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Rp-cAMPS sodium salt

Catalog No. T36679   CAS 142439-94-9

Rp-cAMPS sodium salt, a cAMP analog, is a potent, competitive cAMP-induced activation of cAMP-dependent PKA I and II (Kis of 12.5 μM and 4.5 μM, respectively) antagonist. Rp-cAMPS sodium salt is resistant to hydrolysis by phosphodiesterases[1][2][3][4][5][6].

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Rp-cAMPS sodium salt Chemical Structure
Rp-cAMPS sodium salt, CAS 142439-94-9
Pack Size Availability Price/USD Quantity
25 mg 6-8 weeks $ 1,220.00
50 mg 6-8 weeks $ 1,590.00
100 mg 6-8 weeks $ 2,430.00
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Biological Description
Chemical Properties
Storage & Solubility Information
Description Rp-cAMPS sodium salt, a cAMP analog, is a potent, competitive cAMP-induced activation of cAMP-dependent PKA I and II (Kis of 12.5 μM and 4.5 μM, respectively) antagonist. Rp-cAMPS sodium salt is resistant to hydrolysis by phosphodiesterases[1][2][3][4][5][6].
Targets&IC50 PKA II:9.75 µM (Ki), PKA I:6.05 µM (Ki)
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[2].
In vivo Rp-cAMPS (10 μM, 15 min) reduces the monosynaptic excitatory postsynaptic currents (EPSCs) triggered at the PB-CeLC and BLA-CeLC synapses in tissue slices from arthritic rats, without affecting similar neurons in healthy animals. This inhibition by Rp-cAMPS is notably significant when compared to the pre-drug (ACSF) control measurements in the same cells[2].
Molecular Weight 368.26
Formula C10H12N5NaO5PS
CAS No. 142439-94-9

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Powder: -20°C for 3 years | In solvent: -80°C for 1 year

TargetMolReferences and Literature

1. R J de Wit, et al. Inhibitory action of certain cyclophosphate derivatives of cAMP on cAMP-dependent protein kinases. Eur J Biochem. 1984 Jul 16;142(2):255-60. 2. 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. 3. 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. 4. 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. 5. 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. 6. Van Haastert PJ, et al. Competitive cAMP antagonists for cAMP-receptor proteins. J Biol Chem. 1984 Aug 25;259(16):10020-4.

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