Ivermectin is a broad-spectrum anti-parasite medication. It was first marketed under the name Stromectol® and used against worms (except tapeworms), but, in 2012, it was approved for the topical treatment of head lice infestations in patients 6 months of age and older, and marketed under the name Sklice™ as well. Ivermectin is mainly used in humans in the treatment of onchocerciasis but is also effective against other worm infestations (such as strongyloidiasis, ascariasis, trichuriasis, and enterobiasis). Ivermectin binds selectively and with high affinity to glutamate-gated chloride ion channels in invertebrate muscle and nerve cells of the microfilaria. This binding causes an increase in the permeability of the cell membrane to chloride ions and results in hyperpolarization of the cell, leading to paralysis and death of the parasite. Ivermectin also is believed to act as an agonist of the neurotransmitter gamma-aminobutyric acid (GABA), thereby disrupting GABA-mediated central nervous system (CNS) neurosynaptic transmission. Ivermectin may also impair the normal intrauterine development of O. volvulus microfilariae and may inhibit their release from the uteri of gravid female worms. It is sold under brand names Heartgard, Sklice and Stromectol in the United States, Ivomec worldwide by Merial Animal Health, Mectizan in Canada by Merck, Iver-DT in Nepal by Alive Pharmaceutical and Ivexterm in Mexico by Valeant Pharmaceuticals International. In Southeast Asian countries, it is marketed by Delta Pharma Ltd. under the trade name Scabo 6.

Colistimethate is a methanesulfonate of polymyxin antibacterial colistin. Colistimethate is a nonactive prodrug. In aqueous solutions, colistimethate is hydrolyzed and forms a complex mixture of partially sulfomethylated derivatives and colistin. The antimicrobial activity of colistin is similar to that of polymyxin B and is restricted to gram-negative bacteria, including P aeruginosa, Acinetobacter species, Enterobacter-Klebsiella tribe, Escherichia coli, Salmonella and Shigella species, Citrobacter species, Yersinia pseudotuberculosis, Morganella morganii and Haemophilus influenzae. Colistin has also been shown to possess considerable in vitro activity against Stenotrophomonas maltophilia. Colistin and polymyxin B, however, do not have activity against Proteus, Providencia, Serratia species, Pseudomonas mallei, Burkholderia cepacia, Brucella species, most gram-positive bacteria, gram-negative cocci, anaerobes, fungi and parasites. Parenteral or nebulized colistimethate is indicated for the treatment of acute or chronic infections due to sensitive strains of certain gram-negative bacilli. It is particularly indicated when the infection is caused by sensitive strains of Pseudomonas aeruginosa.

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.

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.

Crilvastatin is an inhibitor of hydroxymethylglutaryl-coenzyme A reductase. In a rat model, the drug was demonstrated to increase low-density lipoprotein (LDL)-cholesterol uptake by the liver more than high-density lipoprotein uptake, thus increasing the clearance of excess plasma cholesterol.