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.
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- CAS 番号: 1643580-44-2
- 分子式: C113H181N39O31S
- 分子量:2613.95
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
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生物活性
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.
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Cell Line:murine breast cancer 4T1 cells, HUVECs
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Concentration:0, 1, 10, 25, 50 and 100 μM
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Incubation Time:24 h
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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.
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Cell Line:murine breast cancer 4T1 cells
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Concentration:0, 1, 10, 25, 50 and 100 μM
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Incubation Time:24 h
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Result:increased the levels of cleaved caspase-3.
| Species | Dose | Route | Tmax | T1/2 |
|---|---|---|---|---|
| Mice[1] | 40 mg/kg | s.c. | 2 h | 10 h |
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.
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Animal Model:BALB/c (female, 5-6 weeks old, orthotopic inoculation of 1×106 4T1 murine breast cancer cells)[1]
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Dosage:40 mg/kg
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Administration:s.c.; every other day; day 7-33
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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.
化学情報
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CAS 番号 1643580-44-2
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分子量 2613.95
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分子式 C113H181N39O31S
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配列
Gly-Gly-Arg-Ser-Phe-Phe-Leu-Leu-Arg-Arg-Ile-Gln-Gly-Cys-Arg-Phe-Arg-Asn-Thr-Val-Asp-Asp
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シーケンスの短縮
GGRSFFLLRRIQGCRFRNTVDD
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)