8-bromo-CyclicAMP is a brominated derivative of cAMP that remains long-acting due to its resistance to degradation by cAMP phosphodiesterase. It can activate cAMP-dependent protein kinase, inhibiting growth, decreasing proliferation, increasing differentiation, and inducing apoptosis of cancer cells.
Cyclic di-AMP (c-di-AMP) is a second messenger produced by bacteria but not by mammals. Generated by a family of diadenylate cyclases, c-di-AMP can impact bacterial cell growth, cell wall homeostasis, pathogenicity, and other cellular functions. Bacteria-derived cyclic dinucleotides, including c-di-AMP, trigger the expression of interferon genes in mammalian cells.
Rp-8-CPT-cAMP is a structural combination of the lipophilic and non-hydrolyzable cAMP analogs, 8-CPT-cyclicAMP and Rp-cyclicAMPS .[1] It functions as a site-selective inhibitor of protein kinase A (PKA) type I and II, with preference towards site A of type I and site B of type II.2 By occupying cAMP binding sites at the regulatory subunit of PKA, Rp-8-CPT-cAMP prevents the kinase holoenzyme from dissociative activation.[2],[3]
Sp-cAMPS sodium salt 作为 cAMP 类似物,是一种依赖 cAMP 的PKA I 和PKA II 的有效激活剂。Sp-cAMPS sodium salt 还是一种有效的竞争性磷酸二酯酶 (PDE3A) 抑制剂,Ki 为 47.6 μM。Sp-cAMPS sodium salt 结合PDE10 GAF 结构域,EC50为 40 μM 。
Rp-8-bromo-CyclicAMPS (Rp-8-bromo-cAMPS) is a cell-permeable cAMP analog that combines an exocyclic sulfur substitution in the equatorial position of the cyclophosphate ring with a bromine substitution in the adenine base of cAMP. It acts as an antagonist of cAMP-dependent protein kinases (PKAs) and is resistant to hydrolysis by cyclic nucleotide phosphodiesterases. Rp-8-bromo-cAMPS more effectively antagonizes cAMP-dependent activation of purified PKA type I from rabbit muscle than PKA type II from bovine heart.