PKA is a ubiquitous cellular kinase, also known as cAMP-dependent protein kinase (cAMP), and it is well-established that plays an important role in regulating several functions of cell processes, including regulation of glycogen, sugar, and lipid metabolism[1]. Bucladesine Calcium is a cell-permeable PKA activator that functions by preferentially activating endogenous cAMP. In vitro assays, Bucladesine Calcium was found to significantly suppress TNF-a production in a dose-dependent manner, with IC50 values of 247, 28.9, and 25.4 μM, respectively in RAW264.7 cells[2]. Additionally, Rat hepatocytes were cultured with cAMP agonists Bucladesine Calcium inhibits Nitric oxide synthesis and inducible nitric oxide synthase (iNOS) expression through effects on the iNOS promoter region and NF-kB-binding activity[3]. In hepatocytes, Bucladesine Calcium can prevent tumor necrosis factor α plus acti-nomycin D (TNFα/ActD)-induced apoptosis via a PKA-dependent mechanism[4]. In vivo model, Bucladesine Calcium shows a distinct anti-fibrotic effect via PKA/p-CREB/CBP signaling. Treatment of Bucladesine Calcium result in the decrease of the number and size of silicosis nodules, inhibition of myofibroblast differentiation, and extracellular matrix deposition[5]. Moreover, 4 days intra-peritoneal injections of Bucladesine Calcium (600 nM/mouse) significantly reversed zinc chloride- and lead acetate-induced avoidance memory retention alterations compared to control animals[6].
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