Phosphocreatine disodium hydrate
Based on 3 publication(s) in Google Scholar
Phosphocreatine (disodium hydrate) is an organic compound found in vertebrate skeletal muscles. Phosphocreatine (disodium hydrate) enhances antioxidant activity, and activates the TAK1 pathway to protect the heart. Phosphocreatine (disodium hydrate) normalizing mitochondrial function and reducing oxidative stress via Akt mediated Nrf2/HO-1 pathway. Phosphocreatine (disodium hydrate) Phosphocreatine (disodium hydrate) provides renal protection by suppressing Apoptosis and ROS (Reactive Oxygen Species) generation through ERK mediated mediated Nrf-2/HO-1 pathway..
For research use only. We do not sell to patients.
- Purity: 99.86%
- CAS No.: 19333-65-4
- Formula: C4H10N3O5P.xH2O.2Na
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Storage:
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Purity & Documentation
- References
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Help & FAQs
Publications Citing Use of MedChemExpress (MCE) Phosphocreatine disodium hydrate
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Biological Activity
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Human Endogenous Metabolite |
Non-salt form:
Phosphocreatine (0-1 mM, 24 h) reveals the effect of anti-oxidant, anti-apoptosis and anti-necroptosis to protect agaist DOX (Doxorubicin) (HY-15142A)-induced cardiomyocytes injury in H9c2 cells by targeting TAK1[2].
Phosphocreatine (0-1 mM, 24 h) alleviates oxidative stress by increasing antioxidant activity, subsequently recovers expression level of TAK1 to baseline and reduces apoptosis and necroptosis in DOX-induced myocardial injury[2].
Phosphocreatine (5-20 mM, 24 h) attenuates cell injury and inhibits apoptosis induced by MGO (Methylglyoxal) (HY-106634) in PC12 cell[3].
Phosphocreatine (5-20 mM, 24 h) prevents loss of mitochondrial membrane permeability of MGO (Methylglyoxal) injured PC-12 cells[3].
Phosphocreatine (5-20 mM, 2 h) exhibits the neuroprotective effects in PC-12 cells relying on normalizing mitochondrial function and reducing oxidative stress via Akt mediated Nrf2/HO-1 pathway[3].
Phosphocreatine (5-40 mM, 24 h) at different concentrations might contribute to protection of the NRK-52E cells against MGO-induced kidney injury[4].
Phosphocreatine (10-40 mM, 4 h) suppresses kidney oxidative stress metabolites[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:PC-12, NRK-52E cells
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Concentration:5, 10, 20, 40 mM
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Incubation Time:2 h
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Result:Significantly suppressed the enhanced early apoptosis in PC-12 cells in a dose-dependent manner.
Increased the expression of Bcl-2, procaspase-3 and procaspase-9 in NRK-52E cells.
Decreased the expression of Bax and cleaved caspase-3 in NRK-52E cells.
Suppressed karyorrhexis and karyopyknosis in NRK-52E cells.
Decreased the apoptotic rate compared with MGO-treated cells in NRK-52E cells.
Prevented the losing of MMP (mitochondrial membrane potential) in NRK-52E cells.
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Cell Line:PC-12, NRK-52E cells
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Concentration:0, 5, 10, 20, 40 mM
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Incubation Time:24 h
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Result:Was not toxic to PC-12 cells under the treatment conditions.
Significantly increased PC-12 cell viability at the concentrations of 5, 10 and 20 mM compared with MGO (Methylglyoxal) (HY-106634) groups.
Contributed to protection of the NRK-52E cells against MGO-induced kidney injury.
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Cell Line:PC-12, NRK-52E cells
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Concentration:20, 40 mM
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Incubation Time:24 h
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Result:Increased the expression levels of Akt, Nrf2 (nuclear factor (erythroid-derived-2)-like 2 (Nrf2)) and HO-1 (Hemeoxygenase-1) in PC12 cells.
Increased the expression of nuclear Nrf2 levels, and decreased Nrf2 level in PC12 cells cytoplasm.
Increased the expression of p-Akt, HO-1 and Nrf2 with compared with pre-treatment for 2 h with LY294002 (a PI3K inhibitor) in PC12 cells.
Significantly increased Bcl-2 and procaspase-9 levels and decreased Bax, cleaved caspase-9 and cleaved caspase-3 C level in NRK-52E cells.
Decreased the expression of p-ERK and increased the Nrf2 and HO-1 expressions in NRK-52E cells.
Phosphocreatine (200 mg/kg, i.p., once every other day, 7 weeks) not only alleviates oxidative stress and myocardial apoptosis, but also rescues myocardial necroptosis in DOX-induced cardiotoxicity of rat[2].
Phosphocreatine (20-40 mg/kg, i.v., daily, 6 weeks) has a protective effect on the kidney tissues against diabetic nephropathy in SD (Sprague Dawley) rats[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male Sprague Dawley (SD) rats, i.p., normal saline, 3 times; i.p., DOX 2 mg/kg, 7 times; i.p., normal saline, 3 times [2]
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Dosage:200 mg/kg
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Administration:i.p., once every other day, 7 weeks
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Result:Improved the heart function abnormality.
Lowered myocardial apoptosis.
Recovered the expression of Nrf2, SOD, FoxO3a and diminished C-Casp3, Bax/Bcl2 in the myocardial tissue of rats.
Markedly improved myocardial necroptosis, as indicated by decreasing expression of RIP3 and CaMKII.
Increased expression level of TAK1.
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Animal Model:Male Sprague Dawley (SD) rats, i.p., 70 mg/kg (STZ(Streptozotocin) (HY-13753)), daily, 6 weeks [4]
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Dosage:20, 40 mg/kg
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Administration:i.p., daily, 6 weeks
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Result:Reduced hyperglycemia compared with STZ (Streptozotocin) (HY-13753) -treated rats.
Increased the weight of rats gradually compared with STZ (Streptozotocin) (HY-13753) group.
Decreased kidney weight index (kidney weight/body weight).
Decreased MDA level and increased of GSH and SOD levels compared with STZ group.
Decreased the apoptotic rate compared with MGO-treated groups.
Chemical Information
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CAS No. 19333-65-4
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Appearance Solid
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Formula C4H10N3O5P.xH2O.2Na
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Color White to off-white
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SMILES
O=C(O)CN(C(NP(O[Na])(O[Na])=O)=N)C.O.[x]
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Publications (3)
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Journal Impact Factor
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Most Recent
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Autophagy
ESCRT III-mediated lysosomal repair improve renal tubular cell injury in cisplatin-induced AKI. [Abstract]2025 Sep;21(9):1927-1944. PMID: 40152606 -
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Toxicol Appl Pharmacol
2022 Apr 15:441:115971. PMID: 35276125
Solvent & Solubility
H2O : 100 mg/mL (Need ultrasonic)
Purity & Documentation
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Data Sheet (281 KB)
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SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Korean - KR (394 KB)
- Portuguese - PT (394 KB)
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Handling Instructions (2659 KB)
References
[1]. Feldman EB, et al. Creatine: a dietary supplement and ergogenic aid. Nutr Rev. 1999 Feb;57(2):45-50. [Content Brief]
[2]. Wang C, et al. Phosphocreatine attenuates doxorubicin-induced cardiotoxicity by inhibiting oxidative stress and activating TAK1 to promote myocardial survival in vivo and in vitro. Toxicology. 2021 Aug;460:152881. [Content Brief]
[3]. Li H, et al. Neuroprotective effect of phosphocreatine on oxidative stress and mitochondrial dysfunction induced apoptosis in vitro and in vivo: Involvement of dual PI3K/Akt and Nrf2/HO-1 pathways. Free Radic Biol Med. 2018 May 20;120:228-238. [Content Brief]
[4]. Shopit A, et al. Protection of diabetes-induced kidney injury by phosphocreatine via the regulation of ERK/Nrf2/HO-1 signaling pathway. Life Sci. 2020 Feb 1;242:117248. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Phosphocreatine disodium hydrate Related Classifications
HY-D0885D Related Classifications
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