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.

Cyclic adenosine monophosphate (cAMP, cyclic AMP or 3'-5'-cyclic adenosine monophosphate) is a molecule that is important in many biological processes; it is derived from adenosine triphosphate (ATP) by adenylate cyclase located on the inner side of the plasma membrane and anchored at various locations in the interior of the cell. Around 1960 Earl W. Sutherland, Jr. showed that cyclic adenosine monophosphate (cAMP) serves as the secondary messenger within the cell. Cyclic AMP works by activating protein kinase A (PKA, or cAMP-dependent protein kinase). PKA is normally inactive as a tetrameric holoenzyme, consisting of two catalytic and two regulatory units with the regulatory units blocking the catalytic centers of the catalytic units. Cyclic AMP binds to specific locations on the regulatory units of the protein kinase, and causes dissociation between the regulatory and catalytic subunits, thus enabling those catalytic units to phosphorylate substrate proteins. It was discovered, that melanocytes require the RAS/RAF/MEK/ERK and the cyclic AMP (cAMP) signaling pathways to maintain the fine balance between proliferation and differentiation. cAMP suppressed CRAF activity in melanocytes and that was essential to suppress the oncogenic potential of CRAF in the cells. When RAS was mutated in melanoma, the cells switched their signaling from BRAF to CRAF. That switch was accompanied by dysregulated cAMP signaling, a step that was necessary to allow CRAF to signal to MEK. Thus, a fundamental switch in RAF isoform usage occurs when RAS was mutated in melanoma, and that occurs in the context of disrupted cAMP signaling. These data have important implications for the development of therapeutic strategies to treat this life-threatening disease.