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MedChemExpressModel Phosphocreatine -67-07-2

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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].
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Phosphocreatine

MCE China:Phosphocreatine

Brand:MedChemExpress (MCE)

Cat. No.HY-D0885

CAS:67-07-2

Synonyms:Creatine phosphate; Creatinephosphoric acid

Purity:95.0%

Storage:4°C, sealed storage, away from moisture *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Shipping:Room temperature in continental US; may vary elsewhere.

Description: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..

In Vitro: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].

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].

IC50 & Target:Human Endogenous Metabolite

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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]

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