| Identification | Back Directory | [Name]
N-(phosphonoamidino)sarcosine, dipotassium salt | [CAS]
18838-38-5 | [Synonyms]
Einecs 242-619-0
Phosphocreatine dipotassium
Creatine phosphate (dipotassium)
Cyclocreatine Phosphate
(AM 285)
Creatine Phosphate (potassium salt)
Creatinephosphoric acid (dipotassium)
N-(phosphonoamidino)sarcosine, dipotassium salt
Sarcosine, N-(phosphonoamidino)-, dipotassium salt
Glycine, N-(imino(phosphonoamino)methyl)-N-methyl-, dipotassium salt
Glycine, N-(imino(phosphonoamino)methyl)-N-methyl-, potassium salt (1:2) | [EINECS(EC#)]
242-619-0 | [Molecular Formula]
C4H8K2N3O5P | [MDL Number]
MFCD00065457 | [MOL File]
18838-38-5.mol | [Molecular Weight]
287.294 |
| Hazard Information | Back Directory | [Uses]
Phosphocreatine (creatine phosphate) is an organic compound found in vertebrate skeletal muscles. Phosphocreatine enhances antioxidant activity, and activates the TAK1 pathway to protect the heart. Phosphocreatine normalizing mitochondrial function and reducing oxidative stress via Akt mediated Nrf2/HO-1 pathway. Phosphocreatine provides renal protection by suppressing Apoptosis and ROS (Reactive Oxygen Species) generation through ERK mediated mediated Nrf-2/HO-1 pathway.[1][2][3][4]. | [in vivo]
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].
| Animal Model: | Male Sprague Dawley (SD) rats were divided into three groups, normal control group, DOX group and phosphocreatine group[2]. | | Dosage: | 200 mg/kg | | Administration: | i.p., once every other day, 7 weeks | | 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 were divided into five groups: control group, model group (STZ(Streptozotocin) (HY-13753)), low dose group
(STZ+ phosphocreatine 22 mg/kg) and high dose group (STZ (HY-13753) + phosphocreatine 40 mg/kg). [4].
| | Dosage: | 20, 40 mg/kg | | Administration: | i.v., daily, 6 weeks | | 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.
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| [IC 50]
Human Endogenous Metabolite | [References]
[1] Feldman EB, et al. Creatine: a dietary supplement and ergogenic aid. Nutr Rev. 1999 Feb;57(2):45-50. DOI:10.1111/j.1753-4887.1999.tb01777.x
[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. DOI:10.1016/j.tox.2021.152881
[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. DOI:10.1016/j.freeradbiomed.2018.03.014
[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. DOI:10.1016/j.lfs.2019.117248 |
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| Company Name: |
Merck KGaA
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21-20338288 |
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www.sigmaaldrich.cn |
| Company Name: |
MedChemExpress
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021-58955995 |
| Website: |
www.medchemexpress.com |
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