C11 peptide-1
C11 peptide-1 is an antifibrotic agent that binds directly to Collagen I. C11 peptide-1 physically disrupts Collagen I interaction with Lumican. C11 peptide-1 reduces inflammatory infiltration and inhibits the ERK1/2 and Smad2/3 signaling pathways. C11 peptide-1 can be used for the research of liver fibrosis.
For research use only. We do not sell to patients.
- Formula: C69H106N18O25S2
- Molecular Weight:1651.82
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
ERK1 |
ERK2 |
In Vitro
C11 peptide-1 (10 μM; 1 h) potently inhibits the human Lumican-Collagen I protein interaction with a 75.99% inhibition rate[1].
C11 peptide-1 (3.125-100 μM) binds directly to purified Collagen I with stronger affinity than peptide C5[1].
C11 peptide-1 (10 μM; 24 h) significantly reduces TGF-β1-induced Collagen I (COL1A1) expression in human LX2 hepatic stellate cells[1].
C11 peptide-1 (10 μM; 24 h) significantly reduces TGF-β1-induced α-SMA expression, a marker of activation, in human LX2 hepatic stellate cells[1].
C11 peptide-1 (10 μM; 24 h) significantly inhibits TGF-β1-induced proliferation of human LX2 hepatic stellate cells[1].
C11 peptide-1 (10 μM; 24 h) significantly reduces TGF-β1-induced Collagen I fluorescence intensity in human LX2 hepatic stellate cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:human LX2 hepatic stellate cells (TGF-β1-stimulated)
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Concentration:10 μM
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Incubation Time:24 h
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Result:Significantly suppressed TGF-β1-induced COL1A1 expression with a statistically significant reduction (P < 0.01) relative to the TGF-β1-only treated group.
Showed superior inhibitory efficacy to peptide C5.\nSignificantly inhibited TGF-β1-induced α-SMA expression with a statistically significant reduction (P < 0.01) relative to the TGF-β1-only treated group.
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Cell Line:human LX2 hepatic stellate cells (TGF-β1-stimulated)
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Concentration:10 μM
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Incubation Time:24 h
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Result:Significantly reduced the ratio of EdU-positive LX2 cells with a statistically significant reduction (P < 0.01) relative to the TGF-β1-only treated group.
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Cell Line:human LX2 hepatic stellate cells (TGF-β1-stimulated)
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Concentration:10 μM
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Incubation Time:24 h
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Result:Visually and quantitatively reduced COL1A1 fluorescence intensity with a statistically significant reduction (P < 0.01) relative to the TGF-β1-only treated group.
Parmacokinetics
| Species | Dose | Route | T1/2 | Cmax | MRT0-inf | AUC0-t | AUC0-inf |
|---|---|---|---|---|---|---|---|
| Rat[1] | 1.0 mg/kg | i.p. | 0.4 h | 878.47 ng/mL | 0.67 h | 809.49 ng·h/mL | 815.38 ng·h/mL |
In Vivo
Peptide C11 (1.0 mg/kg; i.p.; single dose) exhibits favorable pharmacokinetic properties in male Sprague-Dawley rats, with a T1/2 of 0.4 h and an AUC0-inf of 815.38 h × ng/mL[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (male, 6-8 weeks old, 20-24 g, CCl4-induced liver fibrosis)[1]
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Dosage:150 μg/kg
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Administration:i.p.; daily; 3 weeks
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Result:Reversed the CCl4-induced decrease in body weight.
Produced a significant reduction in serum ALT and AST levels.
Significantly decreased hepatic hydroxyproline content.
Reduced inflammatory infiltration and collagen deposition as observed via H&E and PSR staining.
Significantly downregulated hepatic expression of key fibrosis markers including Collagen I, α-SMA, and Timp1.
Significantly decreased phosphorylation levels of ERK1/2 and Smad2/3.
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Animal Model:Sprague-Dawley (male)[1]
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Dosage:1.0 mg/kg
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Administration:i.p.; single dose
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Result:Demonstrated a half-life (t1/2) of 0.4 h.
Reached a maximum concentration (Cmax) of 878.47 ng/mL.
Achieved a mean residence time (MRT0-inf) of 0.67 h.
Exhibited an area under the curve from time zero to the last measurable concentration (AUC0-t) of 809.49 h × ng/mL.
Exhibited an area under the curve from time zero to infinity (AUC0-inf) of 815.38 h × ng/mL.
Chemical Information
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Molecular Weight 1651.82
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Formula C69H106N18O25S2
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Sequence
Cys-Tyr-Leu-Asp-Asn-Asn-Lys-Ile-Cys-Asn-Ile-Pro-Asp-Glu (Disulfide bridge: Cys1-Cys9)
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Sequence Shortening
CYLDNNKICNIPDE (Disulfide bridge: Cys1-Cys9)
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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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Fibrosis/Collagen Morphometry
Fibrosis and collagen morphometry is based on the quantitative visualization of fibrillar collagen deposition in tissue sections using histochemical stains such as Sirius Red (Picrosirius Red) or Masson's trichrome, followed by image-based or polarization-enhanced analysis to estimate collagen proportional area as a surrogate of extracellular matrix accumulation during fibrotic remodeling. Sirius Red combined with polarized light microscopy enhances detection of collagen fibers due to birefringence properties, enabling more specific visualization of collagen type I and III fibrils compared to conventional bright-field histology, while whole-section or region-restricted digital morphometry reduces field-selection bias in fibrosis assessment. Alternative quantitative approaches include second harmonic generation (SHG) and two-photon excited fluorescence microscopy, which enable label-free detection of fibrillar collagen and have been validated against histological staining and biochemica
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Collagen: Sirius Red Staining
Sirius Red or picrosirius red staining is a histochemical method for visualizing collagen-rich extracellular matrix in tissue sections, and collagen fibers are detected as red-stained structures under bright-field microscopy with enhanced birefringence under polarized light. Picrosirius red is useful for assessing total collagen organization, distribution, and fibrosis burden, but polarized color should not be interpreted as a definitive collagen type I versus type III readout because color is affected by fiber orientation, thickness, and packing.
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Connective Tissue: Masson's Trichrome/Collagen Trichrome Staining
Masson’s Trichrome (collagen/trichrome staining) is a histological technique that differentially stains tissue compartments using sequential acidic dyes to distinguish collagen from muscle and cytoplasmic components based on dye affinity and tissue permeability differences, enabling visualization of fibrosis and connective tissue architecture in histological sections. The classical formulation typically uses Weigert's iron hematoxylin for nuclear staining, Biebrich scarlet-acid fuchsin for cytoplasm and muscle, and aniline blue (or light green variants) for collagen, producing a characteristic blue/green collagen signal contrasted against red cytoplasm and dark nuclei. The staining principle relies on selective displacement of smaller dye molecules by larger anionic dyes in collagen-rich regions under controlled acidified conditions, which enhances collagen-specific dye retention. This property makes the method widely used for fibrosis assessment in organs such as heart, liver, lung, a
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Liver Histomorphometry
Liver histomorphometry is a quantitative histological approach used to measure structural alterations in hepatic tissue, including parenchymal loss, steatosis, fibrosis, and vascular remodeling, by combining stained tissue section analysis with stereological or computerized image-based measurements. Classical morphometric frameworks quantify volume fractions of liver compartments and fibrotic regions using systematic sampling and image analysis, enabling objective comparison of pathological changes across experimental groups. These approaches are widely applied in liver cirrhosis and fibrosis studies to reduce subjectivity in histological scoring and improve reproducibility of tissue evaluation. Recent methodological advances integrate automated image analysis and radiomics-based extraction of histological features from standard liver stains (e. g. , H&E and fibrotic stains), enabling quantitative correlation between morphometric features and fibrosis stages in non-alcoholic fatty live
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)