Catalog No.S7077 Synonyms: EMD 121974, NSC 707544
Molecular Weight(MW): 702.68
Cilengitide is a potent integrin inhibitor for αvβ3 receptor and αvβ5 receptor with IC50 of 4.1 nM and 79 nM in cell-free assays, respectively; ~10-fold selectivity against gpIIbIIIa. Phase 2.
Cited by 9 Publications
6 Customer Reviews
WT mice were subjected to BDL and treated with either vehicle or cilengitide (10 mg/kg) daily for 6 days; adjacent liver sections were immunostained for CK19 or PCNA. Data were quantified and expressed as mean ± SD. (n = 6 per group.) *P < 0.02, **P < 0.004, Student’s t test.
J Clin Invest, 2015, 125(5): 1886-900. Cilengitide trifluoroacetate purchased from Selleck.
BrdU incorporation was quantified in freshly isolated primary cholangiocytes treated with BSA (4 μg/ml), CCN1 (4 μg/ml), soluble JAG1 (2 μg/ml), DAPT (10 μM), cilengitide (1 μM), NBD (25 μM), or control peptide (25 μM). Where indicated, CCN1 (4 μg/ml) was added with other inhibitors. *P < 0.04, **P < 0.01, Student’s t test.
J Clin Invest, 2015, 125(5): 1886-900. Cilengitide trifluoroacetate purchased from Selleck.
(A) Comparison of blood vessel count of the linear and grafted peptides. Error bars indicate ± SD (n ≥ 6). The dotted line indicates ~50% inhibition of blood vessels. A one-way ANOVA with Dunnett's post-test using a multiple comparison test was used for statistical analysis. In addition, unpaired t-test was used to test the significance of MCoAA-02 against MCo-SST-01 and MCo-PEDF. ****p ≤ 0.0001 and ***p ≤ 0.05. All peptides were compared to 0.3 nM VEGF (highlighted in grey), which is represented as 100% blood vessel growth.
Sci Rep, 2016, 6:35347.. Cilengitide trifluoroacetate purchased from Selleck.
(D) The treatment more significantly inhibited cell invasion and proliferation in EGFRvIII-expressing GBM than vector cells in the environment of hypoxia and vitronectin-enrichment in vitro. All experiments were performed independently at least three times. *p < 0.05; **p < 0.01.
Oncotarget, 2016, 7(4):4680-94.. Cilengitide trifluoroacetate purchased from Selleck.
Elevated β-catenin expression was observed in OPNa-, OPNb- and OPNc-expressing cells. Addition of cilengitide did not alter β-catenin expression in any of the OPN isoform-expressing cells but induced E-cadherin expression in OPNc-expressing cells. GAPDH or β-actin was included as a loading control.
Oncotarget, 2015, 6(26):22239-57.. Cilengitide trifluoroacetate purchased from Selleck.
Cell growth inhibition of non-small cell lung carcinoma (NSCLC) by Cilengitide. Cilengitide is based on the cyclic peptide cyclo(-RGDfV-), which is selective for αv integrins. Interestingly, it acts differently on HTB183 and A549 cell lines. Cilengitide was more efficient on A549, lung adenocarcinoma, while in HTB183 it showed moderate inhibitory activity. This may be due to the mestastatic nature of HTB183 cells which have already lost the cell adhesion properties.
Dr.Milica Pesic from Institute for Biological Research . Cilengitide trifluoroacetate purchased from Selleck.
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Choose Selective Integrin Inhibitors
|Description||Cilengitide is a potent integrin inhibitor for αvβ3 receptor and αvβ5 receptor with IC50 of 4.1 nM and 79 nM in cell-free assays, respectively; ~10-fold selectivity against gpIIbIIIa. Phase 2.|
Cilengitide is a cyclized pentapeptide peptidomimetic designed to compete for the arginine-glycine-aspartic acid (RGD) peptide sequence that regulates integrin-ligand binding. Cilengitide selectively and potently blocks the ligation of theαvβ3 andαvβ5 integrins to provisional matrix proteins such as vitronectin, fibronectin, fibrinogen, von Willebrand factor, osteopontin, and others.  Cilegitide inhibits angiogenesis in vitro. 10 μM Cilengitide completely inhibits attachment of BAE, BME and HUVE cells on vitronectin and fibronectin. Cilengitide inhibits in vitro angiogenesis of BAE cells on three-dimensional collagen and ﬁbrin gels pretreated with FGF-2(or VEGF-A) with IC50 of 15 μM and 8 μM, 4 μM and 3 μM, respectively.  Cilengitide blocks proliferation and induces apoptosis of endothelial cells as well as differentiation of human endothelial precursor cells (EPCs). 50 μg/mL Cilengitide completely inhibits the proliferation of human microvascular endothelial cell line HMEC-1 and leads to apoptosis in ~30% cells.  1.0 μM Cilengitide treating for 9 days inhibits the proliferation of EPCs by nearly 40%. 1 μM Cilengitide inhibits the differentiation of EPCs by more than 80% at 14 days.  Cilengitide inhibits adhesion and induces apoptosis of tumor cells. 25 μg/mL Cilengitide causes detachment of DAOY cells (medulloblastoma) and U87MG cells (glioblastoma) from vitronectin and tenascin by more than 60%. 25 μg/mL Cilengitide induces a nearly 50% apoptosis rate of these cells. 
|In vivo||Cilengitide is activity against tumor growth and angiogenesis as single-agent. 100 μg Cilengitide induces a significant decrease in the number of CD 31+ vessels seen in tumors (2/high-power field) compared with control tumors (56/high-power field). 100 μg Cilengitide increases cellular apoptosis in the brain tumors of animals (2.2% apoptotic cells/high-power field) compared with those receiving the inactive peptide (1.7% cells/high-power field). Cilengitide treatment results in prolonged survival of the mice bearing melanoma xenografts M21 compared with control treatment group. (36.5 vs 17.3 days).  Cilengitide can augment the therapeutic benefit associated with cytotoxic agents including chemotherapy and radiation therapy in tumor models. Cilengitide (250 mg/dose) alone does not alter tumor growth of breast cancer xenografts when compared with untreated mice, but combined modality RIT (CMRIT) using RIT and six doses of Cilengitide (250 mg/dose) increases efficacy of treatment, with the cure rate for mice that receives only RIT increasing from 15 to 53%. CMRIT significantly increases apoptosis of tumor and endothelial cells 5 days, and decreases tumor proliferation. |
Integrin-binding competition assay:Recombinant soluble integrins are immobilized, and peptides, which are serially diluted in Tris-buffered saline (TBS++) (0.1% (w/v) BSA, 150 mM NaCl, 1 mM CaCl2, 1 mM MgCl2 10 μM MnCl2, 20 mM Tris-HCl; pH 7.4), are added in parallel with biotinylated vitronectin (to 1μg/mL). After a 3-h incubation at 37℃ and washing with Tris–buffered saline, bound ligand is detected by incubation with an antibiotin alkaline phosphatase-conjugated antibody (BioRad) followed by development with p-nitrophenyl phosphatase substrate. The reaction is stopped by the addition of NaOH and the color intensity read at 405 nm.
-  Reardon DA, et al. Genes Cancer, 2011, 2(12):1159-1165.
-  Nisato RE, et al. Angiogenesis, 2003, 6(2), 105-119.
-  Oliveira-Ferrer L, et al. J Exp Clin Cancer Res, 2008, 27:86.
|In vitro||DMSO||100 mg/mL (142.31 mM)|
|Water||8 mg/mL (11.38 mM)|
|Ethanol||slightly soluble or insoluble|
|In vivo||Add solvents individually and in order:
30% propylene glycol, 5% Tween 80, 65% D5W
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
|Synonyms||EMD 121974, NSC 707544|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT01782976||Withdrawn||Glioblastoma||M.D. Anderson Cancer Center|Brain Tumor Trials Collaborative|EMD Serono||June 2013||Phase 2|
|NCT01517776||Terminated||Gliomas||Martin-Luther-Universität Halle-Wittenberg|Merck KGaA||January 2012||Phase 2|
|NCT01504165||Completed||Renal Impairment||Merck KGaA||January 2012||Phase 1|
|NCT01276496||Completed||Adult Solid Neoplasm|Estrogen Receptor Negative|HER2/Neu Negative|Male Breast Carcinoma|Progesterone Receptor Negative|Recurrent Breast Carcinoma|Stage IIIB Breast Cancer|Stage IIIC Breast Cancer|Stage IV Breast Cancer|Triple-Negative Breast Carcinoma||National Cancer Institute (NCI)||December 2010||Phase 1|
|NCT01165333||Completed||Diffuse Intrinsic Pontine Glioma||Centre Oscar Lambret||August 2010||Phase 1|
|NCT00979862||Completed||Adult Giant Cell Glioblastoma|Adult Glioblastoma|Adult Gliosarcoma|Recurrent Adult Brain Neoplasm||National Cancer Institute (NCI)||March 2010||Phase 1|
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