Cilengitide trifluoroacetate

Catalog No.S7077 Synonyms: EMD 121974, NSC 707544

Cilengitide trifluoroacetate 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.

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  • 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.

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  MVPGeY5kfGmxbjDBd5NigQ>? NYnPSJhVOS9zMD:xNFDjiIoQvH2= Mk\JNlQhcA>? NVHudG1tTE2VT9Mg MVjy[YR2[2W|IFTSSUBz\XCxcoTldkBi[3Srdnn0fUBqdiCjIHPvcoNmdnS{YYTpc44u\GWyZX7k[Y51KG2jbn7ldi=> MmXJNlY2ODByNU[=
ZH-161 NXPzd5VCTnWwY4Tpc44hSXO|YYm= NE[1UFMyNzFy4pEJ{txu NUC0dZhQOjRiaB?= NYfmOmRHTE2VT9Mg MWTy[YR2[2W|IFTSSUBz\XCxcoTldkBi[3Srdnn0fS=> MlHMNlY2ODByNU[=
S-24 NY\CbJp3TnWwY4Tpc44hSXO|YYm= MojSNU8yOOLCid88cS=> Mn7qNlQhcA>? NYnXXZI2TE2VT9Mg Ml3adoVlfWOnczDEVmUhemWyb4L0[ZIh[WO2aY\peJk> MUSyOlUxODB3Nh?=
HaCaT  NEH6WZNHfW6ldHnvckBCe3OjeR?= NFLwWGEyOOLCid88cS=> NHnXS4g1QCCq M4T0TWROW00EoB?= NIrKb5Vz\WS3Y3XzJHRITi4QskNCpI1TVkFiZYjwdoV{e2mxbh?= NXvwZYlYOjZ3MECwOVY>
LN-308  MXnGeY5kfGmxbjDBd5NigQ>? NVThb4ZSOTEkgJpOwI0> NUfmO3ZPOjRiaB?= MlH1SG1UV8Li M{\ZU5Jm\HWlZYOgRYhTKHC{b4TlbY4hdGW4ZXzzJIFv\CCGUlWgdoVxd3K2ZYKgZYN1cX[rdIm= MV:yOlUxODB3Nh?=
REN MUjD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MkXBNUBvVS1{MECg{txO M2jGN|czKGh? NGDZZ4Vl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= MYmyOFU6PTJ5NB?=
MSTO-211H MXPD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MWGxJI5ONTJyMDFOwG0> M2qxbFczKGh? NX\IeI16\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy MXmyOFU6PTJ5NB?=
MM05 NVnjO2NSS2WubDDWbYFjcWyrdImgRZN{[Xl? M33KS|Ehdk1vMkCwJO69VQ>? MXq3NkBp MVTk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? M13COFI1PTl3Mke0
H28 NUnZcJB5S2WubDDWbYFjcWyrdImgRZN{[Xl? MnjNNUBvVS1{MECg{txO MXu3NkBp M1HmNIRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= M{O4ZlI1PTl3Mke0
SCC25 M3fZVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH\JOZA3NjJ34pETNlAxyqEEtV2= Mm[0O|IhcA>? NYTy[JRlemW|dXz0d{Bud2SncnH0[Uwh\G:|ZT3k[ZBmdmSnboSg[5Jwf3SqIHnubIljcXSrb36= M1;i[FI1PTV5MEW2
CAL27 MoDKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{TsRVYvOjYkgKOyNFDDqML3TR?= MUW3NkBp MlHvdoV{fWy2czDtc4RmemG2ZTyg[I9{\S2mZYDlcoRmdnRiZ4Lve5RpKGmwaHnibZRqd25? MYmyOFU2PzB3Nh?=
FaDu  NWS3WIs6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIXBRm43NjJ34pETNlAxyqEEtV2= NITCcJM4OiCq MUTy[ZN2dHS|IH3v[IVz[XSnLDDkc5NmNWSncHXu[IVvfCCpcn;3eIghcW6qaXLpeIlwdg>? MoLoNlQ2PTdyNU[=
SCC25 MmjCRZBweHSxc3nzJGF{e2G7 M2HZcFI2yqEEtV5CpC=> M2HR[|Q5yqCqwrC= MkHIbY5lfWOnczDhdI9xfG:|aYO= MVyyOFU2PzB3Nh?=
CAL27 MV;BdI9xfG:|aYOgRZN{[Xl? NVvmcJZlOjYEoNM1UeKh MlXvOFjDqGkEoB?= Mof4bY5lfWOnczDhdI9xfG:|aYO= NFq3ZnQzPDV3N{C1Oi=>
FaDu  NUnzNnBiSXCxcITvd4l{KEG|c3H5 NGDtV|UzPcLiwsXNxsA> NGrvOHk1QMLiaNMg M{LNNolv\HWlZYOgZZBweHSxc3nz M{nNXFI1PTV5MEW2
T-47D M2f5fmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnrSNE0zOCEQvF2= MYO5OkBp MYHpcohq[mm2czDj[YxtKGe{b4f0bEBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MV6yOFE2OzFyMh?=
MCF-7  M1\peGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn:2NE0zOCEQvF2= M2D4XFk3KGh? MYDpcohq[mm2czDj[YxtKGe{b4f0bEBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MWmyOFE2OzFyMh?=
T-47D MYPBdI9xfG:|aYOgRZN{[Xl? MX[wMVIxKM7:TR?= MYq0PEBp MmTBbY5lfWOnczDhdI9xfG:|aYO= M2H1VFI1OTV|MUCy
MCF-7  M1L1NWFxd3C2b4Ppd{BCe3OjeR?= MUCwMVIxKM7:TR?= NXuxS4JDPDhiaB?= MkXjbY5lfWOnczDhdI9xfG:|aYO= M1vuWlI1OTV|MUCy
U87MG MorKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1LOUFAuOjVizszN Mn;iNlQwPDhiaB?= M2rqcolvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHTvd4Uh[W6mIITpcYUh\GWyZX7k[Y51KG2jbn7ldi=> NHToUmMzOzN3NEiwOy=>
U251MG M3vGTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH;nS2oxNTJ3IN88US=> MkfvNlQwPDhiaB?= NHnrOIdqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjDkc5NmKGGwZDD0bY1mKGSncHXu[IVvfCCvYX7u[ZI> MXOyN|M2PDhyNx?=
U87MG NFPpNYhCeG:ydH;zbZMhSXO|YYm= NFH0XoEyKML3TR?= NYj4SolCPDhiaB?= M1nKN4lv\HWlZYOgZZBweHSxc3nz NHH3ZWIzOzN3NEiwOy=>
U251MG M1G1NWFxd3C2b4Ppd{BCe3OjeR?= M3nhTlEhyrWP MWC0PEBp NVnCcJh6cW6mdXPld{BieG:ydH;zbZM> NVq5cFFnOjN|NUS4NFc>
U251 NGrOWVBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NE\FXo4xNTJ3IN88[{9uVA>? M3rPRVAuPDhiaB?= NVf5T5hOcW6qaXLpeJMh[2WubDDndo94fGhiaX6g[I9{\SCjbnSgeIlu\SCmZYDlcoRmdnRibXHucoVz MlfKNlE4QDh|NEO=
U87  NEfsTG5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFW2cZYxNTJ3IN88[{9uVA>? M{Xvc|AuPDhiaB?= M2nVOYlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHTvd4Uh[W6mIITpcYUh\GWyZX7k[Y51KG2jbn7ldi=> NIrP[FIzOTd6OEO0Ny=>
U251 MXHBdI9xfG:|aYOgRZN{[Xl? Mn3nNlUh|rypL33M MnzRNlQwPDhiaB?= Mne2bY5lfWOnczDhdI9xfG:|aYOgZZQhPDhiaDDzbYdvcW[rY3HueIx6 NYSxfWJROjF5OEizOFM>
U87  NEm2VVlCeG:ydH;zbZMhSXO|YYm= Mn7FNlUh|rypL33M Mn3NNlQwPDhiaB?= NWjyXlZncW6mdXPld{BieG:ydH;zbZMh[XRiNEigbEB{cWewaX\pZ4FvfGy7 MXSyNVc5QDN2Mx?=
U251 NH7MU3ZHfW6ldHnvckBCe3OjeR?= MV2wMVI2KM7:Zz;tUC=> NWfJOWhROTJiaNMg MmribY5lfWOnczDheZRweGijZ4mg[I9{\SCmZYDlcoRmdnSueR?= Ml\KNlE4QDh|NEO=
U87  MlHHSpVv[3Srb36gRZN{[Xl? NHjET3QxNTJ3IN88[{9uVA>? MWSxNkBpyqB? MUTpcoR2[2W|IHH1eI9xcGGpeTDkc5NmKGSncHXu[IVvfGy7 M3XadlIyPzh6M{Sz
U87MG MVnGeY5kfGmxbjDBd5NigQ>? NF\ocHQxNjFxMT:xNEDPxE1? NELoSJIzPCCq MlmwbY1x[Wm{czD0bIUh[WSqZYPpc44hd2ZiY3XscJMhfG9idnn0do9v\WO2aX6gbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= NIfMbJoyQTJ{MUG3NS=>
LN-308 MWTGeY5kfGmxbjDBd5NigQ>? NXWyd2RFOC5zL{GvNVAh|ryP M3LNTVI1KGh? MYPpcZBicXK|IITo[UBi\Ginc3nvckBw\iClZXzsd{B1dyC4aYTyc45m[3SrbjDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NWLoc2txOTl{MkGxO|E>
LN-18 NVj4fnBQTnWwY4Tpc44hSXO|YYm= MlTLNE4yNzFxMUCg{txO NXvjXW82OjRiaB?= NHuwO3pqdXCjaYLzJJRp\SCjZHjld4lwdiCxZjDj[YxteyC2bzD2bZRzd26nY4TpckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MnrlNVkzOjFzN{G=
T98G MkHzSpVv[3Srb36gRZN{[Xl? NGPOVHExNjFxMT:xNEDPxE1? NH3HOIMzPCCq NE\yUZNqdXCjaYLzJJRp\SCjZHjld4lwdiCxZjDj[YxteyC2bzD2bZRzd26nY4TpckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MmLINVkzOjFzN{G=
LNT-229  MV3GeY5kfGmxbjDBd5NigQ>? NEfB[2sxNjFxMT:xNEDPxE1? NInZOoczPCCq MYrpcZBicXK|IITo[UBi\Ginc3nvckBw\iClZXzsd{B1dyC4aYTyc45m[3SrbjDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MlXqNVkzOjFzN{G=
HMEC-1  NYDvd3dmTnWwY4Tpc44hSXO|YYm= NFTpW28yNzVxNUCg{txoN22u MoTRNlQhcA>? MmjxbY5lfWOnczDhJIRwe2ViZHXw[Y5l\W62IHTleIFkcG2nboVCpC=> Mnu4NVkyOTRyMEW=
HMEC-1  Mlf1VJJwdGmoZYLheIlwdiCDc4PhfS=> M2nNT|EwPS93MDFOwIcwdWx? NHHIblczPC92OD:3NkBp M2e1XolvcGmkaYTzJJBzd2yrZnXyZZRqd25iaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? M3HzZVE6OTF2MEC1
HMEC-1  NYPzdodDSXCxcITvd4l{KEG|c3H5 Mn\YNU82NzVyIN88[{9udA>? MmjlNlQhcA>? M1\WOIlv\HWlZYOgZZBweHSxc3nz MUGxPVEyPDByNR?=
G28 NXrDU3hEWHKxbHnm[ZJifGmxbjDBd5NigQ>? Ml3FNU82NzVyIN88[{9udA>? MWeyOE81QC95MjDo MV\pcohq[mm2czDwdo9tcW[ncnH0bY9vKGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz NYHoUnR6OTlzMUSwNFU>
G44 MX\Qdo9tcW[ncnH0bY9vKEG|c3H5 MXGxM|UwPTBizsznM41t NVPaTWoxOjRxNEivO|IhcA>? MVHpcohq[mm2czDwdo9tcW[ncnH0bY9vKGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz MoHkNVkyOTRyMEW=
G28 M2\ETGFxd3C2b4Ppd{BCe3OjeR?= NXu1Z5M2OS93L{WwJO69\y:vbB?= M4XWXVI1KGh? NYLpO5JYcW6mdXPld{BieG:ydH;zbZM> NYjrNpFNOTlzMUSwNFU>
G44 NXzJSXFlSXCxcITvd4l{KEG|c3H5 M2PrNFEwPS93MDFOwIcwdWx? NV;xblZ{OjRiaB?= NEjHcI5qdmS3Y3XzJIFxd3C2b4Ppdy=> M4qyTlE6OTF2MEC1
HMEC-1  NV[zW3FrTnWwY4Tpc44hSXO|YYm= MX[yNE81OC94MDFOwIcwdWx? MlTsbY5pcWKrdIOgSmFMKGGwZDDTdoPDqA>? NIDobpEyQTFzNECwOS=>
G28 MX3GeY5kfGmxbjDBd5NigQ>? NIToPVc2OCEQvHevcYw> M3TOXFMxNzZyL{GyNEBucW5? MUXpcohq[mm2czDwbI9{eGixconsZZRqd25ib3[gSmFMNCCVcnOgZY5lKEGtdB?= Mkf2NVkyOTRyMEW=

... 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 Insoluble
In vivo Add solvents individually and in order:
30% propylene glycol, 5% Tween 80, 65% D5W
30 mg/mL

* 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
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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Frequently Asked Questions

  • Question 1:

    The recommend vehicle is 30% propylene glycol, 5% Tween 80, 65% D5W at 30mg/ml, can you let me know if this is a suspension or clear solution?

  • Answer:

    S7077 Cilengitide can be dissolved in 30% propylene glycol/5% Tween 80/65% D5W at 10 mg/ml as a clear solution.

  • Question 2:

    Is Cilengitide a TFA salt?

  • Answer:

    S7077 Cilengitide is actually a TFA salt, and the ratio between Cilengitide and TFA is 1:1.

Integrin Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID