Rp-8-CPT-cAMPS sodium

Rp-8-CPT-cAMPS sodium, a cAMP analog, is a potent and competitive antagonist of cAMP-induced activation of cAMP-dependent PKA I and II. Rp-8-CPT-cAMPS sodium preferentially selects site A of RI compares to site A of RII and site B of RII compares to site B of RI[1][2].

Signaling Pathways >> Protein Tyrosine Kinase/RTK >> PKA

Signaling Pathways >> Stem Cell/Wnt >> PKA

Research Areas >> Inflammation/Immunology

Research Areas >> Neurological Disease

PKA[1]

Rp-8-CPT-cAMPS (100 μM; 15 min) blocks phosphorylation of VASP by 6-Bnz-cAMP and largely reduces VASP phosphorylation by forskolin and fenoterol[2]. Rp-8-CPT-cAMPS (100 μM; 30 min) reduces GTP-loading of Rap1 by both 8-pCPT-2'-O-Me-cAMP and 6-Bnz-cAMP[2]. Rp-8-CPT-cAMPS (100 μM; 30 min) largely diminishes the augmentation of bradykinin-induced IL-8 release by the PKA activator 6-Bnz-cAMP and the Epac activator 8-pCPT-2'-O-Me-cAMP[2]. Rp-8-CPT-cAMPS (10 μM) inhibits the endothelium-dependent and -independent relaxation which induced by Venom in pre-contracted rat mesenteric artery rings[3].

[1]. Dostmann WR , et, al. Probing the cyclic nucleotide binding sites of cAMP-dependent protein kinases I and II with analogs of adenosine 3',5'-cyclic phosphorothioates. J Biol Chem. 1990 Jun 25;265(18):10484-91.

[2]. Roscioni SS, et, al. PKA and Epac cooperate to augment bradykinin-induced interleukin-8 release from human airway smooth muscle cells. Respir Res. 2009 Sep 29;10(1):88.

[3]. Chaisakul J, et, al. In vivo and in vitro cardiovascular effects of Papuan taipan (Oxyuranus scutellatus) venom: Exploring "sudden collapse". Toxicol Lett. 2012 Sep 3;213(2):243-8.