Cilengitide

Catalog No.S7077 Synonyms: EMD 121974, NSC 707544

Cilengitide Chemical Structure

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.

Size Price Stock Quantity  
In DMSO USD 454 In stock
USD 270 In stock

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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 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 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 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 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 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 purchased from Selleck.

Purity & Quality Control

Choose Selective Integrin Inhibitors

Biological Activity

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.
Targets
αvβ3 receptor [1]
(Cell-free assay)
αvβ5 receptor [2]
(Cell-free assay)
4.1 nM 79 nM
In vitro

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. [1] 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. [2] 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. [3] 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. [4] 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. [5]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
LN-308  NXvjbmJmTnWwY4Tpc44hSXO|YYm= NXT0SFUyOS9zMD:xNFDjiIoQvH2= NFmxXm0zPCCq NHTKTVNFVVORwrC= M{LaRpJm\HWlZYOgSHJGKHKncH;yeIVzKGGldHn2bZR6KGmwIHGgZ49v[2WwdILheIlwdi2mZYDlcoRmdnRibXHucoVz MWeyOlUxODB3Nh?=
ZH-161 Ml;CSpVv[3Srb36gRZN{[Xl? NVXXcmNWOS9zMPMAje69dQ>? MkDRNlQhcA>? MkjESG1UV8Li M1XqVpJm\HWlZYOgSHJGKHKncH;yeIVzKGGldHn2bZR6 M1z5VVI3PTByMEW2
S-24 M13Ve2Z2dmO2aX;uJGF{e2G7 M2PqNVEwOTEkgJpOwI0> MmPnNlQhcA>? MkTISG1UV8Li MmXXdoVlfWOnczDEVmUhemWyb4L0[ZIh[WO2aY\peJk> NWDTUlU3OjZ3MECwOVY>
HaCaT  M3XnSmZ2dmO2aX;uJGF{e2G7 NH6zVWwyOOLCid88cS=> M{\qbFQ5KGh? MWjEUXNQyqB? MWfy[YR2[2W|IGTHSk3PujMEoH3SUmEh\XiycnXzd4lwdg>? M2PNNlI3PTByMEW2
LN-308  M2K3T2Z2dmO2aX;uJGF{e2G7 MXyxNQKBkc7:bR?= M1y0e|I1KGh? NUnsZpd5TE2VT9Mg M3nrcJJm\HWlZYOgRYhTKHC{b4TlbY4hdGW4ZXzzJIFv\CCGUlWgdoVxd3K2ZYKgZYN1cX[rdIm= M{[4UlI3PTByMEW2
REN MXfD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NFHvVpAyKG6PLUKwNEDPxE1? NELBR3E4OiCq NFzONWNl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= NYnxRnh6OjR3OUWyO|Q>
MSTO-211H NXrjRnl3S2WubDDWbYFjcWyrdImgRZN{[Xl? NXzQNmJSOSCwTT2yNFAh|ryP NInpdFU4OiCq NWDMbHc2\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NVjDWlN6OjR3OUWyO|Q>
MM05 NGnLXGFE\WyuIG\pZYJqdGm2eTDBd5NigQ>? Mnr3NUBvVS1{MECg{txO MUK3NkBp NI\WSlVl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= NWD4TYlOOjR3OUWyO|Q>
H28 NGjWU3hE\WyuIG\pZYJqdGm2eTDBd5NigQ>? MX2xJI5ONTJyMDFOwG0> Mn7wO|IhcA>? NX\LfFhs\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy M1XjNlI1PTl3Mke0
SCC25 M3rUZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHTk[403NjJ34pETNlAxyqEEtV2= Mm\1O|IhcA>? MWXy[ZN2dHS|IH3v[IVz[XSnLDDkc5NmNWSncHXu[IVvfCCpcn;3eIghcW6qaXLpeIlwdg>? MYCyOFU2PzB3Nh?=
CAL27 MoLXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3rMPVYvOjYkgKOyNFDDqML3TR?= MlfoO|IhcA>? NXO3No9iemW|dXz0d{Bud2SncnH0[Uwh\G:|ZT3k[ZBmdmSnboSg[5Jwf3SqIHnubIljcXSrb36= NWrBbmM4OjR3NUewOVY>
FaDu  MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIjVWFY3NjJ34pETNlAxyqEEtV2= NIrafG44OiCq M2exTpJme3WudIOgcY9l\XKjdHWsJIRwe2VvZHXw[Y5l\W62IHfyc5d1cCCrbnjpZol1cW:w NWXZUWxLOjR3NUewOVY>
SCC25 MXvBdI9xfG:|aYOgRZN{[Xl? NFe3N4szPcLiwsXNxsA> MXe0POKhcMLi NWnncWF3cW6mdXPld{BieG:ydH;zbZM> Mn3LNlQ2PTdyNU[=
CAL27 M3uwcWFxd3C2b4Ppd{BCe3OjeR?= MXyyOeKhyrWPwrC= NGLKWmQ1QMLiaNMg NEm3fXZqdmS3Y3XzJIFxd3C2b4Ppdy=> MoPuNlQ2PTdyNU[=
FaDu  NX7CUINHSXCxcITvd4l{KEG|c3H5 MluyNlXDqML3TdMg NEG1Z5A1QMLiaNMg M4nvUolv\HWlZYOgZZBweHSxc3nz M3njNFI1PTV5MEW2
T-47D NUn6W|c{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYLCU41KOC1{MDFOwG0> MYe5OkBp MWfpcohq[mm2czDj[YxtKGe{b4f0bEBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MUiyOFE2OzFyMh?=
MCF-7  Mnz3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml35NE0zOCEQvF2= NFnLd3c6PiCq MV;pcohq[mm2czDj[YxtKGe{b4f0bEBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MUOyOFE2OzFyMh?=
T-47D M2\oOmFxd3C2b4Ppd{BCe3OjeR?= NVTzOHpTOC1{MDFOwG0> MVm0PEBp NUjnfVNqcW6mdXPld{BieG:ydH;zbZM> M2LYZ|I1OTV|MUCy
MCF-7  MkDhRZBweHSxc3nzJGF{e2G7 M4niblAuOjBizszN MkS0OFghcA>? NVTHeXpIcW6mdXPld{BieG:ydH;zbZM> M1\rblI1OTV|MUCy
U87MG NWjQWG5FT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHfhb48xNTJ3IN88US=> M1Gwe|I1NzR6IHi= MVzpcohq[mm2czDj[YxtKGe{b4f0bEBqdiCmb4PlJIFv\CC2aX3lJIRmeGWwZHXueEBu[W6wZYK= NGSxd2MzOzN3NEiwOy=>
U251MG NVrzOXF4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXOwMVI2KM7:TR?= M3PiSVI1NzR6IHi= MWrpcohq[mm2czDj[YxtKGe{b4f0bEBqdiCmb4PlJIFv\CC2aX3lJIRmeGWwZHXueEBu[W6wZYK= NFr2dIszOzN3NEiwOy=>
U87MG M4f0TGFxd3C2b4Ppd{BCe3OjeR?= M1LXclEhyrWP M4LxRVQ5KGh? NYLNTZo{cW6mdXPld{BieG:ydH;zbZM> MWGyN|M2PDhyNx?=
U251MG NUH6[VY5SXCxcITvd4l{KEG|c3H5 MXmxJOK2VQ>? MVu0PEBp MoXobY5lfWOnczDhdI9xfG:|aYO= MWWyN|M2PDhyNx?=
U251 M4eybmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NW\heY4xOC1{NTFOwIcwdUx? NV:1PFl4OC12ODDo M4TXTYlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHTvd4Uh[W6mIITpcYUh\GWyZX7k[Y51KG2jbn7ldi=> MXWyNVc5QDN2Mx?=
U87  MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NITXdHkxNTJ3IN88[{9uVA>? NULZfFRbOC12ODDo NXTmcYhicW6qaXLpeJMh[2WubDDndo94fGhiaX6g[I9{\SCjbnSgeIlu\SCmZYDlcoRmdnRibXHucoVz MkHTNlE4QDh|NEO=
U251 NHLrXlZCeG:ydH;zbZMhSXO|YYm= MYqyOUDPxGdxbVy= NEXPOJMzPC92ODDo NVz0W4NHcW6mdXPld{BieG:ydH;zbZMh[XRiNEigbEB{cWewaX\pZ4FvfGy7 NYq2NGxROjF5OEizOFM>
U87  M1vYNmFxd3C2b4Ppd{BCe3OjeR?= M3W3clI2KM7:Zz;tUC=> NVjNVpdYOjRxNEigbC=> NInHR3NqdmS3Y3XzJIFxd3C2b4Ppd{BifCB2ODDoJJNq\26rZnnjZY51dHl? NFHETXQzOTd6OEO0Ny=>
U251 Mme5SpVv[3Srb36gRZN{[Xl? MnLSNE0zPSEQvHevcWw> MU[xNkBpyqB? M3T5U4lv\HWlZYOgZZV1d3CqYXf5JIRwe2ViZHXw[Y5l\W62bIm= NXfPcoh{OjF5OEizOFM>
U87  MlHRSpVv[3Srb36gRZN{[Xl? NXfJc2ZSOC1{NTFOwIcwdUx? M3vP[FEzKGkEoB?= M2nrcIlv\HWlZYOgZZV1d3CqYXf5JIRwe2ViZHXw[Y5l\W62bIm= NGjTS20zOTd6OEO0Ny=>
U87MG NYfl[GhUTnWwY4Tpc44hSXO|YYm= MoWzNE4yNzFxMUCg{txO NHnidJAzPCCq NUn5cXQ1cW2yYXnyd{B1cGViYXTo[ZNqd25ib3[gZ4VtdHNidH:geol1em:wZXP0bY4hcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NFXGTm4yQTJ{MUG3NS=>
LN-308 M2TkNGZ2dmO2aX;uJGF{e2G7 NWrLSm1wOC5zL{GvNVAh|ryP MXeyOEBp NEX1PGlqdXCjaYLzJJRp\SCjZHjld4lwdiCxZjDj[YxteyC2bzD2bZRzd26nY4TpckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MU[xPVIzOTF5MR?=
LN-18 M{DWbmZ2dmO2aX;uJGF{e2G7 NEjFbG8xNjFxMT:xNEDPxE1? MlPXNlQhcA>? NV:xb5pVcW2yYXnyd{B1cGViYXTo[ZNqd25ib3[gZ4VtdHNidH:geol1em:wZXP0bY4hcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> MmjhNVkzOjFzN{G=
T98G MUnGeY5kfGmxbjDBd5NigQ>? M{XiSFAvOS9zL{GwJO69VQ>? Mn3MNlQhcA>? NGHCcZFqdXCjaYLzJJRp\SCjZHjld4lwdiCxZjDj[YxteyC2bzD2bZRzd26nY4TpckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> NH\vdY0yQTJ{MUG3NS=>
LNT-229  MXHGeY5kfGmxbjDBd5NigQ>? MVGwMlEwOS9zMDFOwG0> MlvoNlQhcA>? NUGzbmQ1cW2yYXnyd{B1cGViYXTo[ZNqd25ib3[gZ4VtdHNidH:geol1em:wZXP0bY4hcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NH7zdGsyQTJ{MUG3NS=>
HMEC-1  M{LCRWZ2dmO2aX;uJGF{e2G7 MoXLNU82NzVyIN88[{9udA>? NGDWfIQzPCCq MXvpcoR2[2W|IHGg[I9{\SCmZYDlcoRmdnRiZHX0ZYNpdWWwdNMg NYPkcJBpOTlzMUSwNFU>
HMEC-1  MoLLVJJwdGmoZYLheIlwdiCDc4PhfS=> M3;Sd|EwPS93MDFOwIcwdWx? MlPQNlQwPDhxN{KgbC=> NF3YN4xqdmirYnn0d{Bxem:uaX\ldoF1cW:wIHnuJIEh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ Mor0NVkyOTRyMEW=
HMEC-1  NXTLeWxFSXCxcITvd4l{KEG|c3H5 NXHqcYNDOS93L{WwJO69\y:vbB?= MlG1NlQhcA>? M4nDbIlv\HWlZYOgZZBweHSxc3nz MnjsNVkyOTRyMEW=
G28 NXnicnBmWHKxbHnm[ZJifGmxbjDBd5NigQ>? MVuxM|UwPTBizsznM41t NGHVOlUzPC92OD:3NkBp NYT0XYRscW6qaXLpeJMheHKxbHnm[ZJifGmxbjDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= M4TDZ|E6OTF2MEC1
G44 NXezfVgzWHKxbHnm[ZJifGmxbjDBd5NigQ>? NEnyNlQyNzVxNUCg{txoN22u NYLOTm5VOjRxNEivO|IhcA>? M4\3XYlvcGmkaYTzJJBzd2yrZnXyZZRqd25iaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MXWxPVEyPDByNR?=
G28 MmHKRZBweHSxc3nzJGF{e2G7 NEDFN3gyNzVxNUCg{txoN22u NGDQV5AzPCCq MXnpcoR2[2W|IHHwc5B1d3Orcx?= NV75SopOOTlzMUSwNFU>
G44 M4\FXWFxd3C2b4Ppd{BCe3OjeR?= MljVNU82NzVyIN88[{9udA>? MojrNlQhcA>? MnP3bY5lfWOnczDhdI9xfG:|aYO= NYLaZoJ6OTlzMUSwNFU>
HMEC-1  NXzMNHExTnWwY4Tpc44hSXO|YYm= NInFXmQzOC92MD:2NEDPxGdxbXy= Mn7jbY5pcWKrdIOgSmFMKGGwZDDTdoPDqA>? MmXaNVkyOTRyMEW=
G28 NH;RT3FHfW6ldHnvckBCe3OjeR?= M2L3fVUxKM7:Zz;tcC=> NXOwOWlwOzBxNkCvNVIxKG2rbh?= MVXpcohq[mm2czDwbI9{eGixconsZZRqd25ib3[gSmFMNCCVcnOgZY5lKEGtdB?= NYnFVYNvOTlzMUSwNFU>

... Click to View More Cell Line Experimental Data

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). [5] 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. [6]

Protocol

Kinase Assay:[2]
+ Expand

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.
Cell Research:[3]
+ Expand
  • Cell lines: Human microvascular endothelial cell line HMEC-1
  • Concentrations: 1-50 μg/mL
  • Incubation Time: 3 days
  • Method: 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.
    (Only for Reference)
Animal Research:[5]
+ Expand
  • Animal Models: Human glioblastoma xenografts U87 MG
  • Formulation: PBS
  • Dosages: 100μg
  • Administration: Daily i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 100 mg/mL (142.31 mM)
Water 8 mg/mL (11.38 mM)
Ethanol <1 mg/mL
In vivo 30% propylene glycol, 5% Tween 80, 65% D5W 30 mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* 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.

Chemical Information

Molecular Weight 702.68
Formula

C29H41F3N8O9

CAS No. 199807-35-7
Storage powder
in solvent
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

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Integrin Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID