2. GPCR/G Protein Immunology/Inflammation Apoptosis PI3K/Akt/mTOR Stem Cell/Wnt MAPK/ERK Pathway
  3. CXCR Apoptosis Caspase Akt ERK
  4. Peptide E5

Peptide E5 is an antagonist targeting the CXCR4/CXCL12 axis. Peptide E5 blocks the CXCR4/CXCL12 axis, downregulates CXCR4 expression, and inhibits the phosphorylation of downstream Akt and Erk. Peptide E5 induces apoptosis, suppresses migration and adhesion of breast cancer cells. Peptide E5 inhibits CXCL12-mediated endothelial progenitor cell recruitment, thereby suppressing tumor angiogenesis. Peptide E5 is applicable to relevant research on breast cancer.

For research use only. We do not sell to patients.

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Peptide E5

Peptide E5 Chemical Structure

CAS No. : 1643580-44-2

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Peptide E5 Related Antibodies

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CXCR CXCR1 CXCR2 CXCR3 CXCR4 CXCR7 CXCR6

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Caspase 1 Caspase 2 Caspase 3 Caspase 4 Caspase 5 Caspase 6 Caspase 7 Caspase 8 Caspase 9 Caspase 10 Caspase 12 Caspase Caspase 11 Caspase-13

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Akt Akt1 Akt2 Akt3

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ERK ERK1 ERK2 ERK5 ERK8

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Description

Peptide E5 is an antagonist targeting the CXCR4/CXCL12 axis. Peptide E5 blocks the CXCR4/CXCL12 axis, downregulates CXCR4 expression, and inhibits the phosphorylation of downstream Akt and Erk. Peptide E5 induces apoptosis, suppresses migration and adhesion of breast cancer cells. Peptide E5 inhibits CXCL12-mediated endothelial progenitor cell recruitment, thereby suppressing tumor angiogenesis. Peptide E5 is applicable to relevant research on breast cancer[1].

In Vitro

Peptide E5 (0.1 μM; 40 min) exhibits specific binding affinity to CXCR4-overexpressing 4T1 breast cancer cells and HUVEC, but shows no such binding activity to CXCR4-low-expressing MS-5 cells[1].
Peptide E5 (0-100 μM; 24 h) induces concentration-dependent cytotoxicity and apoptosis in 4T1 cells[1].
Peptide E5 (0.1-10 μM; 1 h pre-incubation) inhibits CXCL12-induced migration of 4T1 breast cancer cells and HUVECs, as well as MS-5 conditioned medium-induced migration of 4T1 cells[1].
Peptide E5 (0.1-10 μM; 2 h pre-incubation) inhibits the adhesion of 4T1 breast cancer cells to MS-5 stromal cells in a concentration-dependent manner[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Peptide E5 Related Antibodies

Cell Viability Assay[1]

Cell Line: murine breast cancer 4T1 cells, HUVECs
Concentration: 0, 1, 10, 25, 50 and 100 μM
Incubation Time: 24 h
Result: Maintained 4T1 cell viability above 90% at concentrations ＜25 μM.
Reduced 4T1 cell viability to 72% at 50 μM, 57% at 75 μM, and 49% at 100 μM.
Sustained HUVEC viability above 90% at all tested concentrations up to 100 μM.

Western Blot Analysis[1]

Cell Line: murine breast cancer 4T1 cells
Concentration: 0, 1, 10, 25, 50 and 100 μM
Incubation Time: 24 h
Result: increased the levels of cleaved caspase-3.
Parmacokinetics
Species Dose Route Tmax T1/2
Mice[1] 40 mg/kg s.c. 2 h 10 h
In Vivo

Peptide E5 (40 mg/kg; s.c.; every other day; days 7-33) exhibits only weak single-agent anti-tumor activity, but it significantly enhances the anti-tumor efficacy of paclitaxel and cyclophosphamide[1].
Peptide E5 (40 mg/kg; s.c.; single dose) exhibits a relatively long in vivo half-life (approximately 10 h) in healthy female BALB/c mice, with hepatic metabolism as its primary clearance pathway[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: BALB/c (female, 5-6 weeks old, orthotopic inoculation of 1×106 4T1 murine breast cancer cells)[1]
Dosage: 40 mg/kg
Administration: s.c.; every other day; day 7-33
Result: Did not show a significant inhibitory effect on tumor weight compared to the control group when administered alone.
Significantly reduced tumor weight compared to the control group and paclitaxel-alone group when combined with paclitaxel.
Significantly reduced tumor weight compared to the cyclophosphamide-alone group and prolonged survival compared to the cyclophosphamide-alone group when combined with cyclophosphamide.
Significantly decreased CD31 levels in tumor tissue when administered alone and in combination with paclitaxel or cyclophosphamide.
Downregulated CXCR4 expression in tumor tissue when combined with paclitaxel or cyclophosphamide.
Significantly inhibited Akt and Erk phosphorylation in tumor tissue when administered alone and in combination with cyclophosphamide.
Molecular Weight

2613.95

Formula

C113H181N39O31S
CAS No.
Sequence

Gly-Gly-Arg-Ser-Phe-Phe-Leu-Leu-Arg-Arg-Ile-Gln-Gly-Cys-Arg-Phe-Arg-Asn-Thr-Val-Asp-Asp
Sequence Shortening

GGRSFFLLRRIQGCRFRNTVDD
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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Peptide E5 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:

Peptide E51643580-44-2Peptide E 5Peptide E-5CXCRApoptosisCaspaseAktERKCXC chemokine receptorsC-X-C motif chemokine receptorsPKBProtein kinase BExtracellular signal regulated kinasesCXCL12BALB/c miceendothelial cellsCXCR4MS-5 cellsErkbreast cancer cellsHUVECs4T1 breast cancer cellsInhibitorinhibitorinhibit

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