Cyclocreatine-13C3
Cyclocreatine-13C3 is the 13C-labeled Cyclocreatine (HY-W017540). Cyclocreatine, a creatine analogue, acts as a brain-penetrant and potent bioenergetic protective agent by providing high levels of ATP. Cyclocreatine can be phosphorylated and dephosphorylated by creatine kinases. Cyclocreatine suppresses creatine metabolism ameliorating the cognitive, autistic and epileptic phenotype in a mouse model of creatine transporter defciency. Cyclocreatine protects against ischemic injury and enhances cardiac recovery during early reperfusion in dogs and rats. Cyclocreatine decreases plaque-adjacent neuronal dystrophy in TREM2-deficient mice with amyloid-β pathology. Cyclocreatine is proming for research of ischemic heart disease, cardiovascular diseases, Alzheimer’s disease and other neurodegenerative diseases associated with microglial dysfunction, prostate cancer.
For research use only. We do not sell to patients.
- Formula: C213C3H9N3O2
- Molecular Weight:146.12
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Application
1. This compound can be used as a tracer
2. This compound can be used as an internal standard for quantitative analysis by NMR, GC-MS, or LC-MS.
Chemical Information
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Unlabeled CAS 35404-50-3
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Molecular Weight 146.12
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Formula C213C3H9N3O2
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SMILES
N[13C]1=NCCN1[13CH2][13C](O)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
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Protocol for Hematoxylin-Eosin (H&E) Staining
Hematoxylin-eosin staining is a routine histological method that stains nuclei mainly blue-purple with hemalum and stains cytoplasm, extracellular matrix, and many stromal components pink with eosin, allowing tissue architecture, cell morphology, necrosis, inflammation, fibrosis, tumor growth pattern, and treatment-associated injury to be evaluated by light microscopy. In cancer cells, primary neurons, mouse tumor models, intestinal organoids, inflammatory macrophage preparations, and drug-screening tissues, H&E is a morphology assay rather than a molecular assay; it should be interpreted with complementary molecular or immunostaining assays when the biological question concerns specific proteins, RNA levels, ferroptosis, mitophagy, or immune phenotypes.
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Amyloid: Congo Red Amyloid Staining
Congo red amyloid staining is a histochemical method used to detect extracellular amyloid deposits in tissue sections based on the affinity of Congo red dye for β-pleated sheet-rich protein aggregates. When bound to amyloid, Congo red produces characteristic apple-green birefringence under polarized light microscopy, which is widely regarded as a diagnostic feature of amyloid deposition in histopathology. The diagnostic principle relies on the combination of dye binding (congophilia) and optical anisotropy under polarized illumination, which distinguishes amyloid from most non-amyloid eosinophilic extracellular deposits in routine histological evaluation. Amyloid identification by Congo red staining remains a cornerstone in diagnostic pathology despite the availability of adjunct methods such as immunohistochemistry and mass spectrometry, particularly because of its ability to localize deposits directly within tissue architecture. The specificity of Congo red-positive deposits is incre
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How to Choose the Right Model Animal
Choosing the right model animal is a validity-driven decision in which the species, strain, sex, age, genetic background, disease-induction method, outcome measures, and welfare burden must match the scientific question rather than laboratory tradition or convenience. A model should be selected by judging face validity, construct validity, and predictive validity: whether it resembles the human phenotype, whether it reproduces relevant mechanisms, and whether results are likely to predict human biology or treatment response. Animal studies often fail to translate because of species differences, weak disease resemblance, poor experimental design, inadequate reporting, publication bias, and underuse of randomization, blinding, and sample-size justification. Unresolved questions include how to rank competing models objectively, how much human-disease complexity must be reproduced for a given objective, and when non-animal systems such as organoids, ex vivo tissue, or computational models
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Alzheimer’s Disease Modeling
Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive functions and loss of specific types of neurons and synapses. Alzheimer's symptoms can be simulated in mice by injecting drugs (such as Aβ) or genetically modified.
Purity & Documentation
References
[1]. Salwa A Elgebaly, et al. Cyclocreatine protects against ischemic injury and enhances cardiac recovery during early reperfusion. Expert Rev Cardiovasc Ther. 2019 Sep;17(9):683-697. [Content Brief]
[2]. Tyler K Ulland, et al. TREM2 Maintains Microglial Metabolic Fitness in Alzheimer's Disease. Cell. 2017 Aug 10;170(4):649-663.e13. [Content Brief]
[3]. Patel R, et al. Cyclocreatine Suppresses Creatine Metabolism and Impairs Prostate Cancer Progression[J]. Cancer Res. 2022 Jul 18;82(14):2565-2575. [Content Brief]
[5]. Cacciante F, et al. Cyclocreatine treatment ameliorates the cognitive, autistic and epileptic phenotype in a mouse model of Creatine Transporter Deficiency[J]. Sci Rep. 2020 Oct 27;10(1):18361. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)