Fursultiamine, also known as thiamine tetrahydrofurfuryl disulfide (TTFD) is an oral FDA- approved thiamine derivative for treating vitamin B1 deficiency and is very rapidly metabolized into thiamine. Fursultiamine possesses a mild beneficial effect in patients with Alzheimer's disease. The improvement could be observed not only in their emotional or other mental symptoms but also in intellectual function. Only mildly impaired subjects showed cognitive improvement. In addition was shown, that fursultiamine have a beneficial clinical effect on some autistic children. Some relatively recent experiments have revealed that fursultiamine was a unique antagonist of hepcidin in vitro that could serve as a template for the development of drug candidates that inhibit the hepcidin-ferroportin interaction. This inhibition is a key for the treatment of anemia of inflammation (AI), a common in patients with infection, autoimmune diseases, cancer, and chronic kidney disease.

δ-Tocopherol (δ-T) is a chiral organic molecule belonging to the group of tocopherol, that vary in their degree of methylation of the phenol moiety of the chromanol ring. It was revealed, that δ-Tocopherol had a more potent anticancer activity in solid tumors compared to the other tocopherols, δ-T possessed antileukemic activity of in acute myeloid leukemia (AML). δ-T induced tumor cell death through peroxisome proliferator-activated receptor γ (PPAR-γ) induction, cyclin-D1 inhibition, and modulation of redox balance. In addition, on animal models was found, that δ-tocopherol was more active than α- or γ-tocopherol in inhibiting lung tumor growth, possibly through trapping reactive oxygen and nitrogen species and inducing apoptosis.

Methylcobalamin (also known as mecobalamin, MeCbl, or MeB12) is one of the two forms of biologically active vitamin B12. Methyl-B12 is the principal form of circulating vitamin B12, hence the form, which is transported into peripheral tissue. Methylcobalamin is absorbed by the intestine by a specific mechanism, which uses the intrinsic factor, and by a diffusion process in which approximately 1% of the ingested dose is absorbed. Cyanocobalamin and hydroxycobalamin are forms of the vitamin that require conversion to methylcobalamin. Methylcobalamin alone or in combination with others compound are used to treat different diseases. Being a component of CEREFOLIN NAC it is used to treat Alzheimer's dementia. As a part of METANX® tablets is used for the dietary management of endothelial dysfunction in patients with diabetic peripheral neuropathy. Methylcobalamin exerted therapeutic effects on neuropathic pain in diabetics, possibly through its neurosynthesis and neuroprotective actions. The possible mechanisms can be considered as follows. (1) Methylcobalamin improved nerve conduction velocity; (2) methylcobalamin promoted injured nerve regeneration, recovering the neuromuscular functions in peripheral hyperalgesia and allodynia; and (3) methylcobalamin inhibited the ectopic spontaneous discharges from peripheral primary sensory neurons in neuropathic pain states. Methylcobalamin is the only form that can cross the blood-brain barrier and so can directly protect brain cells from degeneration. While crossing the barrier, it also stimulates production of serotonin, a chemical neurotransmitter responsible for elevated mood; research where Alzheimer’s patients were administered methylcobalamin showcased improvements in memory, communication skills, and emotions. It also helps form the myelin sheath, the insular coating around nerve cells that allow for electrical impulses to travel through the nervous system more efficiently.

Cobamamide is one of the active forms of vitamin B12 that is also known as adenosylcobalamin or dibencozide. This drug is available as a nutritional supplement to prevent the vitamin B12 deficiency. Liposomal formulation of cobamamide was developed for the treatment of atopic dermatitis by a Korean company Hanall Biopharma.

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.

Lutein is a xanthophyll and one of 600 known naturally occurring carotenoids. Lutein is synthesized only by plants and like other xanthophylls is found in high quantities in green leafy vegetables such as spinach, kale and yellow carrots. In green plants, xanthophylls act to modulate light energy and serve as non-photochemical quenching agents to deal with triplet chlorophyll (an excited form of chlorophyll), which is overproduced at very high light levels, during photosynthesis. Xanthophylls are taken for nutritional supplementation, and also for treating dietary shortage or imbalance. Xanthophylls have antioxidant activity and react with active oxygen species, producing biologically active degradation products. They also can inhibit peroxidation of membrane phospholipids and reduce lipofuscin formation, both of which contribute to their antioxidant properties. Lutein is naturally present in the macula of the human retina. It filters out potentially phototoxic blue light and near-ultraviolet radiation from the macula. The protective effect is due in part, to the reactive oxygen species quenching ability of these carotenoids. Lutein is more stable to decomposition by pro-oxidants than are other carotenoids such as beta-carotene and lycopene. Lutein is abundant in the region surrounding the fovea, and lutein is the predominant pigment at the outermost periphery of the macula. Zeaxanthin, which is fully conjugated (lutein is not), may offer somewhat better protection than lutein against phototoxic damage caused by blue and near-ultraviolet light radiation. Lutein is one of only two carotenoids that have been identified in the human lens, may be protective against age-related increases in lens density and cataract formation. Again, the possible protection afforded by lutein may be accounted for, in part, by its reactive oxygen species scavenging abilities. Carotenoids also provide protection from cancer. One of the mechanisms of this is by increasing the expression of the protein connexin-43, thereby stimulating gap junctional communication and preventing unrestrained cell proliferation. Lutein was found to be present in a concentrated area of the macula, a small area of the retina responsible for central vision. The hypothesis for the natural concentration is that lutein helps protect from oxidative stress and high-energy light. Several studies show that an increase in macula pigmentation decreases the risk for eye diseases such as Age-related Macular Degeneration (AMD). There is also epidemiological evidence that increasing lutein and zeaxanthin intake lowers the risk of cataract development. Consumption of more than 2.4 mg of lutein/zeaxanthin daily from foods and supplements was significantly correlated with reduced incidence of nuclear lens opacities, as revealed from data collected during a 13- to 15-year period in the Nutrition and Vision Project (NVP).

Pantethine, dimeric form of pantothenic acid, is a biologically active form of the B5 vitamin and an intermediate in the production of Coenzyme A. It is available as a dietary supplement, and is used support the healthy blood-cholesterol profile. Pantethine has shown an ability to favorably impact a variety of risk factors in people with hypercholesterolemia, arteriosclerosis and diabetes. It is thought that pantethine, in conjunction with the intermediary cysteamine, inhibits acetyl-coenzyme (CoA) carboxylase and 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase, thereby affecting TG synthesis and lipoprotein metabolism. Pantethine increases CoA levels within the cells, which favorably modifies lipoprotein metabolism. The full mechanism of action of pantethine in lowering cholesterol levels is not fully understood. Since homocysteine is believed to contribute to the onset and progression of atherosclerosis and is involved in the biosynthesis of CoA, it is possible that pantethine impacts homocysteine.