Acetylcysteine amide (NACA) is a novel thiol-containing antioxidant. NACA is a modified form of its parent compound N-acetylcysteine (NAC) that is a precursor of the most abundant endogenous antioxidant, glutathione (GSH). NACA demonstrated the multiple therapeutic abilities, including antioxidant, anti-apoptotic, and anti-inflammatory properties with greater efficacy compared to its parent compound. NACA treatment significantly maintained acute mitochondrial bioenergetics and normalized GSH levels following spinal cord injury. It is a new neuroprotective drug, that might be effective at slowing down nigral neuronal degeneration and illness progression in patients with Parkinson's disease.

Verteporfin (trade name Visudyne), a benzoporphyrin derivative, is a medication used for the treatment of patients with predominantly classic subfoveal choroidal neovascularization due to age-related macular degeneration, pathologic myopia or presumed ocular histoplasmosis syndrome. Verteporfin can also be used to destroy tumors. Verteporfin is a 1:1 mixture of two regioisomers (I and II), VISUDYNE therapy is a two-stage process requiring administration of both verteporfin for injection and nonthermal red light. Verteporfin accumulates in these abnormal blood vessels and, when stimulated by nonthermal red light with a wavelength of 689 nm in the presence of oxygen, produces highly reactive short-lived singlet oxygen and other reactive oxygen radicals, resulting in local damage to the endothelium and blockage of the vessels. Verteporfin is also used off-label for the treatment of central serous retinopathy. Verteporfin is given intravenously, 15 minutes before laser treatment. Light activation of verteporfin results in local damage to neovascular endothelium, resulting in vessel occlusion. Damaged endothelium is known to release procoagulant and vasoactive factors through the lipo-oxygenase (leukotriene) and cyclo-oxygenase (eicosanoids such as thromboxane) pathways, resulting in platelet aggregation, fibrin clot formation and vasoconstriction. Verteporfin appears to somewhat preferentially accumulate in neovasculature, including choroidal neovasculature. However, animal models indicate that the drug is also present in the retina. Therefore, there may be collateral damage to retinal structures following photoactivation including the retinal pigmented epithelium and outer nuclear layer of the retina. The temporary occlusion of choroidal neovascularization (CNV) following VISUDYNE therapy has been confirmed in humans by fluorescein angiography.

Permethrin is a synthetic pyrethrin derivative acts as a neurotoxin by depolarizing the nerve cell membrane. Permethrin disrupts the sodium channel current by which membrane repolarization is regulated resulting in fatal paralysis of the nerves in the exoskeletal respiratory muscles of susceptible arthropods, including lice and mite. Permethrin is sold under brand names NIx and Elimite to treat pediculosis, scabies and demodicidosis.

Retonol, also known as Vitamin A1, is a vitamin found in food and used as a dietary supplement. It is used to treat and prevent vitamin A deficiency. It is also used to prevent further issues in those who have measles. Retinol is used as a metabolic precursor of retinoic acid to treat skin-related conditions, such as cellulite, skin aging, photodamage.

Phylloquinone is often called vitamin K1 or phytonadione. It is a fat-soluble vitamin that is stable to air and moisture but decomposes in sunlight. It is found naturally in a wide variety of green plants. Phylloquinone is also an antidote for coumatetralyl. Vitamin K is needed for the posttranslational modification of certain proteins, mostly required for blood coagulation. MEPHYTON (Phytonadione tablets) are indicated in the following coagulation disorders which are due to faulty formation of factors II, VII, IX and X when caused by vitamin K deficiency or interference with vitamin K activity: anticoagulant-induced prothrombin deficiency caused by coumarin or indanedione derivatives; hypoprothrombinemia secondary to antibacterial therapy; hypoprothrombinemia secondary to administration of salicylates; hypoprothrombinemia secondary to obstructive jaundice or biliary fistulas but only if bile salts are administered concurrently, since otherwise the oral vitamin K will not be absorbed. MEPHYTON tablets possess the same type and degree of activity as does naturally-occurring vitamin K, which is necessary for the production via the liver of active prothrombin (factor II), proconvertin (factor VII), plasma thromboplastin component (factor IX), and Stuart factor (factor X). The prothrombin test is sensitive to the levels of three of these four factors II, VII, and X. Vitamin K is an essential cofactor for the gamma-carboxylase enzymes, which catalyze the posttranslational gamma-carboxylation of glutamic acid residues in inactive hepatic precursors of coagulation factors II (prothrombin), VII, IX, and X. Gamma-carboxylation converts these inactive precursors into active coagulation factors, which are secreted by hepatocytes into the blood. Supplementing with Phylloquinone results in a relief of vitamin K deficiency symptoms, which include easy bruisability, epistaxis, gastrointestinal bleeding, menorrhagia and hematuria. Oral phytonadione is adequately absorbed from the gastrointestinal tract only if bile salts are present. After absorption, phytonadione is initially concentrated in the liver, but the concentration declines rapidly. Very little vitamin K accumulates in tissues. Little is known about the metabolic fate of vitamin K. Almost no free unmetabolized vitamin K appears in bile or urine. In normal animals and humans, phytonadione is virtually devoid of pharmacodynamic activity. However, in animals and humans deficient in vitamin K, the pharmacological action of vitamin K is related to its normal physiological function; that is, to promote the hepatic biosynthesis of vitamin K-dependent clotting factors. MEPHYTON tablets generally exert their effect within 6 to 10 hours.

It is known that Vitamin E, traditionally known as α¬ tocopherol, is a mixture of eight different compounds, four tocopherols and four tocotrienols, each one being designated as α, β, γ and δ forms. The two groups differ in the hydrophobic tridecyl side chain which is saturated (phytyl) in tocopherols and unsaturated having three double bonds (geranyl) in tocotrienols. During the last few years, it has been found that all the eight forms are biologically active and perform specific functions. Clinical research has shown that mixture of tocotrienols and tocopherols offer synergistic protective action against heart ailments and cancer that is not exclusively offered by α¬tocopherol. The other advantage of mixed tocopherols and tocotrienols is their role in slowing down aging. Diseases like diabetes 1 and 2, autoimmune diseases, bacterial and viral infections, Alzheimer disease, fungal (Candida) infections are prevented by these compounds. It helps in the maintenance of bones, muscles, eyes (vision), memory, sleep, lungs, infertility, skin and wrinkles. Although all forms of Vitamin E exhibit antioxidant activity, it is known that the antioxidant activity of vitamin E is not sufficient to explain the vitamin's biological activity. Vitamin E's anti-atherogenic activity involves the inhibition of the oxidation of LDL and the accumulation of oxLDL in the arterial wall. Vitamin E's antithrombotic and anticoagulant activities involves the downregulation of the expression of intracellular cell adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 that lowers the adhesion of blood components to the endothelium. Its antioxidant effects explain the neuroprotective effects of vitamin E. The immunomodulatory effects of Vitamin E have been demonstrated in vitro, where alpha-tocopherol increases mitogenic response of T lymphocytes from aged mice. The mechanism of this response by vitamin E is not well understood, however it has been suggested that vitamin E itself may have mitogenic activity independent of its antioxidant activity. The mechanism of action of vitamin E's antiviral effects (primarily against HIV-1) involves its antioxidant activity. Vitamin E reduces oxidative stress, which is thought to contribute to HIV-1 pathogenesis, as well as to the pathogenesis of other viral infections. Vitamin E also affects membrane integrity and fluidity and, since HIV-1 is a membraned virus, altering membrane fluidity of HIV-1 may interfere with its ability to bind to cell-receptor sites, thus decreasing its infectivity.

It is known that Vitamin E, traditionally known as α¬ tocopherol, is a mixture of eight different compounds, four tocopherols and four tocotrienols, each one being designated as α, β, γ and δ forms. The two groups differ in the hydrophobic tridecyl side chain which is saturated (phytyl) in tocopherols and unsaturated having three double bonds (geranyl) in tocotrienols. During the last few years, it has been found that all the eight forms are biologically active and perform specific functions. Clinical research has shown that mixture of tocotrienols and tocopherols offer synergistic protective action against heart ailments and cancer that is not exclusively offered by α¬tocopherol. The other advantage of mixed tocopherols and tocotrienols is their role in slowing down aging. Diseases like diabetes 1 and 2, autoimmune diseases, bacterial and viral infections, Alzheimer disease, fungal (Candida) infections are prevented by these compounds. It helps in the maintenance of bones, muscles, eyes (vision), memory, sleep, lungs, infertility, skin and wrinkles. Although all forms of Vitamin E exhibit antioxidant activity, it is known that the antioxidant activity of vitamin E is not sufficient to explain the vitamin's biological activity. Vitamin E's anti-atherogenic activity involves the inhibition of the oxidation of LDL and the accumulation of oxLDL in the arterial wall. Vitamin E's antithrombotic and anticoagulant activities involves the downregulation of the expression of intracellular cell adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 that lowers the adhesion of blood components to the endothelium. Its antioxidant effects explain the neuroprotective effects of vitamin E. The immunomodulatory effects of Vitamin E have been demonstrated in vitro, where alpha-tocopherol increases mitogenic response of T lymphocytes from aged mice. The mechanism of this response by vitamin E is not well understood, however it has been suggested that vitamin E itself may have mitogenic activity independent of its antioxidant activity. The mechanism of action of vitamin E's antiviral effects (primarily against HIV-1) involves its antioxidant activity. Vitamin E reduces oxidative stress, which is thought to contribute to HIV-1 pathogenesis, as well as to the pathogenesis of other viral infections. Vitamin E also affects membrane integrity and fluidity and, since HIV-1 is a membraned virus, altering membrane fluidity of HIV-1 may interfere with its ability to bind to cell-receptor sites, thus decreasing its infectivity.

Istaroxime is a novel intravenous agent with luso-inotropic properties that acts by inhibition of Na( )/K( ) adenosine triphosphatase and stimulation of sarco/ endoplasmic reticulum calcium ATPase isoform 2. It is significantly decreased left ventricular end-diastolic pressure, pulmonary capillary wedge pressure, heart rate and increased systolic blood pressure and cardiac index with no change in neurohormones, renal function or troponin I. Istaroxime has successfully concluded phase II clinical trials in cardiac failure patients. Istaroxime induced apoptosis, affected the key proliferative and apoptotic mediators c-Myc and caspase-3 and modified actin cytoskeleton dynamics and RhoA activity in prostate cancer cells – this provides novel insights into the anti-cancer properties of istaroxime further supporting the development of this agent as a novel anti-cancer drug candidate.

Troglitazone (TGZ, brand name: Rezulin and Prelay) is a peroxisome proliferator-activated receptor gamma (PPAR gamma) ligand, which was developed by Daiichi Sankyo and approved for the US market for the treatment of Type II diabetes mellitus. The drug is used alone or in combination with a sulfonylurea, metformin, or insulin as an adjunct to diet and exercise, and was not indicated as initial therapy in patients with type 2 diabetes. This drug was withdrawn from the UK market due to liver toxicity. It was removed from the US market in 2000, only 3 years after its introduction and from Japan, shortly afterward. In addition, was conducted a clinical trial for the treatment of patients with advanced liposarcoma by using troglitazone, but the positive result wasn’t obtained. It was shown, that in case of cancer cells troglitazone acted independently of PPAR gamma, by up-regulation of early growth response-1 (Egr-1). Egr-1 transcription factor has been linked to apoptosis and shown to be activated by extracellular signal-regulated kinase (ERK).

Abamectin is a mixture of avermectins containing avermectin B1a and avermectin B1b. These two components, B1a and B1b have very similar biological and toxicological properties. The avermectins are insecticidal or anthelmintic compounds derived from the soil bacterium Streptomyces avermitilis. Abamectin is used to control insect and mite pests of a range of agronomic, fruit, vegetable and ornamental crops and it is used by homeowners for control of fire ants. Abamectin acts on insects by interfering with neural and neuromuscular transmission. Abamectin attenuated ethanol-induced gastric ulceration. Chemical structure and effects on GABAARs and P2X4Rs receptor function play key roles in the ability of avermectin to reduce ethanol intake