is explained by its ability to accelerate epithelialization.

Mepindolol is a selective beta1-adrenoreceptor blocker with intrinsic sympathetic activity. Treatment with mepindolol dose not significantly affect the lipid levels - the total cholesterol in plasma was decreased by mepindolol but HDL-cholesterol increased. During beta-receptor blockade with mepindolol-sulfate angina was compensated, the unfavourable hemodynamic effects seen during placebo did not occur. No signs of congestive heart failure were found during mepindolol-sulfate-therapy. Mepindolol-sulfate showed a pronounced blood-pressure lowering effect.