2. Cytoskeleton Stem Cell/Wnt MAPK/ERK Pathway TGF-beta/Smad
  3. Collagen ERK TGF-beta/Smad
  4. 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.

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C11 peptide-1

C11 peptide-1 Chemical Structure

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C11 peptide-1 Related Antibodies

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Description

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[1].

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.

C11 peptide-1 Related Antibodies

Western Blot Analysis[1]

Cell Line: human LX2 hepatic stellate cells (TGF-β1-stimulated)
Concentration: 10 μM
Incubation Time: 24 h
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.

Cell Proliferation Assay[1]

Cell Line: human LX2 hepatic stellate cells (TGF-β1-stimulated)
Concentration: 10 μM
Incubation Time: 24 h
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.

Immunofluorescence[1]

Cell Line: human LX2 hepatic stellate cells (TGF-β1-stimulated)
Concentration: 10 μM
Incubation Time: 24 h
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 (150 μg/kg; i.p.; daily; 3 weeks) significantly alleviates CCl4-induced liver fibrosis in male C57BL/6J mice by reducing inflammatory infiltration, collagen deposition, and fibrosis marker expression, and by inhibiting ERK1/2 and Smad2/3 signaling pathways[1].
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.

Animal Model: C57BL/6J (male, 6-8 weeks old, 20-24 g, CCl4-induced liver fibrosis)[1]
Dosage: 150 μg/kg
Administration: i.p.; daily; 3 weeks
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.
Animal Model: Sprague-Dawley (male)[1]
Dosage: 1.0 mg/kg
Administration: i.p.; single dose
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.
Molecular Weight

1651.82

Formula

C69H106N18O25S2
Sequence

Cys-Tyr-Leu-Asp-Asn-Asn-Lys-Ile-Cys-Asn-Ile-Pro-Asp-Glu (Disulfide bridge: Cys1-Cys9)
Sequence Shortening

CYLDNNKICNIPDE (Disulfide bridge: Cys1-Cys9)
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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C11 peptide-1 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

C11 peptide-1CollagenERKTGF-beta/SmadExtracellular signal regulated kinasesTransforming growth factor betaSmad2/3Sprague-Dawley ratshuman LX2 hepatic stellate cellsTGF-β1ERK1/2Collagen IC57BL/6J miceα-SMALumicanliver fibrosisInhibitorinhibitorinhibit

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