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.

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

Free Overnight Delivery on orders over $ 500
Next day delivery by 10:00 a.m. Order now.

Cited by 11 Publications

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 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  NH3odmdHfW6ldHnvckBCe3OjeR?= MmHLNU8yOC9zMEFihKnPxG1? NWLGRZMxOjRiaB?= M2nafWROW00EoB?= MnzIdoVlfWOnczDEVmUhemWyb4L0[ZIh[WO2aY\peJkhcW5iYTDjc45k\W62cnH0bY9vNWSncHXu[IVvfCCvYX7u[ZI> NEW1TWIzPjVyMEC1Oi=>
ZH-161 NUP0SZhmTnWwY4Tpc44hSXO|YYm= M3Gwe|EwOTEkgJpOwI0> MlexNlQhcA>? NGjPNJVFVVORwrC= M3fNTZJm\HWlZYOgSHJGKHKncH;yeIVzKGGldHn2bZR6 MkXoNlY2ODByNU[=
S-24 M1nXcGZ2dmO2aX;uJGF{e2G7 MW[xM|Ex6oDLzszt NVO0U3ZyOjRiaB?= NUnIPJZ2TE2VT9Mg NVHFcG11emWmdXPld{BFWkVicnXwc5J1\XJiYXP0bZZqfHl? MX:yOlUxODB3Nh?=
HaCaT  MlK4SpVv[3Srb36gRZN{[Xl? NUHTfHNsOTEkgJpOwI0> NUnES25EPDhiaB?= M3q5[GROW00EoB?= MkOydoVlfWOnczDUS2Yu|rJ{wrDtVm5CKGW6cILld5Nqd25? M3j1ZVI3PTByMEW2
LN-308  M12yRmZ2dmO2aX;uJGF{e2G7 NXvjVm5kOTEkgJpOwI0> MWWyOEBp M3PjUmROW00EoB?= MV7y[YR2[2W|IFHoVkBxem:2ZXnuJIxmfmWuczDhcoQhTFKHIILldI9zfGW{IHHjeIl3cXS7 NF2zW4kzPjVyMEC1Oi=>
REN MXPD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NVKze4pbOSCwTT2yNFAh|ryP NU[xdGFiPzJiaB?= M3i5XYRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MmW2NlQ2QTV{N{S=
MSTO-211H NEPaPZJE\WyuIG\pZYJqdGm2eTDBd5NigQ>? MYqxJI5ONTJyMDFOwG0> MlPlO|IhcA>? Mkfv[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJIEh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ NHqyN20zPDV7NUK3OC=>
MM05 NFX6eFFE\WyuIG\pZYJqdGm2eTDBd5NigQ>? MmDuNUBvVS1{MECg{txO MWe3NkBp MmLz[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJIEh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ M2rseFI1PTl3Mke0
H28 NXWzfWRoS2WubDDWbYFjcWyrdImgRZN{[Xl? MlLuNUBvVS1{MECg{txO MoHhO|IhcA>? MULk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MmexNlQ2QTV{N{S=
SCC25 MmjaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWG2MlI26oDVMkCwxsDDvU1? MnPQO|IhcA>? MmjxdoV{fWy2czDtc4RmemG2ZTyg[I9{\S2mZYDlcoRmdnRiZ4Lve5RpKGmwaHnibZRqd25? MYGyOFU2PzB3Nh?=
CAL27 NHfUS3VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHe3b5A3NjJ34pETNlAxyqEEtV2= NETXNZg4OiCq M2K1R5Jme3WudIOgcY9l\XKjdHWsJIRwe2VvZHXw[Y5l\W62IHfyc5d1cCCrbnjpZol1cW:w NHXiS2UzPDV3N{C1Oi=>
FaDu  M4DoNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NF3I[2k3NjJ34pETNlAxyqEEtV2= M1q2OVczKGh? MUTy[ZN2dHS|IH3v[IVz[XSnLDDkc5NmNWSncHXu[IVvfCCpcn;3eIghcW6qaXLpeIlwdg>? M{PZeFI1PTV5MEW2
SCC25 MkfzRZBweHSxc3nzJGF{e2G7 M4DrbVI2yqEEtV5CpC=> MX20POKhcMLi M2XrR4lv\HWlZYOgZZBweHSxc3nz MVuyOFU2PzB3Nh?=
CAL27 M1PYcGFxd3C2b4Ppd{BCe3OjeR?= NVrvXos5OjYEoNM1UeKh MV20POKhcMLi NEfHO|hqdmS3Y3XzJIFxd3C2b4Ppdy=> NYPWWYFqOjR3NUewOVY>
FaDu  NIPaZYlCeG:ydH;zbZMhSXO|YYm= M1:wWlI2yqEEtV5CpC=> MYO0POKhcMLi NILBb5ZqdmS3Y3XzJIFxd3C2b4Ppdy=> MWqyOFU2PzB3Nh?=
T-47D NVPBPYltT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFK4RoUxNTJyIN88US=> M13JTVk3KGh? MmnabY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NV6yclRpOjRzNUOxNFI>
MCF-7  M{Xw[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXGwMVIxKM7:TR?= NVK1SJFzQTZiaB?= MYTpcohq[mm2czDj[YxtKGe{b4f0bEBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MX[yOFE2OzFyMh?=
T-47D Mlr2RZBweHSxc3nzJGF{e2G7 M1X4O|AuOjBizszN NV[5TpFnPDhiaB?= M{HxWolv\HWlZYOgZZBweHSxc3nz NW\Hd3Y{OjRzNUOxNFI>
MCF-7  NXH1TnFuSXCxcITvd4l{KEG|c3H5 M37TZVAuOjBizszN MkfoOFghcA>? M4TzPYlv\HWlZYOgZZBweHSxc3nz MVSyOFE2OzFyMh?=
U87MG M1zKcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWTiXHptOC1{NTFOwG0> MnKzNlQwPDhiaB?= NYPwdWZvcW6qaXLpeJMh[2WubDDndo94fGhiaX6g[I9{\SCjbnSgeIlu\SCmZYDlcoRmdnRibXHucoVz NFL3SYMzOzN3NEiwOy=>
U251MG NIqxcYxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYmwMVI2KM7:TR?= NHXnfnQzPC92ODDo NHnv[pdqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjDkc5NmKGGwZDD0bY1mKGSncHXu[IVvfCCvYX7u[ZI> M4fmO|I{OzV2OEC3
U87MG M3mwTmFxd3C2b4Ppd{BCe3OjeR?= M4XqflEhyrWP Mm[1OFghcA>? NYr4dHVCcW6mdXPld{BieG:ydH;zbZM> NUSzUHFqOjN|NUS4NFc>
U251MG M2nlO2Fxd3C2b4Ppd{BCe3OjeR?= M4nxRVEhyrWP NH7Ld4k1QCCq NEjVcIRqdmS3Y3XzJIFxd3C2b4Ppdy=> MmDmNlM{PTR6MEe=
U251 M2XkU2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlXBNE0zPSEQvHevcWw> MmjLNE01QCCq NVPK[IVDcW6qaXLpeJMh[2WubDDndo94fGhiaX6g[I9{\SCjbnSgeIlu\SCmZYDlcoRmdnRibXHucoVz MYmyNVc5QDN2Mx?=
U87  MoPWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXGwMVI2KM7:Zz;tUC=> NID4eYExNTR6IHi= MXrpcohq[mm2czDj[YxtKGe{b4f0bEBqdiCmb4PlJIFv\CC2aX3lJIRmeGWwZHXueEBu[W6wZYK= MkTwNlE4QDh|NEO=
U251 NEfBNFVCeG:ydH;zbZMhSXO|YYm= NYjpcJpkOjVizsznM41N M1y2TVI1NzR6IHi= M3LWT4lv\HWlZYOgZZBweHSxc3nzJIF1KDR6IHigd4lodmmoaXPhcpRtgQ>? MVqyNVc5QDN2Mx?=
U87  NWnQV2g{SXCxcITvd4l{KEG|c3H5 M1H4[FI2KM7:Zz;tUC=> M4HmdFI1NzR6IHi= NI\ES|RqdmS3Y3XzJIFxd3C2b4Ppd{BifCB2ODDoJJNq\26rZnnjZY51dHl? M4riUlIyPzh6M{Sz
U251 M{fPRWZ2dmO2aX;uJGF{e2G7 MkLHNE0zPSEQvHevcWw> NIrHb44yOiCqwrC= M4GwS4lv\HWlZYOgZZV1d3CqYXf5JIRwe2ViZHXw[Y5l\W62bIm= NIPxToYzOTd6OEO0Ny=>
U87  M3S0fGZ2dmO2aX;uJGF{e2G7 M4OzVlAuOjVizsznM41N NVXJO3MxOTJiaNMg NUnsT5RycW6mdXPld{BifXSxcHjh[5kh\G:|ZTDk[ZBmdmSnboTsfS=> NVPKZWx4OjF5OEizOFM>
U87MG MU\GeY5kfGmxbjDBd5NigQ>? NWf5bZBUOC5zL{GvNVAh|ryP MWeyOEBp NEP3cGxqdXCjaYLzJJRp\SCjZHjld4lwdiCxZjDj[YxteyC2bzD2bZRzd26nY4TpckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MoOxNVkzOjFzN{G=
LN-308 NIS2Z2xHfW6ldHnvckBCe3OjeR?= NEC5XIMxNjFxMT:xNEDPxE1? Mmr1NlQhcA>? MYrpcZBicXK|IITo[UBi\Ginc3nvckBw\iClZXzsd{B1dyC4aYTyc45m[3SrbjDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= M1f3XVE6OjJzMUex
LN-18 NWHJNZZJTnWwY4Tpc44hSXO|YYm= M3P3TFAvOS9zL{GwJO69VQ>? NYnkR4NCOjRiaB?= NIfnNYRqdXCjaYLzJJRp\SCjZHjld4lwdiCxZjDj[YxteyC2bzD2bZRzd26nY4TpckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> NVLvSWtROTl{MkGxO|E>
T98G NVHEUndlTnWwY4Tpc44hSXO|YYm= MVuwMlEwOS9zMDFOwG0> NETQbYUzPCCq MX;pcZBicXK|IITo[UBi\Ginc3nvckBw\iClZXzsd{B1dyC4aYTyc45m[3SrbjDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MkXvNVkzOjFzN{G=
LNT-229  MWHGeY5kfGmxbjDBd5NigQ>? M3fiNlAvOS9zL{GwJO69VQ>? NU\Cb2V4OjRiaB?= NEewWGJqdXCjaYLzJJRp\SCjZHjld4lwdiCxZjDj[YxteyC2bzD2bZRzd26nY4TpckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> M3\YOVE6OjJzMUex
HMEC-1  MkW4SpVv[3Srb36gRZN{[Xl? M1[5OFEwPS93MDFOwIcwdWx? MVuyOEBp M2K4UYlv\HWlZYOgZUBld3OnIHTldIVv\GWwdDDk[ZRi[2ivZX70xsA> NH:0VVAyQTFzNECwOS=>
HMEC-1  MUPQdo9tcW[ncnH0bY9vKEG|c3H5 MX:xM|UwPTBizsznM41t NFezNY4zPC92OD:3NkBp MonKbY5pcWKrdIOgdJJwdGmoZYLheIlwdiCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? MYexPVEyPDByNR?=
HMEC-1  MYPBdI9xfG:|aYOgRZN{[Xl? NHXD[5EyNzVxNUCg{txoN22u NIfyXFczPCCq NV\kNHJLcW6mdXPld{BieG:ydH;zbZM> NWXQ[mlVOTlzMUSwNFU>
G28 MYrQdo9tcW[ncnH0bY9vKEG|c3H5 NWjub3pQOS93L{WwJO69\y:vbB?= NVrvOYlkOjRxNEivO|IhcA>? NGX3VJhqdmirYnn0d{Bxem:uaX\ldoF1cW:wIHnuJIEh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ NXuzPGNqOTlzMUSwNFU>
G44 M3LIeXBzd2yrZnXyZZRqd25iQYPzZZk> Mn3LNU82NzVyIN88[{9udA>? NY\ld5JyOjRxNEivO|IhcA>? MULpcohq[mm2czDwdo9tcW[ncnH0bY9vKGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz NXjXVotWOTlzMUSwNFU>
G28 NHHjVGRCeG:ydH;zbZMhSXO|YYm= NXTicVk6OS93L{WwJO69\y:vbB?= MnzwNlQhcA>? NHfnZWVqdmS3Y3XzJIFxd3C2b4Ppdy=> NIfPPYwyQTFzNECwOS=>
G44 MUnBdI9xfG:|aYOgRZN{[Xl? MnrhNU82NzVyIN88[{9udA>? MWCyOEBp NVfJWW1IcW6mdXPld{BieG:ydH;zbZM> NF7xUHkyQTFzNECwOS=>
HMEC-1  MVHGeY5kfGmxbjDBd5NigQ>? MUmyNE81OC94MDFOwIcwdWx? MUjpcohq[mm2czDGRWsh[W6mIGPyZ:Kh MVKxPVEyPDByNR?=
G28 MkjRSpVv[3Srb36gRZN{[Xl? Mn3HOVAh|rypL33s NFi4dmE{OC94MD:xNlAhdWmw NY\N[Iw4cW6qaXLpeJMheGixc4Doc5J6dGG2aX;uJI9nKE[DSzygV5JkKGGwZDDBb5Q> NFHJZmUyQTFzNECwOS=>

... 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

Bio Calculators

Molarity Calculator

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

  • Mass
    Concentration
    Volume
    Molecular Weight

*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

  • C1
    V1
    C2
    V2

* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Total Molecular Weight: g/mol

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

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
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 Darmstadt Germany January 2012 Phase 2
NCT01504165 Completed Renal Impairment Merck KGaA Darmstadt Germany January 2012 Phase 1
NCT01517776 Terminated Gliomas Martin-Luther-Universität Halle-Wittenberg|Merck KGaA Darmstadt Germany January 2012 Phase 2
NCT01504165 Completed Renal Impairment Merck KGaA Darmstadt Germany January 2012 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

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

  • * Indicates a Required Field

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

Tags: buy Cilengitide trifluoroacetate | Cilengitide trifluoroacetate supplier | purchase Cilengitide trifluoroacetate | Cilengitide trifluoroacetate cost | Cilengitide trifluoroacetate manufacturer | order Cilengitide trifluoroacetate | Cilengitide trifluoroacetate distributor
×
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID