Disease relevance of NSC707961

• The effects of cyclocreatine in large C6 glioma multicellular spheroids were mapped here by magnetic resonance microscopy [1].
• Enhanced ability of skeletal muscle containing cyclocreatine phosphate to sustain ATP levels during ischemia following beta-adrenergic stimulation [2].
• During ischemia, the heart of control rats developed a rigor-like increase in tonic pressure (ischemic contracture) not seen in the heart of cyclocreatine-fed rats (22 versus 1 mm Hg, p less than 0.01) [3].
• Dietary cyclocreatine offers no cerebral protection against hypoxia in mice [4].
• Dietary cyclocreatine has been reported to increase brain high-energy stores in mice and to prolong the generation and utilization of these stores following decapitation [4].

Psychiatry related information on NSC707961

• Neuroprotective effects of creatine and cyclocreatine in animal models of Huntington's disease [5].

High impact information on NSC707961

• Growth rate inhibition of subcutaneously implanted tumors results from feeding rats and athymic nude mice diets containing 1% cyclocreatine or 1%, 2%, 5%, or 10% creatine [6].
• Cell cycle studies of cyclocreatine, a new anticancer agent [7].
• We used the creatine analogs cyclocreatine (cCr) or beta-guanidopropionate (beta GPA) to test if mass action ratios (gamma) for CK in muscle could be predicted from combined equilibrium constants (Kcomb) measured in solutions mimicking the intracellular environment [8].
• We tested the hypothesis that if ischemia is important for the formation of NCF from the myocardium, then blocking (or delaying) ischemic changes with cyclocreatine should inhibit the release of NCF [9].
• Next the effect of cyclocreatine on neutrophils in the Boyden chamber was determined and it was found that it did not alter neutrophil migration, which excludes a direct inhibitory effect on the cells [9].

Chemical compound and disease context of NSC707961

• ATP levels were sustained at high values substantially longer in breast muscle of cyclocreatine-fed chicks, compared to control-fed chicks, during total ischemia initiated 2 h after injection of both groups with the beta-adrenergic agonist isoproterenol (5 mg/kg subcutaneous) [2].
• Cyclocreatine 0.5% did not increase survival time during hypoxia (5% O2) [4].
• The growth-inhibitory effect of cyclocreatine (CCr) and the kinetics of CCr and Na(+) cotransport were investigated in MCF7 human breast cancer cells and its adriamycin-resistant subline with use of (31)P- and (23)Na-NMR spectroscopy [10].

Biological context of NSC707961

• Furthermore supernatant from cyclocreatine-treated hearts did not inhibit neutrophil chemotaxis to C5a, indicating absence of a chemotaxis inhibitor in this preparation [9].
• Hodgkin disease-derived cell lines expressing ubiquitous mitochondrial creatine kinase show growth inhibition by cyclocreatine treatment independent of apoptosis [11].
• Creatine biosynthesis during embryonic development. False feedback suppression of liver amidinotransferase by N-acetimidoylsarcosine and 1-carboxymethyl-2-iminoimidazolidine (cyclocreatine) [12].
• Post-bypass segmental contractility and cardiac output were significantly better in cyclocreatine hearts compared to that of controls [13].
• The induced uptake was inhibited by beta-guanidinopropionic acid (IC50 approximately 44.4 microM), 2-amino-1-imidazolidineacetic acid (cyclocreatine; IC50 approximately 369.8 microM), gamma-guanidinobutyric acid (IC50 approximately 697.9 microM), gamma-aminobutyric acid (IC50 approximately 6.47 mM), and amiloride (IC50 approximately 2.46 mM) [14].

Anatomical context of NSC707961

• Cyclocreatine inhibits the production of neutrophil chemotactic factors from isolated hearts [9].
• Cyclocreatine (cCr), whose phosphorylated form is a very poor substrate for CK, inhibited proliferation of the L1236 cell line nearly entirely [11].
• Suspensions of chopped whole brain from 11- to 14-day-old chick embryos were incubated with 30 mM cyclocreatine for 90 min, resulting in accumulation of 100 mumol/g dry weight of cyclocreatine-P, and then incubated for up to 1 h with a series of excitatory amino acids of widely differing potencies [15].
• Further experiments utilizing type IV collagen as attractant demonstrated that cyclocreatine inhibited the chemokinetic (91%) and the haptotactic (73%) responses and the in vitro invasion of A2058-055 cells through Matrigel-coated membranes (88%) [16].
• Cyclocreatine-treated dogs (n = 6) were injected intravenously with cyclocreatine solution (600 mg/kg) 1 h before the experiment and during ligation of the coronary artery [17].

Associations of NSC707961 with other chemical compounds

• After 2 weeks, cyclocreatine-fed (n = 8) and control (n = 7) rats were anesthetized, the heart was excised and retrograde perfusion was begun at 10 ml/min per g with 37 degrees C, phosphate-free buffer containing glucose and oxygen [3].
• Creatine and cyclocreatine attenuate MPTP neurotoxicity [18].
• Porcine carotid arteries were superfused for 12 h with Krebs-Henseleit buffer at 22 degrees C, containing 11 mM glucose as substrate, and supplemented with either 20 mM beta-guanidinopropionic acid (beta-GPA), methyl-guanidinopropionic acid (m-GPA), guanidinoacetic acid (GA) or cyclocreatine (cCr) [19].

Gene context of NSC707961

• In addition, motility stimulation of A2058-055 cells by either autotaxin or fibronectin was markedly inhibited by cyclocreatine [16].
• Moreover, the data suggest a possible interplay between p53 mutations, HCC, CK expression, and the growth-inhibitory effects of cyclocreatine in HCC [20].

Analytical, diagnostic and therapeutic context of NSC707961

• Sequential sets of diffusion images, following cyclocreatine administration, showed increasing self-diffusion coefficients of the intracellular water in the viable rim (0.49 x 10(-5) cm2/s for untreated spheroids, 0.62 x 10(-5) cm2/s after 48 h perfusion with 20 mM cyclocreatine) [1].
• Cyclocreatine feeding provides a unique experimental tool for quantitative evaluation of the proposed protective role of ATP against irreversible cellular damage in skeletal and cardiac muscles during ischemic episodes [2].
• With reperfusion, the heart of cyclocreatine-fed rats spontaneously defibrillated sooner than did the heart in control rats (178 versus 346 s, p less than 0.03) [3].
• Enhancement of cardiac function by cyclocreatine in models of cardiopulmonary bypass [13].
• Creatine and cyclocreatine treatment of human colon adenocarcinoma xenografts: 31P and 1H magnetic resonance spectroscopic studies [21].

References