cAMPS-Rp, triethylammonium salt

Modify Date: 2024-01-03 08:23:24

cAMPS-Rp, triethylammonium salt Structure
cAMPS-Rp, triethylammonium salt structure
Common Name cAMPS-Rp, triethylammonium salt
CAS Number 151837-09-1 Molecular Weight 446.46200
Density N/A Boiling Point N/A
Molecular Formula C16H27N6O5PS Melting Point 212 - 213 ℃
MSDS N/A Flash Point N/A

 Use of cAMPS-Rp, triethylammonium salt


Rp-cAMPS triethylammonium salt is an analog of cAMP which acts as a potent, competitive and cell-permeable antagonist of cAMP-induced activation of cAMP-dependent PKA I and II (Kis of 6.05 µM and 9.75 µM, respectively). Rp-cAMPS triethylammonium salt is resistant to hydrolysis by phosphodiesterases[1][2][3][4][5].

 Names

Name Rp-Adenosine 3′,5′-cyclic monophosphorothioate triethylammonium salt hydrate
Synonym More Synonyms

 cAMPS-Rp, triethylammonium salt Biological Activity

Description Rp-cAMPS triethylammonium salt is an analog of cAMP which acts as a potent, competitive and cell-permeable antagonist of cAMP-induced activation of cAMP-dependent PKA I and II (Kis of 6.05 µM and 9.75 µM, respectively). Rp-cAMPS triethylammonium salt is resistant to hydrolysis by phosphodiesterases[1][2][3][4][5].
Related Catalog
Target

Ki: 6.05 µM (PKA I) and 9.75 µM (PKA II)[1]

In Vitro A membrane-permeable competitive cAMP antagonist (Rp-cAMPS) that blocks PKA activation by binding to the regulatory subunits without dissociating the kinase holoenzyme also inhibits synaptic plasticity but has no effect on normal synaptic transmission[1].
In Vivo Rp-cAMPS (10 μM, 15 min) decreases the monosynaptic EPSCs evoked at the PB-CeLC and BLA-CeLC synapses in slices from arthritic rats but not in control neurons from normal animals. The inhibitory effect of Rp-cAMPS is significant compared to predrug (ACSF) control values obtained in the same neurons[1].
References

[1]. Rothermel JD, et al. A mechanistic and kinetic analysis of the interactions of the diastereoisomers of adenosine 3',5'-(cyclic)phosphorothioate with purified cyclic AMP-dependent protein kinase. Biochem J. 1988 May 1;251(3):757-62.

[2]. Fu Y, et al. PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior. Mol Pain. 2008 Jul 16;4:26.

[3]. Kuriyama S, et al. Isoproterenol inhibits rod outer segment phagocytosis by both cAMP-dependent and independent pathways. Invest Ophthalmol Vis Sci. 1995 Mar;36(3):730-6.

[4]. 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.

[5]. Van Haastert PJ, et al. Competitive cAMP antagonists for cAMP-receptor proteins. J Biol Chem. 1984 Aug 25;259(16):10020-4.

 Chemical & Physical Properties

Melting Point 212 - 213 ℃
Molecular Formula C16H27N6O5PS
Molecular Weight 446.46200
Exact Mass 446.15000
PSA 186.46000
LogP 2.04940

 Synonyms

MFCD03703495
cAMPS-Rp,triethylammonium salt
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