Cilengitide trifluoroacetate

For research use only. Not for use in humans.

Catalog No.S7077 Synonyms: EMD 121974, NSC 707544

22 publications

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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Selleck's Cilengitide trifluoroacetate has been cited by 22 publications

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  NVSxZ4VMTnWwY4Tpc44hSXO|YYm= NXqxfZhMOS9zMD:xNFDjiIoQvH2= MWCyOEBp NH7nNVVFVVORwrC= MkfMdoVlfWOnczDEVmUhemWyb4L0[ZIh[WO2aY\peJkhcW5iYTDjc45k\W62cnH0bY9vNWSncHXu[IVvfCCvYX7u[ZI> MVeyOlUxODB3Nh?=
ZH-161 MmPGSpVv[3Srb36gRZN{[Xl? MX2xM|Ex6oDLzszt NEPoPJAzPCCq NIfTSoJFVVORwrC= M3nNSpJm\HWlZYOgSHJGKHKncH;yeIVzKGGldHn2bZR6 NVHuTGp7OjZ3MECwOVY>
S-24 M4TxbGZ2dmO2aX;uJGF{e2G7 M4SwU|EwOTEkgJpOwI0> NFr6ZVAzPCCq MmjPSG1UV8Li NGrRZYdz\WS3Y3XzJGRTTSC{ZYDvdpRmeiCjY4Tpeol1gQ>? M1LFTlI3PTByMEW2
HaCaT  MXzGeY5kfGmxbjDBd5NigQ>? MoWzNVDjiIoQvH2= MoDNOFghcA>? MWfEUXNQyqB? NF3QVnRz\WS3Y3XzJHRITi4QskNCpI1TVkFiZYjwdoV{e2mxbh?= Mn71NlY2ODByNU[=
LN-308  MXHGeY5kfGmxbjDBd5NigQ>? M2f6bFEx6oDLzszt M4fFflI1KGh? M2L4TmROW00EoB?= MUDy[YR2[2W|IFHoVkBxem:2ZXnuJIxmfmWuczDhcoQhTFKHIILldI9zfGW{IHHjeIl3cXS7 MXGyOlUxODB3Nh?=
REN MV7D[YxtKF[rYXLpcIl1gSCDc4PhfS=> M3PRWVEhdk1vMkCwJO69VQ>? MmHHO|IhcA>? M3vuSIRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NF[wVYYzPDV7NUK3OC=>
MSTO-211H MXLD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MWexJI5ONTJyMDFOwG0> NUL4epZJPzJiaB?= M{XIbIRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NUWzfmZNOjR3OUWyO|Q>
MM05 MXXD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MY[xJI5ONTJyMDFOwG0> NGrtdIc4OiCq NU\FfVl2\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NYnWcGExOjR3OUWyO|Q>
H28 NXnMZXZVS2WubDDWbYFjcWyrdImgRZN{[Xl? NV\xbZRiOSCwTT2yNFAh|ryP MVO3NkBp NVLybpRJ\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5JIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy M4rNOVI1PTl3Mke0
SCC25 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3vJS|YvOjYkgKOyNFDDqML3TR?= Mlu0O|IhcA>? NYe5SVlmemW|dXz0d{Bud2SncnH0[Uwh\G:|ZT3k[ZBmdmSnboSg[5Jwf3SqIHnubIljcXSrb36= M1vXb|I1PTV5MEW2
CAL27 NWnYSHdtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3;pVFYvOjYkgKOyNFDDqML3TR?= MW[3NkBp MoG0doV{fWy2czDtc4RmemG2ZTyg[I9{\S2mZYDlcoRmdnRiZ4Lve5RpKGmwaHnibZRqd25? M3HTTFI1PTV5MEW2
FaDu  MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHLqb2c3NjJ34pETNlAxyqEEtV2= MoP2O|IhcA>? NFTqbmtz\XO3bITzJI1w\GW{YYTlMEBld3OnLXTldIVv\GWwdDDndo94fGhiaX7obYJqfGmxbh?= M33WWVI1PTV5MEW2
SCC25 M1TNUGFxd3C2b4Ppd{BCe3OjeR?= NHHUU3UzPcLiwsXNxsA> M{KxcFQ5yqCqwrC= MlzxbY5lfWOnczDhdI9xfG:|aYO= M{LYSlI1PTV5MEW2
CAL27 MVTBdI9xfG:|aYOgRZN{[Xl? MXSyOeKhyrWPwrC= NFXuT4g1QMLiaNMg NHPkc2pqdmS3Y3XzJIFxd3C2b4Ppdy=> Ml32NlQ2PTdyNU[=
FaDu  NEflOmlCeG:ydH;zbZMhSXO|YYm= NETkPZozPcLiwsXNxsA> M{nV[FQ5yqCqwrC= M3rFN4lv\HWlZYOgZZBweHSxc3nz M3n6d|I1PTV5MEW2
T-47D NEfBdJhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{DWTlAuOjBizszN MXO5OkBp MYLpcohq[mm2czDj[YxtKGe{b4f0bEBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MoDLNlQyPTNzMEK=
MCF-7  NHHhNHFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NU[wTZk3OC1{MDFOwG0> M2\QTlk3KGh? M37SOYlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz M{PqR|I1OTV|MUCy
T-47D NI\SdpFCeG:ydH;zbZMhSXO|YYm= NYfuXFB[OC1{MDFOwG0> MnvwOFghcA>? NXvTb2ttcW6mdXPld{BieG:ydH;zbZM> NHjQfXczPDF3M{GwNi=>
MCF-7  MYTBdI9xfG:|aYOgRZN{[Xl? M{XwW|AuOjBizszN M1\RUVQ5KGh? NHrq[4FqdmS3Y3XzJIFxd3C2b4Ppdy=> NEXsNoozPDF3M{GwNi=>
U87MG NY[x[VNJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVvz[pV1OC1{NTFOwG0> MUSyOE81QCCq M3rMdolvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHTvd4Uh[W6mIITpcYUh\GWyZX7k[Y51KG2jbn7ldi=> NE\tW2wzOzN3NEiwOy=>
U251MG M37GSWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFTmd5gxNTJ3IN88US=> NUPjVnMxOjRxNEigbC=> NUHUZo5zcW6qaXLpeJMh[2WubDDndo94fGhiaX6g[I9{\SCjbnSgeIlu\SCmZYDlcoRmdnRibXHucoVz MmmzNlM{PTR6MEe=
U87MG NVP1PZU2SXCxcITvd4l{KEG|c3H5 NVjWT3RROSEEtV2= M1z3S|Q5KGh? M{nOfIlv\HWlZYOgZZBweHSxc3nz NHnHfpYzOzN3NEiwOy=>
U251MG NHX4WpZCeG:ydH;zbZMhSXO|YYm= M4PzbFEhyrWP NVvvUHJiPDhiaB?= NFPLNHpqdmS3Y3XzJIFxd3C2b4Ppdy=> M1n4XVI{OzV2OEC3
U251 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFz5UZIxNTJ3IN88[{9uVA>? MnfuNE01QCCq NUXwOGR2cW6qaXLpeJMh[2WubDDndo94fGhiaX6g[I9{\SCjbnSgeIlu\SCmZYDlcoRmdnRibXHucoVz MXuyNVc5QDN2Mx?=
U87  M3nsbWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH7R[WsxNTJ3IN88[{9uVA>? Mme4NE01QCCq MoHPbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iZH;z[UBidmRidHnt[UBl\XCnbnTlcpQhdWGwbnXy M4HTOlIyPzh6M{Sz
U251 MVzBdI9xfG:|aYOgRZN{[Xl? Mo\LNlUh|rypL33M MoPjNlQwPDhiaB?= Mn;ybY5lfWOnczDhdI9xfG:|aYOgZZQhPDhiaDDzbYdvcW[rY3HueIx6 NGHBVFczOTd6OEO0Ny=>
U87  M3XFe2Fxd3C2b4Ppd{BCe3OjeR?= M1PXNlI2KM7:Zz;tUC=> Ml3PNlQwPDhiaB?= MU\pcoR2[2W|IHHwc5B1d3OrczDheEA1QCCqIIPp[45q\mmlYX70cJk> M{LNbFIyPzh6M{Sz
U251 M{XCWGZ2dmO2aX;uJGF{e2G7 Ml6xNE0zPSEQvHevcWw> MoLXNVIhcMLi M1;LXolv\HWlZYOgZZV1d3CqYXf5JIRwe2ViZHXw[Y5l\W62bIm= NF62WmkzOTd6OEO0Ny=>
U87  M13V[2Z2dmO2aX;uJGF{e2G7 NHjs[44xNTJ3IN88[{9uVA>? M3r3b|EzKGkEoB?= NF[4WYtqdmS3Y3XzJIF2fG:yaHHnfUBld3OnIHTldIVv\GWwdHz5 MnvMNlE4QDh|NEO=
U87MG M2rVT2Z2dmO2aX;uJGF{e2G7 NIXldIMxNjFxMT:xNEDPxE1? MUWyOEBp NWDMWnk{cW2yYXnyd{B1cGViYXTo[ZNqd25ib3[gZ4VtdHNidH:geol1em:wZXP0bY4hcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NFfhT5UyQTJ{MUG3NS=>
LN-308 MnzLSpVv[3Srb36gRZN{[Xl? M4jPOlAvOS9zL{GwJO69VQ>? Mk\XNlQhcA>? MXnpcZBicXK|IITo[UBi\Ginc3nvckBw\iClZXzsd{B1dyC4aYTyc45m[3SrbjDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= M3SwWVE6OjJzMUex
LN-18 Mm\ESpVv[3Srb36gRZN{[Xl? NUXoXm1UOC5zL{GvNVAh|ryP MWiyOEBp NGTIO4lqdXCjaYLzJJRp\SCjZHjld4lwdiCxZjDj[YxteyC2bzD2bZRzd26nY4TpckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> NEnGNIsyQTJ{MUG3NS=>
T98G MVjGeY5kfGmxbjDBd5NigQ>? MmflNE4yNzFxMUCg{txO NX7kUlJHOjRiaB?= NFfldoVqdXCjaYLzJJRp\SCjZHjld4lwdiCxZjDj[YxteyC2bzD2bZRzd26nY4TpckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> MVKxPVIzOTF5MR?=
LNT-229  M2\vN2Z2dmO2aX;uJGF{e2G7 NVLvR2VVOC5zL{GvNVAh|ryP M4XnN|I1KGh? MlW4bY1x[Wm{czD0bIUh[WSqZYPpc44hd2ZiY3XscJMhfG9idnn0do9v\WO2aX6gbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= NIOzPYEyQTJ{MUG3NS=>
HMEC-1  NIrUZ4ZHfW6ldHnvckBCe3OjeR?= NWHFRoIxOS93L{WwJO69\y:vbB?= M4e5eFI1KGh? NFzNPG1qdmS3Y3XzJIEh\G:|ZTDk[ZBmdmSnboSg[IV1[WOqbXXueOKh NWriNJpSOTlzMUSwNFU>
HMEC-1  NV21bWxLWHKxbHnm[ZJifGmxbjDBd5NigQ>? NVn4XJNbOS93L{WwJO69\y:vbB?= M2nwc|I1NzR6L{eyJIg> MmPhbY5pcWKrdIOgdJJwdGmoZYLheIlwdiCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NWC1Ro93OTlzMUSwNFU>
HMEC-1  NXXidnBXSXCxcITvd4l{KEG|c3H5 MUCxM|UwPTBizsznM41t NETGWYEzPCCq MoDDbY5lfWOnczDhdI9xfG:|aYO= NIfsRWIyQTFzNECwOS=>
G28 MV7Qdo9tcW[ncnH0bY9vKEG|c3H5 NFrhdpQyNzVxNUCg{txoN22u MXuyOE81QC95MjDo NVTUWWNycW6qaXLpeJMheHKxbHnm[ZJifGmxbjDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MYSxPVEyPDByNR?=
G44 M1foR3Bzd2yrZnXyZZRqd25iQYPzZZk> NXq2OZdsOS93L{WwJO69\y:vbB?= MYCyOE81QC95MjDo MoiybY5pcWKrdIOgdJJwdGmoZYLheIlwdiCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? NVvIOpYxOTlzMUSwNFU>
G28 NF;xd2lCeG:ydH;zbZMhSXO|YYm= M1HjN|EwPS93MDFOwIcwdWx? NUjE[mFlOjRiaB?= MnfJbY5lfWOnczDhdI9xfG:|aYO= MljKNVkyOTRyMEW=
G44 M3Tye2Fxd3C2b4Ppd{BCe3OjeR?= MXOxM|UwPTBizsznM41t MVGyOEBp NYfVVVNGcW6mdXPld{BieG:ydH;zbZM> NGD0XHUyQTFzNECwOS=>
HMEC-1  MXPGeY5kfGmxbjDBd5NigQ>? MWKyNE81OC94MDFOwIcwdWx? NYrGTJFGcW6qaXLpeJMhTkGNIHHu[EBUemQEoB?= M{D1OFE6OTF2MEC1
G28 NWGyfoFSTnWwY4Tpc44hSXO|YYm= NHXrdZg2OCEQvHevcYw> MknXN|AwPjBxMUKwJI1qdg>? MorubY5pcWKrdIOgdIhwe3Cqb4L5cIF1cW:wIH;mJGZCUyxiU4LjJIFv\CCDa4S= NHP5cIkyQTFzNECwOS=>

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
pFAK / p-AKT ; 

PubMed: 19114005     


G28 cells were treated with 50 μg/ml cilengitide for 30, 60 and 120 minutes at 37°C. Cell lysates containing similar amounts of protein were separated by SDS-PAGE, transferred to a nitrocellulose membrane and probed with specific antibodies for detection of β-actin and phosphorylated FAK and Akt.

GLI1; 

PubMed: 31366904     


Western blottingting showing downregulated GLI1 with Integrin αvβ3 inhibitor Cilengitide and upregulated GLI1 with co-stimulator ligand RGD compared to the blank control in SGC7901 MCAs and BGC823 MCAs. 

19114005 31366904
Immunofluorescence
VE-cadherin / β3 integrin ; 

PubMed: 19212436     


Confluent HUVEC plated on fibronectin or collagen I were exposed to cilengitide (10 µM each) for the indicated time and double stained for VE-cadherin and β3 integrin. Cilengitide disrupted VE-cadherin staining and promoted appearance of β3 at VE-cadherin-depleted cell-cell borders. Higher magnification of HUVEC cultures demonstrate rare co-localization of VE-cadherin and β3 integrin at cellular junctions upon cilengitide stimulation (arrowheads). Bars: 10 µm.

19212436
Growth inhibition assay
Cell number ; 

PubMed: 24153102     


Cell detachment following 1 hr Cilengitide treatment. Cells were treated with cilengitide for 1 hr, washed with PBS, and remaining attached cells were trypsinized and counted. A) T-47D cells showed a strong dose response, with almost complete cell detachment at 20 uM cilengitide treatment. B) MCF-7 cells showed moderate cell detachment similar to C) MDA-MB-231 cells. D) MDA-MB-468 cells showed little to no cell detachment following this short exposure to cilengitide. Figures show Mean ± SEM and represent the average of three experiments. * = ≤ 0.05.

24153102
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]
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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]
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  • 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]
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  • 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

* 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
Smiles CC(C)C1N(C)C(=O)C(CC2=CC=CC=C2)NC(=O)C(CC(O)=O)NC(=O)CNC(=O)C(CCCNC(N)=N)NC1=O.OC(=O)C(F)(F)F

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT01517776 Terminated Drug: Cilengitide|Drug: Temozolomide Gliomas Martin-Luther-Universität Halle-Wittenberg|Merck KGaA Darmstadt Germany January 2012 Phase 2
NCT01118676 Completed Drug: cilengitide radiochemotherapy Locally Advanced Non Small Cell Lung Cancer (NSCLC)* Institut Claudius Regaud|Merck KGaA Darmstadt Germany 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

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

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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