CCZ01048
Based on 4 publication(s) in Google Scholar
CCZ01048, a α-melanocyte-stimulating hormone (α-MSH) analogue, exhibits high binding affinity to melanocortin 1 receptor (MC1R) with a Ki of 0.31 nM. CCZ01048 shows rapid internalization into B16F10 melanoma cells and high in vivo stability. CCZ01048 is a promising candidate for PET imaging of malignant melanoma.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Formel: C71H105N21O16
- Molecular Weight:1508.72
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Publications Citing Use of MedChemExpress (MCE) CCZ01048
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Biologische Aktivität
Beschreibung
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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Molecular Weight 1508.72
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Formel C71H105N21O16
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (4)
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Journal Impact Factor
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Most Recent
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Sci Rep
First-in-human dosimetry and safety evaluation of 68Ga-αMSH derivative for PET imaging of melanoma. [Abstract]2025 May 22;15(1):17748. PMID: 40404705 -
Bioconjug Chem
Radiolabeling Optimization and Preclinical Evaluation of the New PSMA Imaging Agent [18F]AlF-P16-093. [Abstract]2021 May 19;32(5):1017-1026. PMID: 33872489 -
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Iran J Immunol
Letter to the Editor Regarding "An Overview on Serology and Molecular Tests for COVID-19: An Important Challenge of the Current Century (doi: 10.22034/iji.2021.88660.1894.)". [Abstract]2022 Sep;19(3):337. PMID: 36190387
Protokoll
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
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