GR79236 is an adenosine A1 receptor agonist, which possesses cardiovascular and antilipolytic properties. GR79236 was studied in model animals for the treatment of diabetic ketoacidosis and in patients for pain relief. However, these studies were discontinued. In addition, analgesic efficacy of GR79236 was investigated in the dental pain model. Nevertheless, there was no evidence of efficacy of GR79236. A higher dose of GR79236 might have been effective or that was suggested, that intravenous administration of that drug did not achieve appropriate concentrations in the brain or peripheral nerves.

Yohimbine is a plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of impotence. The exact mechanism for its use in impotence has not been fully elucidated. Yohimbine exerts antagonist actions at halpha(2A)-AR, h5-HT(1B), h5-HT(1D), and hD(2) sites, partial agonist actions at h5-HT(1A) sites. Yohimbine-mediated norepinephrine release at the level of the corporeal tissues may also be involved. In addition, beneficial effects may involve other neurotransmitters such as dopamine and serotonin and cholinergic receptors. Yohimbine has a mild anti-diuretic action, probably via stimulation of hypothalmic center and release of posterior pituitary hormone. Reportedly yohimbine exerts no significant influence on cardiac stimulation and other effects mediated by (beta)-adrenergic receptors. Its effect on blood pressure, if any, would be to lower it; however, no adequate studies are at hand to quantitate this effect in terms of Yohimbine dosage. Side effect of Yohimbine include anxiety, tremor, palpitations, diarrhea, and supine hypertension.

Dyphylline is 7-(2,3-dihydroxypropyl)-theophylline, a white, extremely bitter, amorphous powder that is freely soluble in water and soluble in alcohol. Dyphylline is stable in gastrointestinal fluids over a wide range of pH. Dyphylline is a xanthine derivative with pharmacologic actions similar to theophylline and other members of this class of drugs. Its primary action is that of bronchodilation, but it also exhibits peripheral vasodilatory and other smooth muscle relaxant activity to a lesser degree. The bronchodilatory action of dyphylline, as with other xanthines, is thought to be mediated through competitive inhibition of phosphodiesterase with a resulting increase in cyclic AMP producing relaxation of the bronchial smooth muscle. Dyphylline exerts its bronchodilatory effects directly and, unlike theophylline, is excreted unchanged by the kidneys without being metabolized by the liver. Because of this, dyphylline pharmacokinetics and plasma levels are not influenced by various factors that affect liver function and hepatic enzyme activity, such as smoking, age, congestive heart failure, or concomitant use of drugs which affect liver function.

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.

2,4-dinitrophenol (DNP) is a FDA-banned weight-loss agent and EPA-regulated environmental toxicant, traditionally used in research labs as an uncoupler of OXPHOS. Although not licensed for human consumption, DNP and DNP crystal form are used by bodybuilders and extreme dieters for their fat burning properties through inhibiting efficient energy (ATP) production in cells. Through uncoupling mitochondrial oxidative phosphorylation by facilitating proton transport across the mitochondrial membrane, DNP leads to rapid consumption of energy without generating ATP and consequently, to increased fat metabolism. However, the weight-loss effect comes with serious, and in some cases potentially fatal, adverse side effects, namely hyperthermia (the leading cause of fatality with acute DNP toxicity) and cardiac arrest, but also diaphoresis, tachycardia, tachypnea, skin toxicity, Fourier’s gangrene and cataracts with low dose chronic exposure. The proposed mechanism of DNP induced toxicity suggests the activation of ATP-sensitive K channels.

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

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.