Cyclic adenosine monophosphate (cAMP) (cAMP)

Cyclic adenosine monophosphate (cAMP) is a fundamental intracellular second messenger that plays a central role in translating extracellular signals, such as hormones and neurotransmitters, into specific cellular responses [4, 13]. It is synthesized from ATP by the enzyme adenylyl cyclase upon activation of stimulatory G protein-coupled receptors and is subsequently degraded by phosphodiesterases (PDE) to ensure precise signaling [2, 14]. As a universal regulator, cAMP mediates critical physiological processes including glucose and lipid metabolism, cardiac muscle contractility, and smooth muscle relaxation [2]. Its effects are primarily mediated through the activation of protein kinase A (PKA), though it also regulates exchange proteins activated by cAMP (EPACs) and cyclic nucleotide-gated ion channels [4, 9]. In the clinical setting, the cAMP pathway is a major focus for pharmacological intervention; for example, beta-adrenergic agonists increase cAMP to treat asthma, while PDE inhibitors like roflumilast are utilized for chronic obstructive pulmonary disease [6, 15]. Imbalances in cAMP signaling are linked to a broad range of pathologies, including heart failure, diabetes, chronic inflammation, and certain types of cancer [5, 12]. Consequently, monitoring and modulating cAMP levels remain essential strategies in both drug development and therapeutic efficacy monitoring [10, 13].

Other names

3',5'-Cyclic adenosine monophosphateCyclic AMPAdenosine 3',5'-cyclic monophosphateCyclic adenylic acid

Modulation of cAMP concentrations through the activation of adenylyl cyclases via Gs-protein coupled receptors or the inhibition of phosphodiesterase enzymes that degrade cAMP.