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  M3v3T2Z2dmO2aX;uJGF{e2G7 MkPoNU8yOC9zMEFihKnPxG1? MmXjNlQhcA>? NXTlZ4p4TE2VT9Mg NI\6eFBz\WS3Y3XzJGRTTSC{ZYDvdpRmeiCjY4Tpeol1gSCrbjDhJINwdmOnboTyZZRqd25vZHXw[Y5l\W62IH3hco5meg>? MV[yOlUxODB3Nh?=
ZH-161 MXfGeY5kfGmxbjDBd5NigQ>? MWSxM|Ex6oDLzszt NWSySm9NOjRiaB?= NX;zfYx3TE2VT9Mg MoPzdoVlfWOnczDEVmUhemWyb4L0[ZIh[WO2aY\peJk> NXrOcoxHOjZ3MECwOVY>
S-24 NV:0Z|FVTnWwY4Tpc44hSXO|YYm= MYSxM|Ex6oDLzszt NYrXZZNkOjRiaB?= MkLJSG1UV8Li NHm0Umhz\WS3Y3XzJGRTTSC{ZYDvdpRmeiCjY4Tpeol1gQ>? NX;5cnlmOjZ3MECwOVY>
HaCaT  MmnDSpVv[3Srb36gRZN{[Xl? NEfpcGYyOOLCid88cS=> MXO0PEBp NFz0SYRFVVORwrC= M3S3TZJm\HWlZYOgWGdHNc7{MtMgcXJPSSCneIDy[ZN{cW:w NIXaXXIzPjVyMEC1Oi=>
LN-308  M37XS2Z2dmO2aX;uJGF{e2G7 NEHEbmUyOOLCid88cS=> NH;PTYgzPCCq NFrUepZFVVORwrC= MnfHdoVlfWOnczDBbHIheHKxdHXpckBt\X[nbIOgZY5lKESURTDy[ZBwenSncjDhZ5Rqfmm2eR?= MV:yOlUxODB3Nh?=
REN MnLuR4VtdCCYaXHibYxqfHliQYPzZZk> MkTkNUBvVS1{MECg{txO MUS3NkBp NEfXeJNl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= Mn2yNlQ2QTV{N{S=
MSTO-211H MYTD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NXrYc3VCOSCwTT2yNFAh|ryP M4m3c|czKGh? M1rxXIRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MoH4NlQ2QTV{N{S=
MM05 MVLD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MmnyNUBvVS1{MECg{txO NGXYS2I4OiCq Mnn2[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJIEh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ NHmwXG0zPDV7NUK3OC=>
H28 MUDD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MYexJI5ONTJyMDFOwG0> MVq3NkBp NXyyZZVK\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NXrTXnlZOjR3OUWyO|Q>
SCC25 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWHzXWNXPi5{NfMAl|IxOMLiwsXN NYP0S|dbPzJiaB?= Mor6doV{fWy2czDtc4RmemG2ZTyg[I9{\S2mZYDlcoRmdnRiZ4Lve5RpKGmwaHnibZRqd25? MkHVNlQ2PTdyNU[=
CAL27 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnXoOk4zPeLCk{KwNOKhyrWP NFLQPIY4OiCq NELoU5Fz\XO3bITzJI1w\GW{YYTlMEBld3OnLXTldIVv\GWwdDDndo94fGhiaX7obYJqfGmxbh?= M3PoOlI1PTV5MEW2
FaDu  NIPlZ|NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2LPdVYvOjYkgKOyNFDDqML3TR?= M1:1PVczKGh? NGDFUlVz\XO3bITzJI1w\GW{YYTlMEBld3OnLXTldIVv\GWwdDDndo94fGhiaX7obYJqfGmxbh?= MW[yOFU2PzB3Nh?=
SCC25 MULBdI9xfG:|aYOgRZN{[Xl? MmTkNlXDqML3TdMg NGfP[5c1QMLiaNMg NH3Fc2dqdmS3Y3XzJIFxd3C2b4Ppdy=> MnfvNlQ2PTdyNU[=
CAL27 M4DLe2Fxd3C2b4Ppd{BCe3OjeR?= M13D[FI2yqEEtV5CpC=> MUS0POKhcMLi MXXpcoR2[2W|IHHwc5B1d3Orcx?= MkjDNlQ2PTdyNU[=
FaDu  NFXYeWNCeG:ydH;zbZMhSXO|YYm= NI\SRZIzPcLiwsXNxsA> MoG1OFjDqGkEoB?= NETLeIJqdmS3Y3XzJIFxd3C2b4Ppdy=> NYLETFdQOjR3NUewOVY>
T-47D NYPDc2VjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MViwMVIxKM7:TR?= MVq5OkBp MW\pcohq[mm2czDj[YxtKGe{b4f0bEBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> Mki4NlQyPTNzMEK=
MCF-7  NGD2fYRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWewMVIxKM7:TR?= MW[5OkBp MmezbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> M2nWNlI1OTV|MUCy
T-47D NFvBNndCeG:ydH;zbZMhSXO|YYm= MlvsNE0zOCEQvF2= NVztTGw4PDhiaB?= MXTpcoR2[2W|IHHwc5B1d3Orcx?= NEC4[4IzPDF3M{GwNi=>
MCF-7  NWnJdmFtSXCxcITvd4l{KEG|c3H5 M4HnbFAuOjBizszN M{THZlQ5KGh? M33VVYlv\HWlZYOgZZBweHSxc3nz MYKyOFE2OzFyMh?=
U87MG NHP5SnlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NG\admoxNTJ3IN88US=> M2jSRVI1NzR6IHi= NHPrdndqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjDkc5NmKGGwZDD0bY1mKGSncHXu[IVvfCCvYX7u[ZI> MnvONlM{PTR6MEe=
U251MG NHH1ZnFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWfrSpZ[OC1{NTFOwG0> NXvOSmRTOjRxNEigbC=> NVvnSmQxcW6qaXLpeJMh[2WubDDndo94fGhiaX6g[I9{\SCjbnSgeIlu\SCmZYDlcoRmdnRibXHucoVz NXjzTXZrOjN|NUS4NFc>
U87MG MXLBdI9xfG:|aYOgRZN{[Xl? M2HndFEhyrWP NEPZXYY1QCCq MoW2bY5lfWOnczDhdI9xfG:|aYO= NHm4PW8zOzN3NEiwOy=>
U251MG NFqwOWZCeG:ydH;zbZMhSXO|YYm= MlvnNUDDvU1? Ml64OFghcA>? NXjvS4VwcW6mdXPld{BieG:ydH;zbZM> NXfqdnJxOjN|NUS4NFc>
U251 M2Hobmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGj5VlAxNTJ3IN88[{9uVA>? NFP5d3gxNTR6IHi= NVSzc5E4cW6qaXLpeJMh[2WubDDndo94fGhiaX6g[I9{\SCjbnSgeIlu\SCmZYDlcoRmdnRibXHucoVz MkW2NlE4QDh|NEO=
U87  MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MU[wMVI2KM7:Zz;tUC=> MX:wMVQ5KGh? MmDCbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iZH;z[UBidmRidHnt[UBl\XCnbnTlcpQhdWGwbnXy MWqyNVc5QDN2Mx?=
U251 MYLBdI9xfG:|aYOgRZN{[Xl? M2n4U|I2KM7:Zz;tUC=> MYGyOE81QCCq MVfpcoR2[2W|IHHwc5B1d3OrczDheEA1QCCqIIPp[45q\mmlYX70cJk> MVOyNVc5QDN2Mx?=
U87  NF63NW1CeG:ydH;zbZMhSXO|YYm= MWGyOUDPxGdxbVy= MVmyOE81QCCq MUPpcoR2[2W|IHHwc5B1d3OrczDheEA1QCCqIIPp[45q\mmlYX70cJk> NET6c3AzOTd6OEO0Ny=>
U251 NXu2OWE4TnWwY4Tpc44hSXO|YYm= NHjkfYsxNTJ3IN88[{9uVA>? MnjoNVIhcMLi NH;lVYFqdmS3Y3XzJIF2fG:yaHHnfUBld3OnIHTldIVv\GWwdHz5 M3rPSVIyPzh6M{Sz
U87  MVHGeY5kfGmxbjDBd5NigQ>? MXKwMVI2KM7:Zz;tUC=> MU[xNkBpyqB? NUTJbVg3cW6mdXPld{BifXSxcHjh[5kh\G:|ZTDk[ZBmdmSnboTsfS=> NGTmTlUzOTd6OEO0Ny=>
U87MG MYrGeY5kfGmxbjDBd5NigQ>? NEnTVVgxNjFxMT:xNEDPxE1? MVqyOEBp M2i2O4lueGGrcoOgeIhmKGGmaHXzbY9vKG:oIHPlcIx{KHSxII\peJJwdmWldHnuJIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NVuwfHY{OTl{MkGxO|E>
LN-308 NX3YS45bTnWwY4Tpc44hSXO|YYm= M3LEWFAvOS9zL{GwJO69VQ>? NYnSOIlyOjRiaB?= NYPsRVB6cW2yYXnyd{B1cGViYXTo[ZNqd25ib3[gZ4VtdHNidH:geol1em:wZXP0bY4hcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> M4LqO|E6OjJzMUex
LN-18 NVHzW49UTnWwY4Tpc44hSXO|YYm= M{K0fVAvOS9zL{GwJO69VQ>? NEfWRW4zPCCq M{L2VIlueGGrcoOgeIhmKGGmaHXzbY9vKG:oIHPlcIx{KHSxII\peJJwdmWldHnuJIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy M1TrOFE6OjJzMUex
T98G MnHISpVv[3Srb36gRZN{[Xl? NH[x[3IxNjFxMT:xNEDPxE1? MlW3NlQhcA>? NEXR[YJqdXCjaYLzJJRp\SCjZHjld4lwdiCxZjDj[YxteyC2bzD2bZRzd26nY4TpckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MniyNVkzOjFzN{G=
LNT-229  MoX2SpVv[3Srb36gRZN{[Xl? MUiwMlEwOS9zMDFOwG0> MXWyOEBp Mly3bY1x[Wm{czD0bIUh[WSqZYPpc44hd2ZiY3XscJMhfG9idnn0do9v\WO2aX6gbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= M{njOFE6OjJzMUex
HMEC-1  M3zMSWZ2dmO2aX;uJGF{e2G7 MWOxM|UwPTBizsznM41t MV2yOEBp MXHpcoR2[2W|IHGg[I9{\SCmZYDlcoRmdnRiZHX0ZYNpdWWwdNMg MoXpNVkyOTRyMEW=
HMEC-1  NED2VnlRem:uaX\ldoF1cW:wIFHzd4F6 NH3aUmgyNzVxNUCg{txoN22u MnHzNlQwPDhxN{KgbC=> MlHTbY5pcWKrdIOgdJJwdGmoZYLheIlwdiCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NUXaZ5R2OTlzMUSwNFU>
HMEC-1  MlPXRZBweHSxc3nzJGF{e2G7 M{K2V|EwPS93MDFOwIcwdWx? NVPoNpN2OjRiaB?= MVvpcoR2[2W|IHHwc5B1d3Orcx?= NHzuWlgyQTFzNECwOS=>
G28 NFjCeYRRem:uaX\ldoF1cW:wIFHzd4F6 M4nsNlEwPS93MDFOwIcwdWx? NUHte4NqOjRxNEivO|IhcA>? NV7hUI1qcW6qaXLpeJMheHKxbHnm[ZJifGmxbjDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MWqxPVEyPDByNR?=
G44 MXzQdo9tcW[ncnH0bY9vKEG|c3H5 MXixM|UwPTBizsznM41t MlXjNlQwPDhxN{KgbC=> NYHUWIxwcW6qaXLpeJMheHKxbHnm[ZJifGmxbjDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NYnQZ5RYOTlzMUSwNFU>
G28 NUnxelZ4SXCxcITvd4l{KEG|c3H5 Mn3ENU82NzVyIN88[{9udA>? NHfzOVUzPCCq M2XMTIlv\HWlZYOgZZBweHSxc3nz NYXBeVI{OTlzMUSwNFU>
G44 NWP6WZA{SXCxcITvd4l{KEG|c3H5 NYjNN4pUOS93L{WwJO69\y:vbB?= NIrHSJUzPCCq M{nWUIlv\HWlZYOgZZBweHSxc3nz M{LJNFE6OTF2MEC1
HMEC-1  NF7Y[ZNHfW6ldHnvckBCe3OjeR?= NUSzT5JDOjBxNECvOlAh|rypL33s MnPMbY5pcWKrdIOgSmFMKGGwZDDTdoPDqA>? MoL4NVkyOTRyMEW=
G28 NIjNWWlHfW6ldHnvckBCe3OjeR?= NHnINlM2OCEQvHevcYw> MkC0N|AwPjBxMUKwJI1qdg>? MWfpcohq[mm2czDwbI9{eGixconsZZRqd25ib3[gSmFMNCCVcnOgZY5lKEGtdB?= MUexPVEyPDByNR?=

... 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 slightly soluble or 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
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