Guanosine 5'-O-2-thiodiphosphate trisodium
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Guanosine 5'-O-(2-thiodiphosphate) trisodium (GDPβS trisodium) is a non-hydrolyzable derivative of GDP. Guanosine 5'-O-(2-thiodiphosphate) trisodium acts as an inhibitor of adenylyl cyclase (AC) with a Ki value of 600 nM. In the absence of glutamic-pyruvic transaminase (GPT) in cerebral cortex membranes of rodent models, Guanosine 5'-O-(2-thiodiphosphate) trisodium partially activates AC with an EC50 of 400 nM. Guanosine 5'-O-(2-thiodiphosphate) trisodium prevents norepinephrine-induced nitric oxide release in ventricular myocytes.
For research use only. We do not sell to patients.
- Purity : 97.1%
- Formula: C10H12N5Na3O10P2S
- Molecular Weight:525.21
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Storage:
Solution, -20°C, 2 years
Biological Activity
Description
In Vitro
Guanosine 5'-O-(2-thiodiphosphate) (1 µM) blocks norepinephrine-induced nitric oxide release in adult rat ventricular myocytes[1].
Guanosine 5'-O-(2-thiodiphosphate) acts as a partial agonist for adenylate cyclase activation in synaptic membranes of the rat cerebral cortex, with an EC50 of 4×10-7 M and a maximum activation level equivalent to 60% of that of the GTP triphosphate analog[2].
Guanosine 5'-O-(2-thiodiphosphate) (1 μM) enhances adenylate cyclase activation mediated by low-dose GTPγS (HY-137677), while inhibiting activation induced by high-dose GTPγS in synaptic membranes from rat cerebral cortex[2].
Guanosine 5'-O-(2-thiodiphosphate) promotes partial nucleotide exchange from Gi/o to Gs (EC50 = 2×10-5 M) and partially reverses the inhibitory effect of adenylate cyclase (EC50 = 5×10-6 M). Its potency and efficacy in rat cerebral cortical synaptic membranes are both lower than those of GppNHp[2].
Guanosine 5'-O-(2-thiodiphosphate) competitively inhibits GTP-stimulated adenylate cyclase activity in cholera toxin-pretreated rat pancreatic plasma membranes, with a Ki range of 0.3-0.6 μM[3].
Guanosine 5'-O-(2-thiodiphosphate) inhibits cholecystokinin-8 (CCK-8)-stimulated adenylate cyclase activity in native rat pancreatic plasma membranes; in the presence of 0.3 μM GTP, its I50 is 2.2 μM and Ki is 0.5 μM[3].
Guanosine 5'-O-(2-thiodiphosphate) inhibits secretin+GTP-stimulated adenylate cyclase activity in native rat pancreatic plasma membranes, with an IC50 of 8 μM and a Ki of 3.2 μM[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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Appearance Liquid
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Molecular Weight 525.21
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Formula C10H12N5Na3O10P2S
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Color Colorless to light yellow
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SMILES
NC1=NC(C2=C(N1)N(C=N2)[C@@H]3O[C@H](COP(OP(O[Na])(S[Na])=O)(O[Na])=O)[C@@H](O)[C@H]3O)=O
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Synonyms
GDPβS trisodium
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Solution, -20°C, 2 years
Purity & Documentation
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Data Sheet (275 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Kanai AJ, et al. Beta-adrenergic regulation of constitutive nitric oxide synthase in cardiac myocytes. Am J Physiol. 1997;273(4):C1371-C1377. [Content Brief]
[2]. Rasenick MM, et al. Guanosine-5'-O-thiodiphosphate functions as a partial agonist for the receptor-independent stimulation of neural adenylate cyclase. Brain Res. 1989;488(1-2):105-113. [Content Brief]
[3]. Svoboda M, et al. Guanosine 5'-O-(2-thiodiphosphate) as a competitive inhibitor of GTP in hormone or cholera toxin-stimulated pancreatic adenylate cyclase. FEBS Lett. 1980 Jan 14;109(2):275-9. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keywords
- Guanosine 5'-O-2-thiodiphosphate trisodium
- GDPβS trisodium
- Adenylate Cyclase
- rat ventricular myocytes
- G_s proteins
- G_i/o proteins
- G_i proteins
- G protein-dependent signaling
- adenylate cyclase
- nitric oxide
- C6 glioma cells
- rat pancreatic plasma membranes
- rat cerebral cortex synaptic membranes
- Inhibitor
- inhibitor
- inhibit