2. Metabolic Enzyme/Protease MAPK/ERK Pathway PI3K/Akt/mTOR Stem Cell/Wnt Apoptosis Protein Tyrosine Kinase/RTK
  3. Endogenous Metabolite MAP3K Akt Mitochondrial Metabolism ERK Apoptosis ROS Kinase
  4. Phosphocreatine disodium hydrate

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..

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Phosphocreatine disodium hydrate Chemical Structure

Phosphocreatine disodium hydrate Chemical Structure

CAS No. : 19333-65-4

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MAP3K7/TAK1 MAP3K8 ASK2 MAP3K5/ASK1

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Akt Akt1 Akt2 Akt3

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ERK ERK1 ERK2 ERK5 ERK8

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Description

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.[1][2][3][4].

IC50 & Target

Human Endogenous Metabolite

 

In Vitro

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.

Apoptosis Analysis[3][4]

Cell Line: PC-12, NRK-52E cells
Concentration: 5, 10, 20, 40 mM
Incubation Time: 2 h
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.

Cell Viability Assay[3][4]

Cell Line: PC-12, NRK-52E cells
Concentration: 0, 5, 10, 20, 40 mM
Incubation Time: 24 h
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.

Western Blot Analysis[3][4]

Cell Line: PC-12, NRK-52E cells
Concentration: 20, 40 mM
Incubation Time: 24 h
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.
In Vivo

Non-salt form:
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.

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]
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.
Animal Model: Male Sprague Dawley (SD) rats, i.p., 70 mg/kg (STZ(Streptozotocin) (HY-13753)), daily, 6 weeks [4]
Dosage: 20, 40 mg/kg
Administration: i.p., 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.
Clinical Trial
Formula

C4H10N3O5P.xH2O.2Na
CAS No.
Appearance

Solid

Color

White to off-white

SMILES

O=C(O)CN(C(NP(O[Na])(O[Na])=O)=N)C.O.[x]
Structure Classification
Initial Source

skeletal muscles of vertebrates
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

4°C, sealed storage, away from moisture

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

Solvent & Solubility
In Vitro: 

H2O : 116.67 mg/mL (Need ultrasonic)

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Keywords:

Phosphocreatine disodium19333-65-4Endogenous MetaboliteMAP3KAktMitochondrial MetabolismERKApoptosisROS KinaseMAP kinase kinase kinase, MEKK, MAPKKKPKBProtein kinase BExtracellular signal regulated kinasesATPmuscle contractioncardiotoxicitymitochondrial functionoxidative stressInhibitorinhibitorinhibit

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