Cilengitide trifluoroacetate

For research use only.

Catalog No.S7077 Synonyms: EMD 121974, NSC 707544

28 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 28 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  MXLGeY5kfGmxbjDBd5NigQ>? NVztTlI4OS9zMD:xNFDjiIoQvH2= Mnj4NlQhcA>? NIPrNnZFVVORwrC= MYPy[YR2[2W|IFTSSUBz\XCxcoTldkBi[3Srdnn0fUBqdiCjIHPvcoNmdnS{YYTpc44u\GWyZX7k[Y51KG2jbn7ldi=> NI\qfXkzPjVyMEC1Oi=>
ZH-161 Mn3tSpVv[3Srb36gRZN{[Xl? MX:xM|Ex6oDLzszt MUmyOEBp NWLNXmVFTE2VT9Mg NH75ZZZz\WS3Y3XzJGRTTSC{ZYDvdpRmeiCjY4Tpeol1gQ>? MVSyOlUxODB3Nh?=
S-24 NXzCUYR5TnWwY4Tpc44hSXO|YYm= NH76dWUyNzFy4pEJ{txu MV2yOEBp NXnnfYwzTE2VT9Mg NEHCcFdz\WS3Y3XzJGRTTSC{ZYDvdpRmeiCjY4Tpeol1gQ>? M1;QdFI3PTByMEW2
HaCaT  M37FRmZ2dmO2aX;uJGF{e2G7 NVnxVXVtOTEkgJpOwI0> NITBN401QCCq MVHEUXNQyqB? MkX1doVlfWOnczDUS2Yu|rJ{wrDtVm5CKGW6cILld5Nqd25? MXyyOlUxODB3Nh?=
LN-308  MVTGeY5kfGmxbjDBd5NigQ>? MnHLNVDjiIoQvH2= NX3ySG5LOjRiaB?= M3nYUWROW00EoB?= M1HxSJJm\HWlZYOgRYhTKHC{b4TlbY4hdGW4ZXzzJIFv\CCGUlWgdoVxd3K2ZYKgZYN1cX[rdIm= Mn:yNlY2ODByNU[=
REN MUHD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MnyzNUBvVS1{MECg{txO NH3lcoY4OiCq NEnHdY5l\WO{ZXHz[ZMh[2WubDD2bYFjcWyrdImgbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= M4PpOFI1PTl3Mke0
MSTO-211H MnLER4VtdCCYaXHibYxqfHliQYPzZZk> MUWxJI5ONTJyMDFOwG0> NUXlR2QyPzJiaB?= MUXk[YNz\WG|ZYOgZ4VtdCC4aXHibYxqfHliaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? NU\sfpB[OjR3OUWyO|Q>
MM05 NGLYbJRE\WyuIG\pZYJqdGm2eTDBd5NigQ>? MVGxJI5ONTJyMDFOwG0> NWDhNmhVPzJiaB?= MkK5[IVkemWjc3XzJINmdGxidnnhZoltcXS7IHnuJIEh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ MlHJNlQ2QTV{N{S=
H28 MUXD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NH\sO|YyKG6PLUKwNEDPxE1? M3;3TlczKGh? M{fLcIRm[3KnYYPld{Bk\WyuII\pZYJqdGm2eTDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NIm4PFgzPDV7NUK3OC=>
SCC25 NWjxeVZwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXHBTY53Pi5{NfMAl|IxOMLiwsXN M1fUfVczKGh? M37Yc5Jme3WudIOgcY9l\XKjdHWsJIRwe2VvZHXw[Y5l\W62IHfyc5d1cCCrbnjpZol1cW:w M1;jOVI1PTV5MEW2
CAL27 M4mzVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIPQdpc3NjJ34pETNlAxyqEEtV2= MXu3NkBp M1zPXpJme3WudIOgcY9l\XKjdHWsJIRwe2VvZHXw[Y5l\W62IHfyc5d1cCCrbnjpZol1cW:w M4PHZlI1PTV5MEW2
FaDu  NFvQSXFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUX2NXVIPi5{NfMAl|IxOMLiwsXN MkG0O|IhcA>? MnrFdoV{fWy2czDtc4RmemG2ZTyg[I9{\S2mZYDlcoRmdnRiZ4Lve5RpKGmwaHnibZRqd25? MVuyOFU2PzB3Nh?=
SCC25 NHfpUnRCeG:ydH;zbZMhSXO|YYm= M2nOZ|I2yqEEtV5CpC=> M3\2VFQ5yqCqwrC= Mn:0bY5lfWOnczDhdI9xfG:|aYO= NH;EZpUzPDV3N{C1Oi=>
CAL27 MVfBdI9xfG:|aYOgRZN{[Xl? MoKwNlXDqML3TdMg NE\MbYc1QMLiaNMg NHPjbJVqdmS3Y3XzJIFxd3C2b4Ppdy=> NVTSWHd5OjR3NUewOVY>
FaDu  NVfHU5k2SXCxcITvd4l{KEG|c3H5 MlTxNlXDqML3TdMg NED1bZE1QMLiaNMg NH\2dI1qdmS3Y3XzJIFxd3C2b4Ppdy=> NVi4RndROjR3NUewOVY>
T-47D NEHSd|hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVGwMVIxKM7:TR?= MkHJPVYhcA>? NILIVnVqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjDhJIRwe2ViZHXw[Y5l\W62IH3hco5meg>? MV6yOFE2OzFyMh?=
MCF-7  M2\Zfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MV:wMVIxKM7:TR?= Mn\ZPVYhcA>? Mn3pbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NU\4foU1OjRzNUOxNFI>
T-47D NVvEU5ZxSXCxcITvd4l{KEG|c3H5 NVWwOVlUOC1{MDFOwG0> NXe0S2F2PDhiaB?= MXXpcoR2[2W|IHHwc5B1d3Orcx?= MnPiNlQyPTNzMEK=
MCF-7  NHT2RohCeG:ydH;zbZMhSXO|YYm= NX3jSJJHOC1{MDFOwG0> MUe0PEBp NWrMdFZTcW6mdXPld{BieG:ydH;zbZM> NI[zUZAzPDF3M{GwNi=>
U87MG NFLUTYRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF[0ZZoxNTJ3IN88US=> M2LOeFI1NzR6IHi= M3LBUYlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHTvd4Uh[W6mIITpcYUh\GWyZX7k[Y51KG2jbn7ldi=> NYHBR4k{OjN|NUS4NFc>
U251MG Mnj1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXqwMVI2KM7:TR?= M1z2SlI1NzR6IHi= MmPZbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iZH;z[UBidmRidHnt[UBl\XCnbnTlcpQhdWGwbnXy MUGyN|M2PDhyNx?=
U87MG M1LhSWFxd3C2b4Ppd{BCe3OjeR?= MnzpNUDDvU1? Mnq4OFghcA>? NVHFd4hDcW6mdXPld{BieG:ydH;zbZM> NXvMS2JQOjN|NUS4NFc>
U251MG NGrwOFNCeG:ydH;zbZMhSXO|YYm= NEDZWXgyKML3TR?= NF3xSXc1QCCq M3uyTolv\HWlZYOgZZBweHSxc3nz NIS5Z48zOzN3NEiwOy=>
U251 M17F[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYqwMVI2KM7:Zz;tUC=> MXywMVQ5KGh? NUPjT2N3cW6qaXLpeJMh[2WubDDndo94fGhiaX6g[I9{\SCjbnSgeIlu\SCmZYDlcoRmdnRibXHucoVz MoDpNlE4QDh|NEO=
U87  M1\HOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXSwMVI2KM7:Zz;tUC=> NI\DfFUxNTR6IHi= MXXpcohq[mm2czDj[YxtKGe{b4f0bEBqdiCmb4PlJIFv\CC2aX3lJIRmeGWwZHXueEBu[W6wZYK= MVSyNVc5QDN2Mx?=
U251 MlGxRZBweHSxc3nzJGF{e2G7 MUOyOUDPxGdxbVy= MlzWNlQwPDhiaB?= NFr4TWxqdmS3Y3XzJIFxd3C2b4Ppd{BifCB2ODDoJJNq\26rZnnjZY51dHl? NEPKV3AzOTd6OEO0Ny=>
U87  NYizV5FsSXCxcITvd4l{KEG|c3H5 NUHjS4sxOjVizsznM41N NIjKNI0zPC92ODDo M1PKOYlv\HWlZYOgZZBweHSxc3nzJIF1KDR6IHigd4lodmmoaXPhcpRtgQ>? NYTQd|FpOjF5OEizOFM>
U251 M4nvSWZ2dmO2aX;uJGF{e2G7 NVX0VVlWOC1{NTFOwIcwdUx? MUixNkBpyqB? MVTpcoR2[2W|IHH1eI9xcGGpeTDkc5NmKGSncHXu[IVvfGy7 NFTMd4wzOTd6OEO0Ny=>
U87  M336U2Z2dmO2aX;uJGF{e2G7 M3uyZ|AuOjVizsznM41N MoSxNVIhcMLi NWLFVnBscW6mdXPld{BifXSxcHjh[5kh\G:|ZTDk[ZBmdmSnboTsfS=> NVW3O5JxOjF5OEizOFM>
U87MG NG\NZYFHfW6ldHnvckBCe3OjeR?= MXqwMlEwOS9zMDFOwG0> MlPBNlQhcA>? M37ONYlueGGrcoOgeIhmKGGmaHXzbY9vKG:oIHPlcIx{KHSxII\peJJwdmWldHnuJIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy MorKNVkzOjFzN{G=
LN-308 MorUSpVv[3Srb36gRZN{[Xl? NHe1U20xNjFxMT:xNEDPxE1? NWjNO4szOjRiaB?= MYnpcZBicXK|IITo[UBi\Ginc3nvckBw\iClZXzsd{B1dyC4aYTyc45m[3SrbjDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MmPCNVkzOjFzN{G=
LN-18 NVzDd3FUTnWwY4Tpc44hSXO|YYm= Mm\2NE4yNzFxMUCg{txO MmHONlQhcA>? MWrpcZBicXK|IITo[UBi\Ginc3nvckBw\iClZXzsd{B1dyC4aYTyc45m[3SrbjDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= MnjoNVkzOjFzN{G=
T98G MYTGeY5kfGmxbjDBd5NigQ>? NGnCSmgxNjFxMT:xNEDPxE1? MVuyOEBp MULpcZBicXK|IITo[UBi\Ginc3nvckBw\iClZXzsd{B1dyC4aYTyc45m[3SrbjDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= Ml\4NVkzOjFzN{G=
LNT-229  MoPiSpVv[3Srb36gRZN{[Xl? NV\FXVlDOC5zL{GvNVAh|ryP MVKyOEBp M2ThNYlueGGrcoOgeIhmKGGmaHXzbY9vKG:oIHPlcIx{KHSxII\peJJwdmWldHnuJIlvKGFiZH;z[UBl\XCnbnTlcpQhdWGwbnXy NXfYR2k2OTl{MkGxO|E>
HMEC-1  MnHLSpVv[3Srb36gRZN{[Xl? NYXJPHBlOS93L{WwJO69\y:vbB?= M3;KUFI1KGh? M3KzWYlv\HWlZYOgZUBld3OnIHTldIVv\GWwdDDk[ZRi[2ivZX70xsA> NIrNTGEyQTFzNECwOS=>
HMEC-1  NGq2XFlRem:uaX\ldoF1cW:wIFHzd4F6 NXPIXpd{OS93L{WwJO69\y:vbB?= MVyyOE81QC95MjDo NWTpdHREcW6qaXLpeJMheHKxbHnm[ZJifGmxbjDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= M3rLcVE6OTF2MEC1
HMEC-1  NWPTbXl7SXCxcITvd4l{KEG|c3H5 MmrSNU82NzVyIN88[{9udA>? Mm\KNlQhcA>? NFrFNppqdmS3Y3XzJIFxd3C2b4Ppdy=> Mor0NVkyOTRyMEW=
G28 NXHSOFdDWHKxbHnm[ZJifGmxbjDBd5NigQ>? NITQ[5cyNzVxNUCg{txoN22u M1qwd|I1NzR6L{eyJIg> MUfpcohq[mm2czDwdo9tcW[ncnH0bY9vKGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz MUCxPVEyPDByNR?=
G44 NHvmeHVRem:uaX\ldoF1cW:wIFHzd4F6 MlrTNU82NzVyIN88[{9udA>? NF65[ZczPC92OD:3NkBp MX\pcohq[mm2czDwdo9tcW[ncnH0bY9vKGmwIHGg[I9{\SCmZYDlcoRmdnRibXHucoVz MXyxPVEyPDByNR?=
G28 NYL1[ndHSXCxcITvd4l{KEG|c3H5 MWexM|UwPTBizsznM41t MnzjNlQhcA>? MWHpcoR2[2W|IHHwc5B1d3Orcx?= NEjhS2YyQTFzNECwOS=>
G44 MkXuRZBweHSxc3nzJGF{e2G7 NH;ZXlQyNzVxNUCg{txoN22u M13GcFI1KGh? M4jxZ4lv\HWlZYOgZZBweHSxc3nz MYWxPVEyPDByNR?=
HMEC-1  MULGeY5kfGmxbjDBd5NigQ>? NW\icXdoOjBxNECvOlAh|rypL33s MoPsbY5pcWKrdIOgSmFMKGGwZDDTdoPDqA>? NFm3Um4yQTFzNECwOS=>
G28 NWTFb3NGTnWwY4Tpc44hSXO|YYm= MUO1NEDPxGdxbXy= MYKzNE83OC9zMkCgcYlv NXzTUnpxcW6qaXLpeJMheGixc4Doc5J6dGG2aX;uJI9nKE[DSzygV5JkKGGwZDDBb5Q> NVvUV|M{OTlzMUSwNFU>

... 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
  • 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

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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