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Rp-8-CPT-Cyclic AMP (sodium salt)

(Synonyms: Rp-8-CPT-cAMP) 目录号 : GC44853

A PKA inhibitor

Rp-8-CPT-Cyclic AMP (sodium salt) Chemical Structure

Cas No.:221905-35-7

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500μg
¥2,552.00
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1mg
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产品描述

Rp-8-CPT-cAMP is a structural combination of the lipophilic and non-hydrolyzable cAMP analogs, 8-CPT-cyclic AMP and Rp-cyclic AMPS .[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]

Reference:
[1]. Schwede, F., Maronde, F., Genieser, H., et al. Cyclic nucleotide analogs as biochemical tools and prospective drugs. Pharmacology & Therapeutics 87(2), 199-226 (2000).
[2]. Dostmann, W.R., Taylor, S.S., Genieser, H.G., 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. 265(18), 10484-10491 (1990).
[3]. Gjertsen, B.T., Mellgran, G., Otten, A., et al. Novel (Rp)-cAMPS analogs as tools for inhibition of cAMP-kinase in cell culture. Basal cAMP-kinase activity modulates interleukin-1β action. J. Biol. Chem. 270(35), 20599-20607 (1995).

Chemical Properties

Cas No. 221905-35-7 SDF
别名 Rp-8-CPT-cAMP
化学名 8-[(4-chlorophenyl)thio]-adenosine cyclic 3',5'-[hydrogen (R)-phosphorothioate], monosodium salt
Canonical SMILES O[C@H]1[C@H](N2C(SC3=CC=C(Cl)C=C3)=NC4=C2N=CN=C4N)O[C@H]5[C@H]1O[P@@](OC5)([S-])=O.[Na+]
分子式 C16H14ClN5O5PS2•Na 分子量 509.8
溶解度 25mg/mL in DMSO, 30mg/mL in DMF, 0.5mg/mL in Ethanol 储存条件 Store at -20°C
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1 mM 1.9616 mL 9.8078 mL 19.6155 mL
5 mM 0.3923 mL 1.9616 mL 3.9231 mL
10 mM 0.1962 mL 0.9808 mL 1.9616 mL
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Research Update

The Inhibitory Effect of Adenylic Acid on the Bitterness of the Antibacterial Combination Drug Trimethoprim/Sulfamethoxazole

Chem Pharm Bull (Tokyo) 2023;71(3):198-205.PMID:36858524DOI:10.1248/cpb.c22-00618.

The purpose of the present study was to evaluate bitterness suppression effect of adenylic acid (AMP) as a nucleotide-derived nutrient enhancer on a bitter commercial drug. In the present study, we evaluated peripheral bitterness inhibition effect of AMP on the trimethoprim (TMP) and sulfamethoxazole (SMZ) combination formulation based on taste sensor. The taste sensor values of TMP solutions with different concentrations show large sensor output in correlation with the concentration of TMP, whereas no sensor output in shown for the SMZ solutions. Therefore, the bitterness of this combination formulation is mainly due to TMP. We evaluated the TMP bitterness inhibitory effects of AMP, sodium salt of AMP (AMP Na; sodium adenylate), sodium salt of GMP (GMP Na; sodium guanylate), and sodium salt of inosine monophosphate (IMP Na; sodium inosinate), and found that only AMP displayed very effective bitterness inhibition. MarvinSketch analysis revealed that potential electrostatic interaction between cationized TMP and anionized forms (II and III) of AMP may cause bitterness suppression. 1H-NMR study suggested an interaction of TMP and AMP molecules based on chemical shift perturbations and an interaction between the phosphate group of AMP and amino group of TMP. Lastly, conventional elution analysis simulating oral cavity capacity for up to one minute were performed using commercial TMP/SMZ combination granules. The sensor output gradually increased up to 60 s. The addition of AMP solution to the eluted sample at 60 s significantly decreased the bitterness sensor output of the eluted sample.

Regulation of Expression of Hyperalgesic Priming by Estrogen Receptor α in the Rat

J Pain 2017 May;18(5):574-582.PMID:28089711DOI:10.1016/j.jpain.2016.12.017.

Hyperalgesic priming, a sexually dimorphic model of transition to chronic pain, is expressed as prolongation of prostaglandin E2-induced hyperalgesia by the activation of an additional pathway including an autocrine mechanism at the plasma membrane. The autocrine mechanism involves the transport of cyclic adenosine monophosphate (AMP) to the extracellular space, and its conversion to AMP and adenosine, by ecto-5'phosphodiesterase and ecto-5'nucleotidase, respectively. The end product, adenosine, activates A1 receptors, producing delayed onset prolongation of prostaglandin E2 hyperalgesia. We tested the hypothesis that the previously reported, estrogen-dependent, sexual dimorphism observed in the induction of priming is present in the mechanisms involved in its expression, as a regulatory effect on ecto-5'nucleotidase by estrogen receptor α (EsRα), in female rats. In the primed paw AMP hyperalgesia was dependent on conversion to adenosine, being prevented by ecto-5'nucleotidase inhibitor α,β-methyleneadenosine 5'-diphosphate sodium salt and A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine. To investigate an interaction between EsRα and ecto-5'nucleotidase, we treated primed female rats with oligodeoxynucleotide antisense or mismatch against EsRα messenger RNA. Whereas in rats treated with antisense AMP-induced hyperalgesia was abolished, the A1 receptor agonist N6-cyclopentiladenosine still produced hyperalgesia. Thus, EsRα interacts with this autocrine pathway at the level of ecto-5'nucleotidase. These results demonstrate a sexually dimorphic mechanism for the expression of priming. Perspective: This study presents evidence of an estrogen-dependent mechanism of expression of chronic pain in female rats, supporting the suggestion that differential targets must be considered when establishing protocols for the treatment of painful conditions in men and women.