Quercetin is a unique bioflavonoid that has been extensively studied by researchers over the past 30 years. Quercetin, the most abundant of the flavonoids (the name comes from the Latin –quercetum, meaning oak forest, quercus oak) consists of 3 rings and 5 hydroxyl groups. Quercetin is a member of the class of flavonoids called flavonoles and forms the backbone for many other flavonoids including the citrus flavonoids like rutin, hesperidins, Naringenin and tangeritin. It is widely distributed in the plant kingdom in rinds and barks. The best described property of Quercetin is its ability to act as antioxidant. Quercetin seems to be the most powerful flavonoids for protecting the body against reactive oxygen species, produced during the normal oxygen metabolism or are induced by exogenous damage [9, 10]. One of the most important mechanisms and the sequence of events by which free radicals interfere with the cellular functions seem to be the lipid peroxidation leading eventually the cell death. To protect this cellular death to happen from reactive oxygen species, living organisms have developed antioxidant line of defense systems [11]. These include enzymatic and non-enzymatic antioxidants that keep in check ROS/RNS level and repair oxidative cellular damage. The major enzymes, constituting the first line of defence, directly involved in the neutralization of ROS/RNS are: superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) The second line of defence is represented by radical scavenging antioxidants such as vitamin C, vitamin A and plant phytochemicals including quercetin that inhibit the oxidation chain initiation and prevent chain propagation. This may also include the termination of a chain by the reaction of two radicals. The repair and de novo enzymes act as the third line of defence by repairing damage and reconstituting membranes. These include lipases, proteases, DNA repair enzymes and transferases. Quercetin is a specific quinone reductase 2 (QR2) inhibitor, an enzyme (along with the human QR1 homolog) which catalyzes metabolism of toxic quinolines. Inhibition of QR2 in plasmodium may potentially cause lethal oxidative stress. The inhibition of antioxidant activity in plasmodium may contribute to killing the malaria causing parasites.

Gallic acid is a polyphenol found in a variety of foods and herbs. Several studies have shown thta gallic acid has neuroprotective and anti-oxidant properties and can be a promising candidate for the treatment of cancer, cardiovascular diseases, neurodegenerative disorders, fatty liver disease and many others. Gallic acid acts by protecting cells against oxidative damage caused by reactive species often encountered in biological systems including, hydroxyl, superoxide and peroxyl and the non-radicals, hydrogen peroxide and hypochlorous acid. However, its ability to induce apoptosis, is mainly associated with its prooxidant, rather than antioxidant behavior.

2′-Deoxycytidine (deoxyC) is one of the deoxy nucleosides, which after phosphorylation to dCTP is used to synthesize DNA via various DNA polymerases or reverse transcriptases. Deoxycytidine is phosphorylated by deoxycytidine kinase (dCK). This enzyme catalyzes the initial conversion of the nucleosides deoxyadenosine (dA), deoxyguanosine (dG), and deoxycytidine (dC) into their monophosphate forms, with subsequent phosphorylation to the triphosphate forms performed by additional enzymes.

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.

Ethyl Ferulate is an ester type of Ferulic Acid and has powerful antioxidant, free radical scavenging and UV adsorption properties. Ethyl Ferulate can be incorporated into various cosmetic formulations including aqueous, ethanolic and emulsion-based creams, sun creams or moisturizers. Ethyl ferulate demonstrated the cytoprotective effects against oxidative damage in neuronal cells. Ethyl ferulate has also been widely studied and some recent findings include its anticholinesterase activity; inhibition of nuclear factor-kappa B (NF-κB) activity in LPS-stimulated RAW 264.7 macrophages; inhibition of inducible nitric oxide synthase (iNOS) induction in UV-induced oxidative stress in melanocytes; induction of heme oxygenase (HO-1) activity in rat astrocytes and neurons, which is a putative pathway against oxidative stress that underline neurodegenerative diseases; and cytoprotective effect against reactive oxygen species (ROS)-induced damage through the stimulation of dermal fibroblasts stress response.

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.

Resveratrol, a natural non-flavonoid polyphenol, exhibits a wide range of beneficial properties as an anticancer agent, a platelet anti-aggregation agent, and an antioxidant, as well as its anti-aging, anti-inflammatory, antiallergenic. This compound is in phase III clinical trials in combination with carboxymethyl-β-glucan for improving nasal symptoms in children with pollen-induced allergic rhinitis. Also in phase III clinical trial in the treatment of painful knee osteoarthritis and in type 2 diabetic patients. It has been demonstrated that resveratrol may prevent type 2 diabetic by targeting Sirtuin type 1 (SIRT1), indicating that SIRT1 may be a novel therapeutic target for diabetes prevention.

Tramiprosate is a glycosaminoglycan mimetic designed to interfere with the actions of beta-amyloid peptides (Abeta) early in the cascade of amyloidogenic events. It is a patented variant of the amino acid taurine, which is reported to inhibit the interaction of Abeta with endogenous glycosaminoglycans and thereby prevent beta-sheet formation. Preclinical data have shown that tramiprosate reduces brain and plasma levels of Abeta, prevents fibril formation and exerts cytoprotective effects in the brain. The pharmacological effects have also been demonstrated in clinical trials of patients with mild to moderate Alzheimer's disease. Promising findings for the efficacy of tramiprosate, indicated by improvement or stabilization of cognitive function, have been shown in phase II clinical trials and open-label extensions of these studies. Furthermore, tramiprosate appears to be well tolerated with no reports of safety concerns. Tramiprosate is in phase III clinical trial for the treatment of Alzheimer's disease.

Idebenone is a synthetic short-chain benzoquinone and a substrate for the enzyme NAD(P)H:quinone oxidoreductase (NQO1) capable of stimulating mitochondrial electron transport and supplementing cellular energy levels. Idebenone was initially developed by Takeda Pharmaceutical Company for the treatment of Alzheimer’s disease and other cognitive defects. This has been met with limited success. The Swiss company Santhera Pharmaceuticals has started to investigate it for the treatment of neuromuscular diseases. In 2010, early clinical trials for the treatment of Friedreich’s ataxia and Duchenne muscular dystrophy have been completed. In clinical trials, Idebenone (Raxone/Catena) had a positive impact on a measurement of respiratory function (Peak Expiratory Flow, or PEF) in non-ambulatory Duchenne muscular dystrophy patients who were not taking steroids. As of December 2013 the drug is not approved for these indications in North America or Europe. It is approved for the treatment of Leber's hereditary optic neuropathy (LHON) in Europe. Idebenone (Raxone) is indicated for the treatment of visual impairment in adolescent and adult patients with Leber’s Hereditary Optic Neuropathy (LHON). Because the number of patients with Leber's hereditary optic neuropathy is low, the disease is considered ‘rare’, and Raxone was designated an ‘orphan medicine’ on 15 February 2007. Idebenone is thought to help improve production of energy by restoring mitochondrial function, thereby preventing the cellular damage and the loss of sight seen in LHON. Idebenone is a rapidly absorbed, safe and well-tolerated drug and is currently the only clinically proven treatment option for Leber's hereditary optic neuropathy (LHON) patients.