Cilengitide trifluoroacetate

For research use only.

Catalog No.S7077 Synonyms: EMD 121974, NSC 707544

45 publications

Cilengitide trifluoroacetate Chemical Structure

CAS No. 199807-35-7

Cilengitide (EMD 121974, NSC 707544) 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 45 publications

Purity & Quality Control

Choose Selective Integrin Inhibitors

Biological Activity

Description Cilengitide (EMD 121974, NSC 707544) 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
G28 MmLOSpVv[3Srb36gRZN{[Xl? MWG1NEDPxGdxbXy= MU[zNE83OC9zMkCgcYlv MXHpcohq[mm2czDwbI9{eGixconsZZRqd25ib3[gSmFMNCCVcnOgZY5lKEGtdB?= NYrVdmlnRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMUmxNVQxODVpPkG5NVE1ODB3PD;hQi=>
HMEC-1  NG\sNFNHfW6ldHnvckBCe3OjeR?= MmLQNlAwPDBxNkCg{txoN22u NXXlNGhEcW6qaXLpeJMhTkGNIHHu[EBUemQEoB?= M{PCOFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzF7MUG0NFA2Lz5zOUGxOFAxPTxxYU6=
G44 NV65NmdmSXCxcITvd4l{KEG|c3H5 MYKxM|UwPTBizsznM41t Ml\QNlQhcA>? MUDpcoR2[2W|IHHwc5B1d3Orcx?= NXWzeGlXRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMUmxNVQxODVpPkG5NVE1ODB3PD;hQi=>
G28 MnXjRZBweHSxc3nzJGF{e2G7 M4LzeVEwPS93MDFOwIcwdWx? MXWyOEBp MmfBbY5lfWOnczDhdI9xfG:|aYO= M{P0OFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzF7MUG0NFA2Lz5zOUGxOFAxPTxxYU6=
G44 MlL6VJJwdGmoZYLheIlwdiCDc4PhfS=> NFnjTVEyNzVxNUCg{txoN22u MX:yOE81QC95MjDo NHrhbpVqdmirYnn0d{Bxem:uaX\ldoF1cW:wIHnuJIEh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ NVvmfmlxRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMUmxNVQxODVpPkG5NVE1ODB3PD;hQi=>
G28 M3m0XHBzd2yrZnXyZZRqd25iQYPzZZk> M2W5S|EwPS93MDFOwIcwdWx? MlTkNlQwPDhxN{KgbC=> NFn2OY5qdmirYnn0d{Bxem:uaX\ldoF1cW:wIHnuJIEh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ NEHYfWs9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9zOUGxOFAxPSd-MUmxNVQxODV:L3G+
HMEC-1  NYrkd|JFSXCxcITvd4l{KEG|c3H5 MmrQNU82NzVyIN88[{9udA>? NUO1dHQ{OjRiaB?= NGDYN2ZqdmS3Y3XzJIFxd3C2b4Ppdy=> NH3NVGo9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9zOUGxOFAxPSd-MUmxNVQxODV:L3G+
HMEC-1  M4HBN3Bzd2yrZnXyZZRqd25iQYPzZZk> NF3xZnkyNzVxNUCg{txoN22u MkiyNlQwPDhxN{KgbC=> NHPnbZhqdmirYnn0d{Bxem:uaX\ldoF1cW:wIHnuJIEh\G:|ZTDk[ZBmdmSnboSgcYFvdmW{ NWXqW3NrRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMUmxNVQxODVpPkG5NVE1ODB3PD;hQi=>
HMEC-1  NWSzUlRJTnWwY4Tpc44hSXO|YYm= NHX6UHEyNzVxNUCg{txoN22u MWOyOEBp MU\pcoR2[2W|IHGg[I9{\SCmZYDlcoRmdnRiZHX0ZYNpdWWwdNMg NXLzfnNFRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMUmxNVQxODVpPkG5NVE1ODB3PD;hQi=>
LNT-229  NYHsOXFYTnWwY4Tpc44hSXO|YYm= MknjNE4yNzFxMUCg{txO NWLJXZJMOjRiaB?= MnLvbY1x[Wm{czD0bIUh[WSqZYPpc44hd2ZiY3XscJMhfG9idnn0do9v\WO2aX6gbY4h[SCmb4PlJIRmeGWwZHXueEBu[W6wZYK= NXSyfmFKRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMUmyNlEyPzFpPkG5NlIyOTdzPD;hQi=>
T98G NWTGVFlmTnWwY4Tpc44hSXO|YYm= NEW1[HcxNjFxMT:xNEDPxE1? NYmzRYhZOjRiaB?= MVHpcZBicXK|IITo[UBi\Ginc3nvckBw\iClZXzsd{B1dyC4aYTyc45m[3SrbjDpckBiKGSxc3Wg[IVx\W6mZX70JI1idm6nch?= NYOzfm1qRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMUmyNlEyPzFpPkG5NlIyOTdzPD;hQi=>
LN-18 MVPGeY5kfGmxbjDBd5NigQ>? M1TkTFAvOS9zL{GwJO69VQ>? NVzIT29XOjRiaB?= NUi1fIRicW2yYXnyd{B1cGViYXTo[ZNqd25ib3[gZ4VtdHNidH:geol1em:wZXP0bY4hcW5iYTDkc5NmKGSncHXu[IVvfCCvYX7u[ZI> NFTN[oY9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9zOUKyNVE4OSd-MUmyNlEyPzF:L3G+
LN-308 M2nDUmZ2dmO2aX;uJGF{e2G7 M3TtUFAvOS9zL{GwJO69VQ>? MWeyOEBp NFfnWldqdXCjaYLzJJRp\SCjZHjld4lwdiCxZjDj[YxteyC2bzD2bZRzd26nY4TpckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> Mmr6QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOTl{MkGxO|EoRjF7MkKxNVcyRC:jPh?=
U87MG M3u0OmZ2dmO2aX;uJGF{e2G7 MojGNE4yNzFxMUCg{txO NXS1RY5oOjRiaB?= NFPt[GlqdXCjaYLzJJRp\SCjZHjld4lwdiCxZjDj[YxteyC2bzD2bZRzd26nY4TpckBqdiCjIHTvd4Uh\GWyZX7k[Y51KG2jbn7ldi=> NUjuZm1nRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMUmyNlEyPzFpPkG5NlIyOTdzPD;hQi=>
U87  NEHyO2pHfW6ldHnvckBCe3OjeR?= Mn;6NE0zPSEQvHevcWw> NEnO[ogyOiCqwrC= NVLiZ|ZncW6mdXPld{BifXSxcHjh[5kh\G:|ZTDk[ZBmdmSnboTsfS=> MVS8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zOTd6OEO0N{c,OjF5OEizOFM9N2F-
U251 MnnoSpVv[3Srb36gRZN{[Xl? MmiyNE0zPSEQvHevcWw> MV6xNkBpyqB? M4TYU4lv\HWlZYOgZZV1d3CqYXf5JIRwe2ViZHXw[Y5l\W62bIm= NUe2XnRsRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkG3PFg{PDNpPkKxO|g5OzR|PD;hQi=>
U87  MU\BdI9xfG:|aYOgRZN{[Xl? NF:2WI0zPSEQvHevcWw> MYeyOE81QCCq MUXpcoR2[2W|IHHwc5B1d3OrczDheEA1QCCqIIPp[45q\mmlYX70cJk> M2jnWFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJzN{i4N|Q{Lz5{MUe4PFM1OzxxYU6=
U251 MkfIRZBweHSxc3nzJGF{e2G7 NXL1OZFXOjVizsznM41N M2XLfFI1NzR6IHi= NXXNfppLcW6mdXPld{BieG:ydH;zbZMh[XRiNEigbEB{cWewaX\pZ4FvfGy7 MWm8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zOTd6OEO0N{c,OjF5OEizOFM9N2F-
U87  M1zyc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NITBVYQxNTJ3IN88[{9uVA>? NWD0U5c{OC12ODDo NX:2bXRscW6qaXLpeJMh[2WubDDndo94fGhiaX6g[I9{\SCjbnSgeIlu\SCmZYDlcoRmdnRibXHucoVz MnXHQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjF5OEizOFMoRjJzN{i4N|Q{RC:jPh?=
U251 NH;aPHJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MofwNE0zPSEQvHevcWw> NITiZ|cxNTR6IHi= M17pPYlvcGmkaYTzJINmdGxiZ4Lve5RpKGmwIHTvd4Uh[W6mIITpcYUh\GWyZX7k[Y51KG2jbn7ldi=> MXu8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zOTd6OEO0N{c,OjF5OEizOFM9N2F-
U251MG NF65WVJCeG:ydH;zbZMhSXO|YYm= M3LrblEhyrWP MV60PEBp Ml\5bY5lfWOnczDhdI9xfG:|aYO= M4TKfVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ|M{W0PFA4Lz5{M{O1OFgxPzxxYU6=
U87MG NFK2dVdCeG:ydH;zbZMhSXO|YYm= Mk\qNUDDvU1? NGrWblE1QCCq NVKydVh7cW6mdXPld{BieG:ydH;zbZM> NYPHeo9FRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkOzOVQ5ODdpPkKzN|U1QDB5PD;hQi=>
U251MG NXjt[G1sT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWmwMVI2KM7:TR?= MmTyNlQwPDhiaB?= NIjzSWVqdmirYnn0d{Bk\WyuIHfyc5d1cCCrbjDkc5NmKGGwZDD0bY1mKGSncHXu[IVvfCCvYX7u[ZI> NWDObJc4RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkOzOVQ5ODdpPkKzN|U1QDB5PD;hQi=>
U87MG NInBcWVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF;Bbm8xNTJ3IN88US=> NEXnWG4zPC92ODDo MofIbY5pcWKrdIOgZ4VtdCCpcn;3eIghcW5iZH;z[UBidmRidHnt[UBl\XCnbnTlcpQhdWGwbnXy MYS8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zOzN3NEiwO{c,OjN|NUS4NFc9N2F-
MCF-7  MXPBdI9xfG:|aYOgRZN{[Xl? NEPF[IUxNTJyIN88US=> MkPxOFghcA>? MW\pcoR2[2W|IHHwc5B1d3Orcx?= MV:8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPDF3M{GwNkc,OjRzNUOxNFI9N2F-
T-47D MV3BdI9xfG:|aYOgRZN{[Xl? MoXQNE0zOCEQvF2= M17DZlQ5KGh? MWTpcoR2[2W|IHHwc5B1d3Orcx?= MmTHQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjRzNUOxNFIoRjJ2MUWzNVAzRC:jPh?=
MCF-7  NYP2U4xYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVGwMVIxKM7:TR?= NVvoN5Y3QTZiaB?= NWGxR4JYcW6qaXLpeJMh[2WubDDndo94fGhiaX6gZUBld3OnIHTldIVv\GWwdDDtZY5v\XJ? MYO8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPDF3M{GwNkc,OjRzNUOxNFI9N2F-
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... 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)C1C(=O)NC(C(=O)NCC(=O)NC(C(=O)NC(C(=O)N1C)CC2=CC=CC=C2)CC(=O)O)CCCN=C(N)N.C(=O)(C(F)(F)F)O

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
Dosage mg/kg Average weight of animals g Dosing volume per animal ul Number of animals
Step 2: Enter the in vivo formulation ()
% DMSO % % Tween 80 % ddH2O
CalculateReset

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 (mg) = Concentration (mM) × Volume (mL) × 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 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

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

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID