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.
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]
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.
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.
ZK110841 is an agonist of prostaglandin DP-receptors on human platelet. ZK110841 elevated the cyclicAMP level in EBTr cells dose-dependently, being more than 100 fold over the basal level at 1 microM.
CU-32 is an inhibitor of cyclic GMP-AMP (cGAMP) synthase (cGAS; IC50= 0.45 μM).1It reduces DNA-, but not Sendai virus-, induced dimerization of IFN regulatory factor 3 in THP-1 cells, indicating selectivity for the cGAS DNA sensing pathway over the RIG-I-MAVS RNA sensing pathway. It is also selective for cGAS over toll-like receptors (TLRs) at 50 μM. CU-32 decreases IFN-stimulatory DNA-induced production of IFN-β in THP-1 cells when used at concentrations of 10, 30, and 100 μM. 1.Padilla-Salinas, R., Sun, L., Anderson, R., et al.Discovery of small-molecule cyclic GMP-AMP synthase inhibitorsJ. Org. Chem.85(3)1579-1600(2020)