Phosphocreatine (disodium)

Phosphocreatine (disodium) is an organic compound found in vertebrate skeletal muscles. Phosphocreatine (disodium) enhances antioxidant activity, and activates the TAK1 pathway to protect the heart. Phosphocreatine (disodium) normalizing mitochondrial function and reducing oxidative stress via Akt mediated Nrf2/HO-1 pathway. Phosphocreatine (disodium) 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 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].
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].