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Fig. 1 · Structure
Cat. No.
A12371
CAS No.
199807-35-7
Formula
C29H41N8O9F3
Mol. Weight
702.7

Documents & Downloads

Cilengitide trifluoroacetate

Cat. No. A12371 CAS 199807-35-7

Integrin inhibitor

Cilengitide is a cyclic Arg-Gly-Asp peptide with potential antineoplastic activity. Cilengitide binds to and inhibits the activities of the alpha(v)beta(3) and alpha(v)beta(5) integrins, thereby inhibiting endothelial cell-cell interactions, endothelial cell-matrix interactions, and angiogenesis.

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Publications for Cilengitide trifluoroacetate

1 publication citing this product

  1. Yi Han Tan, .et al. , Cell Microbiol, 2017, Aug;19(8) PMID: 28186697
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Biological Activity

Target & Activity

Target Activity Value
αvβ3 receptor (Cell-free assay) 4.1 nM
αvβ5 receptor (Cell-free assay) 79 nM

In Vitro Studies

Cilengitide inhibited endothelial cell counts in HMEC-1 cells. In suspended HUVEC, Cilengitide induced LIBS expression, whereas EMD135981 did not. In untransfected A2780 ovarian cancer cells, Cilengitide added during the recycling period increased α5β1 recycling to the plasma membrane. [1,2,3]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Cilengitide inhibits endothelial cell counts

Cell-based study · HMEC-1 cells [1]

HMEC-1 cells were incubated with Cilengitide at 1 μg/ml. Endothelial cell counts showed 33%, 59% and 44% inhibition after 24, 48 and 72 hours, respectively.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
endothelial cell countsproliferation 33%, 59% and 44% inhibition after 24, 48 and 72 hours, respectively[1]

Literature-Reported Treatment Conditions

Treatment concentration
1 μg/ml
Exposure duration
24, 48 and 72 hours
Method
incubated
Vehicle
sterile physiological saline solution
Methods and source locations

Compound reported in the paper: Cilengitide

The paper names Cilengitide without stating the salt or form; not verified as the trifluoroacetate form supplied as A12371. No dose conversion or lot validation.

Methods > Cell culture and Reagents (S6); Methods > Proliferation (S13); Results > Cilengitide inhibits proliferation and induces apoptosis in endothelial cells (S50, S51, S52)

endothelial cell counts: endothelial cell counts; comparator: medium containing 4% FCS — Results > Cilengitide inhibits proliferation and induces apoptosis in endothelial cells (S51, S52)

LIBS expression in suspended endothelial cells

Cell-based study · HUVEC in suspension [2]

HUVEC in suspension were exposed to Cilengitide at 10 µM for 10 minutes. Cilengitide, but not EMD135981, induced LIBS expression.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
β3 LIBSReported result HUVEC in suspension were exposed to 10 µM of cilengitide or EMD135981 for 10 minutes. Cilengitide, but not EMD135981, induced LIBS expression.[2]

Literature-Reported Treatment Conditions

Treatment concentration
10 µM
Exposure duration
10 minutes
Method
exposed
Reported limits
Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: Cilengitide

The paper names Cilengitide without stating the salt or form; not verified as the trifluoroacetate form supplied as A12371. No dose conversion or lot validation.

Figure 3 legend (S148, S149)

β3 LIBS: β3 LIBS; comparator: EMD135981 — Figure 3 legend (S148, S149)

Integrin recycling in ovarian cancer cells

Cell-based study · A2780 ovarian cancer cells [3]

Untransfected A2780 ovarian cancer cells received Cilengitide at 1 μM during the recycling period. Treatment increased α5β1 recycling to the plasma membrane.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
proportion of integrin recycled to the plasma membraneα5β1 recycling A2780 cells left untransfected; 1 μM cilengitide: α5β1 recycling increased by at least twofold[3]

Literature-Reported Treatment Conditions

Treatment concentration
1 μM
Exposure duration
during the recycling period
Method
added to the cells only during the recycling period
Reported limits
Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: Cilengitide

The paper names Cilengitide without stating the salt or form; not verified as the trifluoroacetate form supplied as A12371. No dose conversion or lot validation.

Results > Inhibition of αvβ3 promotes α5β1 recycling in A2780 cells (S3, S4, S6); Materials and methods > Receptor internalization and recycling assays (S112); Figure 1. legend (S151, S153, S155)

proportion of integrin recycled to the plasma membrane: proportion of integrin recycled to the plasma membrane; comparator: absence (BAS) — Results > Inhibition of αvβ3 promotes α5β1 recycling in A2780 cells (S3, S4); Figure 1. legend (S151, S153, S155)

In Vivo Studies

ZIKV-infected mice receiving IFNAR1-blocking antibody were treated with Cilengitide or PBS vehicle control. Within this design, Cilengitide treatment significantly suppressed whole-brain ZIKV RNA levels. [4]

Whole-brain viral RNA suppression in infected mice

Animal study · C57BL/6J mice (4 to 5 week old, male, from Jackson Laboratories) [4]

ZIKV-infected mice receiving IFNAR1-blocking antibody were treated with Cilengitide or PBS vehicle control. Within this design, Cilengitide treatment significantly suppressed whole-brain ZIKV RNA levels.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
viral levels were analyzed by qRT-PCRReported result C57BL/6 mice were administered with IFNAR1 blocking Ab before ZIKV infection and treated daily with cilengitide (20 mg/kg body weight) or PBS only. Animals were euthanized at 6 days post-infection, and viral levels were analyzed by qRT-PCR or by immunohistochemistry. At the whole brain level, cilengitide treatment significantly suppressed levels of ZIKV RNA.[4]

Conditions shared by the study groups

Route
i.p.
Treatment course
daily for 6 days
Vehicle
PBS
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Cilengitide 20 mg/kg body weightPBS was used as a vehicle control.C57BL/6 mice were administered with IFNAR1 blocking Ab before ZIKV infection and treated daily with cilengitide (20 mg/kg body weight) or PBS only. Animals were euthanized at 6 days post-infection, and viral levels were analyzed by qRT-PCR or by immunohistochemistry. At the whole brain level, cilengitide treatment significantly suppressed levels of ZIKV RNA.[4]
Cilengitide 20 mg/kg body weight
Model: C57BL/6J mice (4 to 5 week old, male, from Jackson Laboratories)
Methods and source locations

Compound reported in the paper: Cilengitide

The paper names Cilengitide without stating the salt or form; not verified as the trifluoroacetate form supplied as A12371. No dose conversion or lot validation.

RESULTS > Inhibition of Integrin αvβ5 Alleviates ZIKV-Induced Pathology in hNSCs and Mouse Brain (S153, S154, S155); STAR★METHODS > METHOD DETAILS > ZIKV infection in mice (S203, S204); Figure 6. legend (S387)

viral levels were analyzed by qRT-PCR: viral levels were analyzed by qRT-PCR; comparator: PBS was used as a vehicle control. — RESULTS > Inhibition of Integrin αvβ5 Alleviates ZIKV-Induced Pathology in hNSCs and Mouse Brain (S153, S154, S155)

Cilengitide 20 mg/kg body weight · RESULTS > Inhibition of Integrin αvβ5 Alleviates ZIKV-Induced Pathology in hNSCs and Mouse Brain (S153, S154, S155); STAR★METHODS > METHOD DETAILS > ZIKV infection in mice (S204)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 199807-35-7
Applications Integrin inhibitor
Formula C29H41N8O9F3
Molecular Weight 702.7
Synonyms EMD 12197; EMD-85189; EMD-121974; NSC-707544; D03497
SMILES
CC(C)[C@H]1C(=O)N[C@H](C(=O)NCC(=O)N[C@H](C(=O)N[C@@H](C(=O)N1C)Cc2ccccc2)CC(=O)O)CCCNC(=N)N.C(=O)(C(F)(F)F)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 89 mg/mL (126.66 mM)
Water 7 mg/mL (9.96 mM)
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Oliveira-Ferrer L, Hauschild J, Fiedler W, et al. Cilengitide induces cellular detachment and apoptosis in endothelial and glioma cells mediated by inhibition of FAK/src/AKT pathway. J Exp Clin Cancer Res (2008). PMID: 19114005 DOI: 10.1186/1756-9966-27-86 Source material
  2. [2] Alghisi GC, Ponsonnet L, Rüegg C. The integrin antagonist cilengitide activates alphaVbeta3, disrupts VE-cadherin localization at cell junctions and enhances permeability in endothelial cells. PLoS One (2009). PMID: 19212436 DOI: 10.1371/journal.pone.0004449 Source material
  3. [3] Caswell PT, Chan M, Lindsay AJ, et al. Rab-coupling protein coordinates recycling of alpha5beta1 integrin and EGFR1 to promote cell migration in 3D microenvironments. J Cell Biol (2008). PMID: 18838556 DOI: 10.1083/jcb.200804140 Source material
  4. [4] Wang S, Zhang Q, Tiwari SK, et al. Integrin αvβ5 Internalizes Zika Virus during Neural Stem Cells Infection and Provides a Promising Target for Antiviral Therapy. Cell Rep (2020). PMID: 31956073 DOI: 10.1016/j.celrep.2019.11.020 Source material

Publications

1 publication citing this product

  1. Yi Han Tan, .et al. , Cell Microbiol, 2017, Aug;19(8) PMID: 28186697

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