| Field | Specification |
|---|---|
| Target | |
| Alternative names | EMD 121974 TFA |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C29H41F3N8O9 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Cilengitide TFA, also known as EMD 121974 TFA, is a blood-brain-barrier-permeable integrin inhibitor with IC50 values against human targets of 0.61 nM (αvβ3), 8.4 nM (αvβ5), 14.9 nM (α5β1), 5400 nM (αIIbβ3), 2050 nM (αvβ6), and 2350 nM (αvβ8). It blocks the binding of integrins to vitronectin, fibronectin, fibrinogen, and LAP (TGF-β), and can be used as an internal standard in solid-phase integrin binding assays. In cell-based studies it reduces tumor cell viability, induces apoptosis, lowers phosphorylation of STAT3, AKT, and mTOR, downregulates PD-L1 expression, inhibits angiogenesis, modulates anti-tumor immune responses, and slows tumor growth, with reported use in research on glioblastoma, melanoma, advanced solid tumors, and refractory brain tumors[1][2][3][4]. It is supplied as a white to off-white solid (C29H41F3N8O9, MW 702.68) at 99.92% purity.
Physical & Chemical Properties
| CAS Number | 199807-35-7 |
|---|---|
| Molecular Formula | C29H41F3N8O9 |
| Molecular Weight | 702.68 g/mol |
| Purity | 99.92% |
| Appearance | Solid |
| Color | White to off-white |
| SMILES | O=C(NCC(N[C@H](C(N[C@H](CC1=CC=CC=C1)C(N([C@H]2C(C)C)C)=O)=O)CC(O)=O)=O)[C@H](CCCNC(N)=N)NC2=O.FC(F)(C(O)=O)F |
| Target | αvβ3, αvβ5, α5β1, αIIbβ3, αvβ6, αvβ8 |
| Signaling Pathway | Cytoskeleton; TGF-beta/Smad; Apoptosis; Immunology/Inflammation; Stem Cell/Wnt; JAK/STAT Signaling; PI3K/Akt/mTOR |
| Solubility | In Vitro: DMF: 100 mg/mL (142.31 mM; Requires sonication) DMSO: 100 mg/mL (142.31 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) H2O: 50 mg/mL (71.16 mM; Requires sonication) |
| Storage | -20°C, sealed storage, away from moisture. In solvent: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
IC50 & Target
|
αvβ3 0.61 nM (IC50) |
αvβ5 8.4 nM (IC50) |
α5β1 14.9 nM (IC50) |
αIIbβ3 5400 nM (IC50) |
αvβ6 2050 nM (IC50) |
αvβ8 2350 nM (IC50) |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMF | 100 mg/mL (142.31 mM) | requires sonication |
| DMSO | 100 mg/mL (142.31 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
| H2O | 50 mg/mL (71.16 mM) | requires sonication |
Aliquot the stock solution and store it at -80°C (up to 6 months) or -20°C (up to 1 month); sealed storage, away from moisture; avoid repeated freeze-thaw cycles.
If water is used as the stock solvent, dilute to the working solution and sterilize it through a 0.22 μm filter before use.
In Vivo
Choose the formulation that suits the animal model and route of administration. Percentages are volume ratios of the final working solution. Prepare the working solution fresh on the day of dosing; if precipitation or phase separation occurs, gentle warming or sonication can help.
Direct preparation of the working solution
These formulations are prepared directly, without a DMSO stock; use them promptly after preparation.
Protocol 1
| Composition | PBS |
|---|---|
| Result | 16.67 mg/mL (23.72 mM); clear solution; requires sonication |
Data provided by the manufacturer.
In Vitro
In a time- and dose-dependent manner, Cilengitide (1-1000 μg/mL; 24-72 h) TFA lowers the viability of B16 and A375 cells[2]. Colony formation by B16 and A375 melanoma cells is suppressed by Cilengitide (5-10 μg/mL; two weeks) TFA[2]. Apoptosis is triggered in B16 and A375 melanoma cells by Cilengitide (5-10 μg/mL; 12 h) TFA[2]. Cilengitide (5 μg/mL; 12 h) TFA changes the transcriptome of B16 melanoma cells and regulates genes and pathways involved in cell growth, apoptosis and integrin signaling, among them lower phosphorylation levels of AKT and mTOR[2]. By immunofluorescence staining, Cilengitide (5 μg/mL; 12 h) TFA lowers PD-L1 expression in B16 and A375 melanoma cells and decreases the proportion of PD-L1-positive B16 and A375 melanoma cells; after 12 hours of incubation, the positive rate falls from 38.1-41.1% to 17.9-18.2%[2]. Cilengitide (5-20 μg/mL; 12 h) TFA decreases PD-L1 expression and STAT3Tyr705 phosphorylation in B16 and A375 melanoma cells, while total STAT3 protein expression is not altered[2]. Through reduced STAT3 phosphorylation, Cilengitide (5 μg/mL; 12 h) TFA lowers PD-L1 expression in B16 and A375 melanoma cells, and IL-6-induced STAT3 activation reverses this PD-L1 downregulation[2]. Binding of human αvβ3 integrin to vitronectin is most strongly inhibited by Cilengitide (6.4 nM-20 μM; 1 h) TFA (IC50 = 0.61 nM), which also binds αvβ5 (IC50 = 8.4 nM) and α5β1 (IC50 = 14.9 nM) with high affinity. Affinity for αvβ6, αvβ8 and αIIbβ3 integrins is significantly reduced by comparison[1]. Adhesion of human umbilical vein endothelial cells to vitronectin, which is integrin-mediated, is inhibited by Cilengitide (2 μM) TFA, with an IC50 of 2 μM[3].
Cell Viability Assay[2]
| Cell Line | B16, A375 melanoma cell lines |
|---|---|
| Concentration | 0, 1, 10, 100, 1000 μg/mL |
| Incubation Time | 24 h; 48 h; 72 h |
| Result | Inhibited B16 and A375 cell growth in a time- and dose-dependent manner. Reduced B16 cell viability with IC50 values of 12 μg/mL (24 h), 10 μg/mL (48 h), 8 μg/mL (72 h). Reduced A375 cell viability with IC50 values of 4 μg/mL (24 h), 1.5 μg/mL (48 h), 0.5 μg/mL (72 h). |
Apoptosis Analysis[2]
| Cell Line | B16, A375 melanoma cell lines |
|---|---|
| Concentration | 0, 5, 10 μg/mL |
| Incubation Time | 12 h |
| Result | Increased B16 cell apoptosis rate from ~7% (untreated) to ~15.27% (5 μg/mL) and ~21.71% (10 μg/mL). Increased A375 cell apoptosis rate from ~3% (untreated) to ~14.89% (5 μg/mL) and ~36.6% (10 μg/mL). |
Immunofluorescence[2]
| Cell Line | B16, A375 melanoma cell lines |
|---|---|
| Concentration | 5 μg/mL |
| Incubation Time | 12 h |
| Result | Downregulated PD-L1 expression in B16 and A375 cells, as shown by reduced fluorescent signal compared to untreated controls. |
Western Blot Analysis[2]
| Cell Line | B16, A375 melanoma cell lines |
|---|---|
| Concentration | 0, 5, 10, 20 μg/mL |
| Incubation Time | 12 h |
| Result | Reduced PD-L1 protein levels by ~50% (5 μg/mL), ~60% (10 μg/mL), and ~70% (20 μg/mL) in both cell lines. Reduced STAT3 (Tyr705) phosphorylation by ~30% (5 μg/mL), ~40% (10 μg/mL), and ~60% (20 μg/mL) in both cell lines. Caused no significant change in total STAT3 protein levels across groups. |
Western Blot Analysis[2]
| Cell Line | B16, A375 melanoma cell lines |
|---|---|
| Concentration | 5 μg/mL (alone or combined with 20 ng/mL IL-6) |
| Incubation Time | 12 h |
| Result | Reduced PD-L1 expression and STAT3 phosphorylation when used alone. Reversed IL-6-induced increases in STAT3 phosphorylation and PD-L1 expression, restoring PD-L1 levels and STAT3 phosphorylation to near-control levels in co-treatment groups. |
In Vivo
In mice, Cilengitide (50 mg/kg; i.p.; once daily; for 7 consecutive days) TFA reduces PD-L1 expression in subcutaneous melanoma tumors, shows moderate anti-tumor activity by enhancing CD8+ T cell-mediated immune responses, and lowers the bioluminescent signal of luciferase-expressing subcutaneous melanoma[2]. Cilengitide (10-250 μg; intraperitoneal injection; three times per week) TFA suppresses the growth of M21-L melanoma tumors in nude mice in a dose-dependent manner[3]. In nude mice bearing medulloblastoma and glioblastoma xenografts, Cilengitide (100 μg; i.p.) TFA gives a 100% survival rate and nearly complete tumor clearance at day 28[3].
| Animal Model | C57BL/6[2] |
|---|---|
| Dosage | 50 mg/kg |
| Administration | i.p.; daily; 7 days |
| Result | Reduced PD-L1 protein expression in subcutaneous B16 melanoma tumors. Showed moderate antitumor activity, with smaller tumor volumes compared to control at day 20 post-implantation. Increased intratumoral CD8+ T cell infiltration and tumor granzyme B and IFN-γ levels relative to control. Reduced bioluminescent tumor signal strength relative to control at day 20 post-implantation. When combined with anti-PD1 therapy, caused significantly weaker tumor signal than with either monotherapy. |
| Animal Model | Nude mice[3] |
|---|---|
| Dosage | 10 μg; 50 μg; 250 μg |
| Administration | i.p.; three times per week |
| Result | Reduced tumor volume by 55% and tumor weight by 23%. Reduced tumor volume by 75% and tumor weight by 38%. Reduced tumor volume by 89% and tumor weight by 61%. |
| Animal Model | Nude mice[3] |
|---|---|
| Dosage | 100 μg |
| Administration | i.p. |
| Result | Resulted in 100% survival of mice at 28 days. Induced almost complete histological disappearance of tumors. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Need this compound in a format that drops straight into your assay? We can tailor formulation, chemistry, and documentation so your results stay consistent across runs and re-orders.
- Format options: solid or pre-dissolved solution (choose solvent), target concentration, aliquots, light/moisture-protected packaging
- Chemistry options: free base/acid vs salt forms, hydrate/solvate preference, stereoisomer control (single enantiomer or racemate), close analogs
- Add-on labels & handles: D/¹³C/¹⁵N isotopes (LC-MS/internal standards), azide/alkyne or other functional handles for conjugation
- QC & documentation: standard COA or enhanced analytical pack (HPLC/LC-MS/NMR), chiral purity, residual solvents, water content (KF), method-specific specs
- Scale & continuity: mg to gram scale, bulk pricing, lot reservation, repeat-order continuity
To quote quickly, tell us: compound name + CAS/structure (SMILES or mol file), intended assay context, solvent preference, salt/stereochemistry requirements, purity/QC level, and the amount (mg–g).
Can’t find the compound you’re looking for?
Send the CAS or structure and your specs. We can help source it, suggest close equivalents, or discuss custom synthesis with the right QC documentation (RUO).
Three subtypes of lung cancer fibroblasts define distinct therapeutic paradigms. Cancer Cell 2021 Nov 8;39(11):1531-1547.e10. PMID: 34624218
Type V Collagen in Scar Tissue Regulates the Size of Scar after Heart Injury. Cell 2020 Aug 6;182(3):545-562.e23. PMID: 32621799
Peptide codes for organ-selective mRNA delivery. Nat Mater 2025 Sep 1. PMID: 40890497
Crosstalk with lung epithelial cells regulates Sfrp2-mediated latency in breast cancer dissemination. Nat Cell Biol 2020 Mar;22(3):289-296.
Excessive collagen type VII mediates pleural fibrosis via increasing extracellular matrix stiffness. J Clin Invest 2025 Oct 16:e188822. PMID: 41100460
Cancer Immunotherapy via Disruption of Integrin αvβ3 and CD47 Costabilization on Cancer Cell Surface. Adv Sci (Weinh) 2025 Oct 30:e01602. PMID: 41168993
Drug Screening of Primary Human Endometriotic Cells Based on Micro-Encapsulating Microfluidic Chip. Adv Sci (Weinh) 2025 May;12(20):e2504647. PMID: 40289897
MFGE8 induces anti-PD-1 therapy resistance by promoting extracellular vesicle sorting of PD-L1. Cell Rep Med 2025 Feb 18;6(2):101922. PMID: 39842432
Integrin inhibition facilitates fibrocartilaginous transformation in connective tissue in osteoarthritis. Sci Adv 2026 Jan 2;12(1):eady4112. PMID: 41481715
Dynamic adaptive coassembled sericin protein orchestrating stem cell development for nucleus pulposus regeneration. Sci Adv 2026 Jan 2;12(1):eadx2768. PMID: 41477862
