ADK
Adenosine (ADO) is an endogenous homeostatic inhibitory neuromodulator that reduces cellular excitability at sites of tissue injury and inflammation. The effects of ADOon cellular excitability are mediated via interactions with different cell surface receptor subtypes (termed P1 receptors: A1, A2A, A2B, and A3 receptor subtypes) and can result in cellular protection during conditions of physiological stress or trauma, including ischemia, seizures, inflammation, and pain[1]. The effects of extracellular ADO are terminated by its reuptake and phosphorylation by ADO kinase (ADK; EC 2.7.1.20) and via deamination by adenosine deaminase (ADA; EC 3.5.4.4). By preventing ADO phosphorylation, ADK inhibition increases intracellular ADO concentrations, altering the equilibrium of the bidirectional transport systems responsible for ADO reuptake with the net effect of increasing the local concentration of ADO in the extracellular compartment. Therefore, ADK inhibitors may have therapeutic potential as analgesic and anti-inflammatory agents[2].
[1] M.F. Jarvis et al. ABT-702 (4-amino-5-(3-bromophenyl)-7-(6-morpholinopyridin-3-yl)pyrido[2, 3-d]pyrimidine), a novel orally effective adenosine kinase inhibitor with analgesic and anti-inflammatory... J Pharmacol Exp Ther. 2000 Dec;295(3):1156-64.
[2] C.H. Lee et al. Discovery of 4-amino-5-(3-bromophenyl)-7-(6-morpholino-pyridin-3-yl)pyrido[2,3-d]pyrimidine, an orally active, non-nucleoside adenosine kinase inhibitor. J Med Chem. 2001 Jun 21;44(13):2133-8.