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    Cilengitide (EMD 121974)
    Cilengitide (EMD 121974)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V2806
    CAS #: 188968-51-6Purity ≥98%

    Description: Cilengitide (also known as EMD 121974, NSC 707544) is a highly potent integrin inhibitor for the αvβ3 receptor and the αvβ5 receptor with IC50 of 4.1 nM and 79 nM in cell-free assays, respectively; it showed ~10-fold selectivity against gpIIbIIIa. Cilengitide is a cyclic Arg-Gly-Asp based peptide with potential antineoplastic activity and has been extensively studied for its anticancer application. The mechanism of action for cilengitide is to bind to and inhibit the activities of the alpha(v)beta(3) and alpha(v)beta(5) integrins, thereby inhibiting endothelial cell-cell interactions, endothelial cell-matrix interactions, and angiogenesis. Cilengitide is currently undergoing phase 2 clinical trials, and the European Medicines Agency has granted cilengitide orphan drug status.

    References: . 2017; 9(9): 117; Genes Cancer. 2011;2(12):1159-65; Cancer Res. 2002;62(15):4263-72.

    Related CAS#: 188968-51-6 (free base)199807-35-7 (TFA salt)

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    Molecular Weight (MW)588.66
    FormulaC₂₇H₄₀N₈O₇  
    CAS No.188968-51-6 (free base); 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: >40 mg/mL 
    Water:  ≥ 30 mg/mL
    Ethanol: N/A
    SMILES CodeO=C(NCC(N[[email protected]](C(N[[email protected]](CC1=CC=CC=C1)C(N([[email protected]]2C(C)C)C)=O)=O)CC(O)=O)=O)[[email protected]](CCCNC(N)=N)NC2=O 
    SynonymsCilengitide; EMD 121974; EMD-121974; EMD121974; NSC-707544; NSC 707544; NSC707544; EMD-85189; EMD 85189; EMD85189; D-03497; D03497; D 03497
    Chemical Name2-((2S,5R,8S,11S)-5-benzyl-11-(3-((diaminomethylene)amino)propyl)-8-isopropyl-7-methyl-3,6,9,12,15-pentaoxo-1,4,7,10,13-pentaazacyclopentadecan-2-yl)acetic acid


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    In Vitro

    In vitro activity: 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.


    Kinase 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.


    Cell Assay: HMEC-1 (1×104 per well) are seeded on uncoated 48 well plates and incubated in medium containing 4% FCS with Cilengitide. After incubation for 72 hours at 37℃, cells are trypsinized and counted.

    In VivoCilengitide 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.
    Animal modelHuman glioblastoma xenografts U87 MG 
    Formulation & DosageDissolved in PBS; 100μg; i.p. injection 
    References

    Genes Cancer. 2011 Dec;2(12):1159-65; Cancer Res. 2002 Aug 1;62(15):4263-72.


    These protocols are for reference only. InvivoChem does not independently validate these methods.

    Cilengitide


    Inhibition of adhesion of human BCEC to (a) and detachment from vitronectin (b,c) by EMD 121974 (Cilengitide, or RGD).  2002 Apr 10;98(5):690-7.

     Cilengitide


    Effect of antibodies to αvβ3 and αvβ5 on adhesion of human BCEC to (a) and detachment from vitronectin (b) and influence of FCS on detachment from regular tissue culture dishes (c). EMD 121974 (Cilengitide, or RGDp) was included as positive control.  2002 Apr 10;98(5):690-7.

     Cilengitide


    Detachment by EMD 121974 (Cilengitide) of human (HBCEC) and mouse MBCEC, DAOY and U87MG cells from vitronectin (a), tenascin (b) and collagen type 1 (c).  2002 Apr 10;98(5):690-7.

     Cilengitide


    Induction of apoptosis by EMD 121974 (Cilengitide) in human and mouse BCEC, DAOY and U87MG cells plated onto wells covered with vitronectin (a), tenascin (b) and collagen type 1 (c).  2002 Apr 10;98(5):690-7.

     Cilengitide


    Immunohistochemistry and immunofluorescence of brain tumor cells in vivoand in vitro. Immunohistochemistry of vitronectin in vivo (a1) and in vitro (a2), tenascin in vivo (b1) and in vitro (b2) and trichrome‐positive material in vivo(c1) and in vitro (c2), shown in light blue. Immunofluorescence of murine αv(d1) and β3 (d2) in vivo showing angiogenic vessels. Staining for CD 31 for blood vessels in vivo, control (e1) and after treatment with EMD 121974 (e2,  Cilengitide). Immunofluorescence in vivo of tumoral αvβ3 (f1) and αvβ5 (f2). Apoptosis in vivo, control (g1) and after treatment with EMD 121974 (g2).  2002 Apr 10;98(5):690-7.

     Cilengitide


    Heterogeneity in response of 39 HNSCC in the FLAVINO assay according to the readouts of colony formation (CF), release of MCP-1, and interleukin 6. Cil, cilengitide; E, Erbitux (cetuximab)

    Cilengitide

    Colony formation of epithelial cells (CFec) and release of MCP-1 and IL-6 are prognostic factors for tumor-specific (a,c,e) and overall survival (b,d,f) of HNSCC patients. (a,b) Colony formation; (c,d) release of MCP-1, (e,f) release of IL-6 as optimized classifiers for survival derived from significant receiver-operating characteristic curves obtained from n = 39 HNSCC patients. . 2017 Sep; 9(9): 117.


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