3-Deaza-adenosine (BW 91Y) is a potent inhibitor of adenosine deaminase and S-Adenosylhomocysteine (SAH) hydrolase, with potent antitumor activity against a range of leukemia cell lines. 3-Deaza-adenosine has anti-inflammatory properties, inhibiting leukocyte adhesion and chemotaxis, lymphocyte-mediated cytolysis, phagocytosis, degranulation, and NF-κB signaling. 3-Deaza-adenosine also has antiviral and antibacterial activities. 3-Deaza-adenosine has previously been shown to inhibit a variety of cellular functions, which could be critical for the development of atherosclerosis and restenosis. These include the thrombin-stimulated production of platelet-derived growth factor and the expression of endothelial leukocyte adhesion molecule-1 as well as cellular arachidonic acid and ROS production. Moreover, c3Ado prevents tumor necrosis factor (TNF)-alpha production, reduces TNF- alpha-induced macrophage adhesion to endothelial cells in vitro via the inhibition of ICAM-1 synthesis, and promotes monocyte apoptosis.

Adenosine monophosphate (AMP) is a nucleotide, consisting of a phosphate group, the sugar ribose, and the nucleobase adenine. AMP is an activator of several enzymes in the tissues. In the glycolytic pathway, the enzyme phosphofructokinase is inhibited by ATP but the inhibition is reversed by AMP, the deciding factor for the reaction being the ratio between ATP and AMP. In medicine, AMP is used mainly as an alternative to adenosine for treatment of ischemia and as a tool compound to measure hyperresponsiveness of airways.

2′-Deoxyadenosine, a pair of deoxythymidine (T) in double-stranded DNA, is a substrate of adenosine deaminase. In case of absence of this enzyme, 2′-deoxyadenosine accumulates in T lymphocytes and kills these cells resulting in a genetic disorder known as adenosine deaminase severe combined immunodeficiency disease (ADA-SCID).

α,β-methylene adenosine 5′-diphosphate (AOPCP, adenosine-5′-O-[(phosphonomethyl)phosphonic acid] or α,β-methylene-ADP) is an analog of adenosine 5′-diphosphate (ADP). It acts as a CD73/ecto-5′-nucleotidase inhibitor. Blocks ecto-5'-nucleotidase-mediated adenosine production by preventing the conversion of AMP to adenosine.

Cordycepin, or 3'-deoxyadenosine, is a derivative of the nucleoside adenosine, differing from the latter by the absence of the hydroxy group in the 3' position of its ribose part. Cytostatic effect of cordycepin is due to incorporation of phospho-cordycepin into mRNA and inhibition of mRNA synthesis. Cordycepin exhibit rapid antidepressant effect due to potentiation of AMPA receptors

Nicotinamide adenine nucleotide (NAD) is a cofactor found in all living cells. It exists in oxidized form (NAD+) and reduced form (NADH). NADH is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). NADH supplements are used for improving mental clarity, alertness, concentration, and memory; as well as for treating Alzheimer’s disease and dementia. Because of its role in energy production, NADH is also used for improving athletic performance and treating chronic fatigue syndrome (CFS). Some people use NADH for treating high blood pressure, high cholesterol, jet lag, depression, and Parkinson’s disease; opposing alcohol’s effects on the liver; reducing signs of aging; protecting against the side effects of an AIDS drug called zidovudine (AZT).

Flavin adenine dinucleotide is a coenzyme form of vitamin B2. Many oxidoreductases, called flavoenzymes or flavoproteins, require FAD as a prosthetic group, which functions in electron transfers. It is usually used for the prevention and treatment of various diseases that are caused by Vitamin B2 deficiency or metabolic disorder including stomatitis, eczema, etc. No adverse reactions were reported.

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.

Guanosine is an endogenous guanine nucleoside. Guanosine was shown to be protective in several in vitro and/or in vivo experimental models of central nervous system (CNS) diseases including ischemic stroke, Alzheimer's disease, Parkinson's disease, spinal cord injury, nociception, and depression. The mechanisms underlying the neurobiological properties of guanosine seem to involve the activation of several intracellular signaling pathways and a close interaction with the adenosinergic system, with a consequent stimulation of neuroprotective and regenerative processes in the CNS. Several guanosine analogues, i.e. acyclovir (and its oral prodrug valaciclovir), penciclovir (in its oral prodrug form, famciclovir) and ganciclovir, are widely used for the treatment of herpesvirus (i.e. HSV-1, HSV-2, VZV and HCMV) infections.