C(RGDf-Me-V)
Cilengitide
CAS: 188968-51-6
Molecular Formula: C27H40N8O7
C(RGDf-Me-V) - Names and Identifiers
C(RGDf-Me-V) - Physico-chemical Properties
| Molecular Formula | C27H40N8O7 |
| Molar Mass | 588.66 |
| Density | 1.41±0.1 g/cm3(Predicted) |
| Appearance | powder |
| Color | white to beige |
| pKa | 4.01±0.10(Predicted) |
| Storage Condition | -20°C |
| MDL | MFCD04307743 |
| In vitro study | Cilengitide is a cyclic pentapeptide peptide that competes for the arginine-glycine-aspartic acid (RGD) peptide sequence. Regulates integrin-ligand binding. Cilengitide selectively and effectively inhibits the binding of αvβ3 and αvβ5 integrins to matrix proteins, such as Vitronectin, Fibronectin, Fibrinogen, von Willebrand Factor, Osteopontin, and others. 10 μm Cilengitide completely inhibited the attachment of BAE,BME and HUVE cells to Vitronectin and Fibronectin. Cilengitide inhibits angiogenesis in vitro with three-dimensional collagen and fibrin gel using FGF-2 (or VEGF-A) pretreated BAE cells with IC50 of 15 μm and 8 μm, respectively, 4 M and 3 M. Cilengitide inhibits cell proliferation, induces apoptosis of endothelial cells, and induces differentiation of human endothelial progenitor cells. 50 μg/mL Cilengitide completely inhibited the proliferation of human microvascular endothelial cell line HMEC-1, resulting in-30% cell apoptosis. Treatment with 1 μm Cilengitide for 9 days inhibited nearly 40% of EPCs proliferation. Treatment with 1 μm Cilengitide for 14 days inhibited EPCs differentiation by more than 80%. Cilengitide inhibits adhesion and induces apoptosis of tumor cells. 25 μg/mL Cilengitide separated more than 60% of Dao y cells (medulloblastoma) and U87MG cells (glioblastoma) from Vitronectin and Tenascin. 25 μg/mL Cilengitide induced nearly 50% apoptosis. |
| In vivo study | Cilengitide alone was effective against tumor growth and angiogenesis. Tumors treated with 100 μg Cilengitide significantly reduced the number of CD31 + vessels compared to the control group. Tumors in the brains of animals treated with 100 μg Cilengitide promoted apoptosis compared to those treated with the null peptide. Cilengitide treatment of mice carrying melanoma xenograft M21 prolonged the lifespan of the mice compared to the control group, 36.5 days vs 17.3 days, respectively. Cilengitide can increase the benefits of cytotoxic drug-associated therapies, including chemotherapy and radiation therapy for tumor models. Cilengitide (250 mg/dose) alone did not alter the tumor growth of breast cancer xenografts compared to untreated mice, but was treated in combination with RIT(CMRIT), the use of RIT and six doses of Cilengitide (250 mg/dose) increased the efficacy of the treatment, increasing Recovery Rate of mice from 15% treated with RIT alone to 53%. CMRIT treatment of endothelial cells for 5 days significantly promoted tumor cell apoptosis and reduced tumor cell proliferation. |
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