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  NHvVRXVHfW6ldHnvckBCe3OjeR?= MoLqNU8yOC9zMEFihKnPxG1? NU\ZWXFEOjRiaB?= NFKybpVFVVORwrC= M1zWWZJm\HWlZYOgSHJGKHKncH;yeIVzKGGldHn2bZR6KGmwIHGgZ49v[2WwdILheIlwdi2mZYDlcoRmdnRibXHucoVz NXHM[mRGOjZ3MECwOVY>
ZH-161 MojrSpVv[3Srb36gRZN{[Xl? NWHHeIxQOS9zMPMAje69dQ>? Mk\qNlQhcA>? M2PBdWROW00EoB?= NHTRemFz\WS3Y3XzJGRTTSC{ZYDvdpRmeiCjY4Tpeol1gQ>? NGX1VZQzPjVyMEC1Oi=>
S-24 M3rsZWZ2dmO2aX;uJGF{e2G7 NIq4SI0yNzFy4pEJ{txu NW\xSW17OjRiaB?= M1vIPGROW00EoB?= MmfhdoVlfWOnczDEVmUhemWyb4L0[ZIh[WO2aY\peJk> NIezcJQzPjVyMEC1Oi=>
HaCaT  MVjGeY5kfGmxbjDBd5NigQ>? MUSxNQKBkc7:bR?= NEfPWZA1QCCq NIPJTFlFVVORwrC= M{\BdZJm\HWlZYOgWGdHNc7{MtMgcXJPSSCneIDy[ZN{cW:w MlTINlY2ODByNU[=
LN-308  NXXpeG5STnWwY4Tpc44hSXO|YYm= MkHoNVDjiIoQvH2= MlvCNlQhcA>? MUPEUXNQyqB? M2HxOZJm\HWlZYOgRYhTKHC{b4TlbY4hdGW4ZXzzJIFv\CCGUlWgdoVxd3K2ZYKgZYN1cX[rdIm= NH\mTZgzPjVyMEC1Oi=>
REN MXXD[YxtKF[rYXLpcIl1gSCDc4PhfS=> M3nWXVEhdk1vMkCwJO69VQ>? M3rTVFczKGh? M1HCd4Rm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NVPDc|VvOjR3OUWyO|Q>
MSTO-211H M1nrS2NmdGxiVnnhZoltcXS7IFHzd4F6 MkLpNUBvVS1{MECg{txO MVK3NkBp NFPFWpRl\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= NWKyWId2OjR3OUWyO|Q>
MM05 MnPIR4VtdCCYaXHibYxqfHliQYPzZZk> NELiW3QyKG6PLUKwNEDPxE1? M4P5b|czKGh? MXTk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? NH:3R20zPDV7NUK3OC=>
H28 NXywZXR[S2WubDDWbYFjcWyrdImgRZN{[Xl? NXnjZYY5OSCwTT2yNFAh|ryP MlXhO|IhcA>? MVnk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MlHHNlQ2QTV{N{S=
SCC25 MkXHS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWrnNZZKPi5{NfMAl|IxOMLiwsXN NWnXeIhkPzJiaB?= MYjy[ZN2dHS|IH3v[IVz[XSnLDDkc5NmNWSncHXu[IVvfCCpcn;3eIghcW6qaXLpeIlwdg>? M1rIWFI1PTV5MEW2
CAL27 MlrtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYKxOVM5Pi5{NfMAl|IxOMLiwsXN NXrnR|FoPzJiaB?= M1\vVpJme3WudIOgcY9l\XKjdHWsJIRwe2VvZHXw[Y5l\W62IHfyc5d1cCCrbnjpZol1cW:w MoXmNlQ2PTdyNU[=
FaDu  MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3r0NlYvOjYkgKOyNFDDqML3TR?= NInOZ4U4OiCq MVfy[ZN2dHS|IH3v[IVz[XSnLDDkc5NmNWSncHXu[IVvfCCpcn;3eIghcW6qaXLpeIlwdg>? MXiyOFU2PzB3Nh?=
SCC25 NXHib3MzSXCxcITvd4l{KEG|c3H5 NFLnWYUzPcLiwsXNxsA> NUizeoJJPDkEoHlCpC=> MXjpcoR2[2W|IHHwc5B1d3Orcx?= NVviZ291OjR3NUewOVY>
CAL27 NWH0Sm1qSXCxcITvd4l{KEG|c3H5 M3\3O|I2yqEEtV5CpC=> MUS0POKhcMLi Mm\EbY5lfWOnczDhdI9xfG:|aYO= MkjqNlQ2PTdyNU[=
FaDu  NVLreJF2SXCxcITvd4l{KEG|c3H5 NYX4PXJOOjYEoNM1UeKh MYC0POKhcMLi NIS0NI5qdmS3Y3XzJIFxd3C2b4Ppdy=> NWLUVFV[OjR3NUewOVY>
T-47D NXO1U4VzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX[wMVIxKM7:TR?= MVi5OkBp NGn0e5FqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? MkLhNlQyPTNzMEK=
MCF-7  MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWiwMVIxKM7:TR?= NF32PGI6PiCq M12wTIlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz NInRcZMzPDF3M{GwNi=>
T-47D NU\SPVR3SXCxcITvd4l{KEG|c3H5 MVKwMVIxKM7:TR?= M{D2eFQ5KGh? NXnPZlhYcW6mdXPld{BieG:ydH;zbZM> MmTMNlQyPTNzMEK=
MCF-7  NInvZXJCeG:ydH;zbZMhSXO|YYm= Mn7LNE0zOCEQvF2= MlOxOFghcA>? MWXpcoR2[2W|IHHwc5B1d3Orcx?= MYGyOFE2OzFyMh?=
U87MG NFT6dZpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3zQR|AuOjVizszN MmDaNlQwPDhiaB?= M{TnNYlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHTvd4Uh[W6mIITpcYUh\GWyZX7k[Y51KG2jbn7ldi=> M3HxO|I{OzV2OEC3
U251MG NXXuTJhFT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWDxWJFOOC1{NTFOwG0> MWeyOE81QCCq MoTmbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iZH;z[UBidmRidHnt[UBl\XCnbnTlcpQhdWGwbnXy M3;CW|I{OzV2OEC3
U87MG Mn7ERZBweHSxc3nzJGF{e2G7 MVyxJOK2VQ>? NYT1[FJnPDhiaB?= MWnpcoR2[2W|IHHwc5B1d3Orcx?= NUS1bGFxOjN|NUS4NFc>
U251MG Mlu5RZBweHSxc3nzJGF{e2G7 MYixJOK2VQ>? NYnY[oJjPDhiaB?= NUTScoVscW6mdXPld{BieG:ydH;zbZM> MniwNlM{PTR6MEe=
U251 NGi5bmpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHv4bFQxNTJ3IN88[{9uVA>? NYrERVYxOC12ODDo MnzjbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iZH;z[UBidmRidHnt[UBl\XCnbnTlcpQhdWGwbnXy NF72S2YzOTd6OEO0Ny=>
U87  MojXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVXkN3NwOC1{NTFOwIcwdUx? NVPReGV{OC12ODDo M2jne4lvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHTvd4Uh[W6mIITpcYUh\GWyZX7k[Y51KG2jbn7ldi=> NGPMRVYzOTd6OEO0Ny=>
U251 M2rGT2Fxd3C2b4Ppd{BCe3OjeR?= MWSyOUDPxGdxbVy= MXuyOE81QCCq MlrybY5lfWOnczDhdI9xfG:|aYOgZZQhPDhiaDDzbYdvcW[rY3HueIx6 NEHwZogzOTd6OEO0Ny=>
U87  MYrBdI9xfG:|aYOgRZN{[Xl? MUeyOUDPxGdxbVy= MlTrNlQwPDhiaB?= NVvVUnVNcW6mdXPld{BieG:ydH;zbZMh[XRiNEigbEB{cWewaX\pZ4FvfGy7 NVj5UlV[OjF5OEizOFM>
U251 MXPGeY5kfGmxbjDBd5NigQ>? NIe1UIExNTJ3IN88[{9uVA>? MW[xNkBpyqB? NWXidYM{cW6mdXPld{BifXSxcHjh[5kh\G:|ZTDk[ZBmdmSnboTsfS=> NEjOeGYzOTd6OEO0Ny=>
U87  MUfGeY5kfGmxbjDBd5NigQ>? NGHaXlQxNTJ3IN88[{9uVA>? MVOxNkBpyqB? MVnpcoR2[2W|IHH1eI9xcGGpeTDkc5NmKGSncHXu[IVvfGy7 Mnv0NlE4QDh|NEO=
U87MG NYq2cXpJTnWwY4Tpc44hSXO|YYm= NHOxd5cxNjFxMT:xNEDPxE1? NIXZVY8zPCCq MkH5bY1x[Wm{czD0bIUh[WSqZYPpc44hd2ZiY3XscJMhfG9idnn0do9v\WO2aX6gbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= M2H6cFE6OjJzMUex
LN-308 NFHwRndHfW6ldHnvckBCe3OjeR?= NV3iR3pmOC5zL{GvNVAh|ryP NHfmNXIzPCCq M4fCcIlueGGrcoOgeIhmKGGmaHXzbY9vKG:oIHPlcIx{KHSxII\peJJwdmWldHnuJIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy M1j6XlE6OjJzMUex
LN-18 MX\GeY5kfGmxbjDBd5NigQ>? M1nRUFAvOS9zL{GwJO69VQ>? NXvzWZZzOjRiaB?= NYqw[XFGcW2yYXnyd{B1cGViYXTo[ZNqd25ib3[gZ4VtdHNidH:geol1em:wZXP0bY4hcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> MkD0NVkzOjFzN{G=
T98G MoP0SpVv[3Srb36gRZN{[Xl? NWDPUFBrOC5zL{GvNVAh|ryP NHn1fYUzPCCq NV;rU2ZxcW2yYXnyd{B1cGViYXTo[ZNqd25ib3[gZ4VtdHNidH:geol1em:wZXP0bY4hcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> MlLUNVkzOjFzN{G=
LNT-229  M17TeGZ2dmO2aX;uJGF{e2G7 MYCwMlEwOS9zMDFOwG0> M1iyO|I1KGh? NITRRlJqdXCjaYLzJJRp\SCjZHjld4lwdiCxZjDj[YxteyC2bzD2bZRzd26nY4TpckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> M1rNe|E6OjJzMUex
HMEC-1  MXTGeY5kfGmxbjDBd5NigQ>? NILU[3oyNzVxNUCg{txoN22u MVOyOEBp M3fGcIlv\HWlZYOgZUBld3OnIHTldIVv\GWwdDDk[ZRi[2ivZX70xsA> NIrSeVUyQTFzNECwOS=>
HMEC-1  MnuxVJJwdGmoZYLheIlwdiCDc4PhfS=> NXy2bJFQOS93L{WwJO69\y:vbB?= MVGyOE81QC95MjDo Ml3hbY5pcWKrdIOgdJJwdGmoZYLheIlwdiCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? MoPDNVkyOTRyMEW=
HMEC-1  NU\v[XBWSXCxcITvd4l{KEG|c3H5 M1exUlEwPS93MDFOwIcwdWx? NIrPe3AzPCCq M2q1bolv\HWlZYOgZZBweHSxc3nz NHL5[4IyQTFzNECwOS=>
G28 NUHRcFkxWHKxbHnm[ZJifGmxbjDBd5NigQ>? NFzuPWQyNzVxNUCg{txoN22u NUnLOollOjRxNEivO|IhcA>? Mn;ubY5pcWKrdIOgdJJwdGmoZYLheIlwdiCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NXW5T48{OTlzMUSwNFU>
G44 NFi4NpRRem:uaX\ldoF1cW:wIFHzd4F6 M{jvPFEwPS93MDFOwIcwdWx? M1n1V|I1NzR6L{eyJIg> MniybY5pcWKrdIOgdJJwdGmoZYLheIlwdiCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? MYOxPVEyPDByNR?=
G28 NFW1coxCeG:ydH;zbZMhSXO|YYm= MnzYNU82NzVyIN88[{9udA>? NVH1TW1kOjRiaB?= NIWxc5dqdmS3Y3XzJIFxd3C2b4Ppdy=> M2r1elE6OTF2MEC1
G44 M1f2dWFxd3C2b4Ppd{BCe3OjeR?= MWGxM|UwPTBizsznM41t NEfLOYIzPCCq NY\hU21[cW6mdXPld{BieG:ydH;zbZM> MVexPVEyPDByNR?=
HMEC-1  NIHSbGZHfW6ldHnvckBCe3OjeR?= MX:yNE81OC94MDFOwIcwdWx? MYDpcohq[mm2czDGRWsh[W6mIGPyZ:Kh M1\tUVE6OTF2MEC1
G28 NYPtSYJPTnWwY4Tpc44hSXO|YYm= NFe2UI42OCEQvHevcYw> NUTtWnduOzBxNkCvNVIxKG2rbh?= M{S5UolvcGmkaYTzJJBpd3OyaH;yfYxifGmxbjDv[kBHSUtuIGPyZ{BidmRiQXv0 MVOxPVEyPDByNR?=

... 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 to the product individually and in order(Data is from Selleck tests instead of citations):
30% propylene glycol, 5% Tween 80, 65% D5W
For best results, use promptly after mixing.
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
NCT01118676 Completed Locally Advanced Non Small Cell Lung Cancer (NSCLC)* Institut Claudius Regaud|Merck KGaA 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