Creatine Phosphate (potassium salt)
(Synonyms: Phosphocreatine) 目录号 : GC43323
磷酸肌酸（钾盐）主要存在于脊椎动物的骨骼肌中，是一种称为 α 氨基酸和衍生物的有机化合物，是测定肌酸激酶的底物，用于在骨骼肌收缩过程中再生 ATP。
Cas No.:18838-38-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Phosphocreatine dipotassium, primarily found in the skeletal muscles of vertebrates and one of organic compounds known as alpha amino acids and derivatives, is a substrate for the determination of creatine kinase and used to regenerate ATP during skeletal muscle contraction[1].
References:
[1]. Feldman EB, et al. Creatine: a dietary supplement and ergogenic aid. Nutr Rev. 1999 Feb;57(2):45-50.
| Cas No. | 18838-38-5 | SDF | |
| 别名 | Phosphocreatine | ||
| 化学名 | N-[imino(phosphonoamino)methyl]-N-methyl-glycine, dipotassium salt | ||
| Canonical SMILES | OC(CN(C)C(NP([O-])([O-])=O)=N)=O.[K+].[K+] | ||
| 分子式 | C4H8N3O5P•2K | 分子量 | 287.3 |
| 溶解度 | 5 mg/ml in PBS (pH 7.2) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.4807 mL | 17.4034 mL | 34.8068 mL |
| 5 mM | 0.6961 mL | 3.4807 mL | 6.9614 mL |
| 10 mM | 0.3481 mL | 1.7403 mL | 3.4807 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
The roles of ionic processes in muscular fatigue during intense exercise
Sports Med 1992 Feb;13(2):134-45.PMID:1373245DOI:10.2165/00007256-199213020-00009.
Muscular fatigue is manifested by a decline in force- or power-generating capacity and may be prominent in both submaximal and maximal contractions. Disturbances in muscle electrolytes play an important role in the development of muscular fatigue. Intense muscular contraction is accompanied by an increased muscle water content, distributed in both intracellular and extracellular spaces. This water influx will modify ionic changes in both compartments. Changes in muscle intracellular electrolyte concentrations with intense contraction may be summarised as including decreases in potassium (6 to 20%) and in Creatine Phosphate (up to 70 to 100%) and increases in lactate (more than 10-fold), sodium (2-fold) and small, variable increases in chloride. The net result of these intracellular ionic concentration changes with exercise will be a reduction in the intracellular strong ion difference, with a consequent marked rise in intracellular hydrogen ion concentration. This intracellular acidosis has been linked with fatigue via impairment of regulatory and contractile protein function, calcium regulation and metabolism. Potassium efflux from the contracting muscle cell dramatically decreases the intracellular to extracellular potassium ratio, leading to depolarisation of sarcolemmal and t-tubular membranes. Surprisingly little research has investigated the effects of intense exercise training on electrolyte regulation and fatigue.
Creatine Phosphate (Neoton) as an additive to St. Thomas' Hospital cardioplegic solution (Plegisol). Results of a clinical study
Eur J Cardiothorac Surg 1991;5(2):74-81.PMID:2018658DOI:10.1016/1010-7940(91)90004-4.
Experimentally, Creatine Phosphate (CP) added to St. Thomas' Hospital cardioplegic solution (STH) improved post-ischaemic recovery of cardiac function in the rat heart. We investigated the effect of adding CP (10.0 mmol/l) to STH. Fifty open-heart surgery patients were randomized into control (STH) and treated (STH + CP) groups (25 per group). Patients underwent (a) monitoring for peri- and postoperative arrhythmias (48-h Holter monitoring). (b) quantitative birefringence assessment of intraoperative myocardial protection in left and right ventricular biopsies sampled at start of bypass (pre-isch.), end of bypass (end-isch.) and after 10 min reperfusion (post-isch.), and (c) measurement of serum creatine kinase-MB isozyme (CK-MB) values for up to 4 days postoperatively; results were assessed with respect to (d) haemodynamics and postoperative clinical outcome. Inotropic support (adrenaline) was required in three patients (12%) from each group; no patient died. All patients required defibrillation, and the number of direct current shocks required for sinus rhythm was the same in each group. The occurrence and incidence of reperfusion-induced arrhythmias were the same in both groups. Serum CK and CK-MB values were similar throughout the sampling period in both groups of patients; one patient in the control group had raised CK-MB levels postoperatively, but perioperative infarction was not indicated by the electrocardiogram.(ABSTRACT TRUNCATED AT 250 WORDS)
Purification and localization of brain-type creatine kinase in sodium chloride transporting epithelia of the spiny dogfish, Squalus acanthias
J Biol Chem 1992 Feb 25;267(6):4270-6.PMID:1310991doi
The targeting of creatine kinase isoenzymes to specific sites within muscle cells provides a system for the regeneration of ATP in situ from ADP and Creatine Phosphate. We have recently reported the colocalization of brain-type (B) creatine kinase and the nonsarcomeric mitochondrial creatine kinase isoenzymes in the thick ascending limb of the loop of Henle in the rat kidney, suggesting that creatine kinase may regenerate ATP for sodium transport (Friedman, D.L., and Perryman, M.B. (1991) J. Biol. Chem. 266, 22404-22410). In order to test the hypothesis regarding the association of B creatine kinase with sodium transport, we examined the creatine kinase enzymes in the rectal (salt-secreting) gland of the dogfish shark which contains high levels of the Na+/K(+)-ATPase. The creatine kinase isoform composition was determined by non-denaturing electrophoresis, immunoblotting, protein purification, and amino acid sequence analysis. The results demonstrate both B creatine kinase and mitochondrial creatine kinase proteins are present in the rectal gland, an isoform composition which is the same as in the mammalian kidney. By using a combination of chromatographic techniques, shark B creatine kinase was purified to homogeneity and partial sequence data was obtained from two cyanogen bromide peptide fragments. One of these fragments contains the active site and is identical at all sequenced residues with the corresponding region from the echinoderm sperm flagellar creatine kinase, and is 96% homologous with both chicken and rat B creatine kinase subunits. The other fragment corresponds to a region near the N-terminal of mammalian creatine kinases and is 89% homologous with B creatine kinase from chicken. The localization of these isoforms was examined by immunocytochemistry using subunit specific antisera. Mitochondrial creatine kinase and B creatine kinase immunoreactivity are detected in all tubules, and is restricted to the basal region of the cells, which is the site of the Na+/K(+)-ATPase. The conservation of creatine kinase isoform expression in excretory tissue, and the localization of creatine kinase immunoreactivity in the basal region of the tubule cells, demonstrate that subcellular compartmentation of B creatine kinase may underly the functional coupling of creatine kinase activity with sodium transport.
The use of exogenous Creatine Phosphate for myocardial protection in patients undergoing coronary artery bypass surgery
J Cardiovasc Surg (Torino) 1996 Dec;37(6 Suppl 1):75-80.PMID:10064355doi
A key component in the development of ischemic functional and structural myocardial injury during cardiosurgical procedures is an inadequate cellular energy supply which occurs as a consequence of the cessation of oxidative metabolism. In such conditions high energy phosphates are rapidly depleted. As they play a critical role in the maintenance of cell viability and postischemic recovery of contractile function, their conservation is therefore a primary objective in any procedure designed to reduce ischemic injury. Exogenous administration of phosphocreatine (CP) has been suggested as being beneficial to the ischemic heart. The aim of present study was to evaluate the possible cardioprotective effect of exogenous CP during coronary artery surgery (CABG). Forty patients undergoing CABG procedure were randomly assigned to receive creatine phosphate-enriched (group I) or standard-St. Thomas' Hospital (group II) cardioplegic solution; each group comprised 20 patients. Group I received: 6.0 g of exogenous CP (Neoton) daily in two 20-min intravenous infusions during 3 days preoperatively; during surgical procedure they were administered standard cardioplegic solution enriched in CP at the concentration of 10 mmol/l and -- 2 days postoperatively -- 4.0 g CP daily in two intravenous injections. Group II did not receive CP at all In both groups were analysed. Haemodynamic parameters. Continuous 48-h ECG recording (Holter monitoring) outcome. Laboratory values of serum CK and CK-MB. Inotropic support required (drugs, mechanical support). Ultrastructural findings (biopsy data). Statistical analysis was carried out using Student's "t"-test and the chi2 test. Values of p<0.05 were taken as the criterion of significant difference. The results of the study were: Significantly lower average number and energy of DC-shocks needed to restore cardiac function after cardiopulmonary bypass procedure in group 1. Statistically significant beneficial effect on the presence of ventricular arrhythmias during surgery and in early postoperative period in group I. Significantly lower requirements for inotropic drugs postoperatively in group I. Statistically significant lower degree of sarcolemmal damages in myocardial biopsies in group I. Concluding, the authors wish to state that: Exogenous phosphocreatine (Neoton) perioperative administration in coronary artery bypass patients reduced the need for inotropic drugs, which is clinically manifested in lower frequency of low cardiac output syndrome. Perioperative administration of exogenous CP improves electrophysiological stability of the myocardium. Advantageous clinical and electrophysiological effect of exogenous CP may result from its properties to protect sarcolemma of the cardiomyocytes.
St. Thomas' Hospital cardioplegia: enhanced protection with exogenous Creatine Phosphate
Ann Thorac Surg 1996 Jan;61(1):67-75.PMID:8561641DOI:10.1016/0003-4975(95)00819-5.
Background: Experimentally, Creatine Phosphate (CP) improves postischemic recovery of function and reduces postischemic arrhythmias. Methods: We studied 50 patients undergoing valve replacement. They were randomized into either a control group, who received St. Thomas' Hospital cardioplegic solution No. 1, or a CP-treated group, receiving the same cardioplegic solution plus CP (10 mmol/L). There were no preoperative clinical differences between groups. Assessment was by electrocardiographic analysis, inotropic drug requirement, quantitative birefringence, myocardial high-energy phosphate content, function, and semiquantitative ultrastructural assessment. Results: Direct-current shocks were reduced in the CP-treated group (0.88 +/- 0.15) compared with the control group (1.40 +/- 0.14; p < 0.02), as was the total number of joules (22.0 +/- 3.5 versus 34.4 +/- 3.7, respectively; p <0.02). The incidence of spontaneous sinus rhythm was higher in the CP-treated group (40% versus 8%; p < 0.05) and the incidence of postoperative arrhythmias, lower (8% versus 32%; p < 0.05). Prolonged inotropic administration (12 hours or longer) occurred in fewer patients in the CP-treated group (4% versus 28%; p < 0.05). Response to inotropic support (in the subset of patients requiring this treatment) was significantly greater in the CP-treated group than in the control group. There were no differences in recovery of function, birefringence changes, myocardial high-energy phosphate content, or ultrastructure between groups. Conclusions: St. Thomas' Hospital cardioplegic solution No. 1 plus CP enhanced myocardial protection and conferred a direct benefit to the patient by reducing postoperative arrhythmias and need of prolonged inotropic support.