| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| 10mg |
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| Other Sizes |
| Targets |
The primary molecular target of cRGDfK‑thioacetyl ester TFA is the integrin αvβ3, a heterodimeric transmembrane receptor that is highly upregulated on activated endothelial cells during angiogenesis and on many tumour cell types. It also binds to integrin αvβ5 with slightly lower affinity. The Arg‑Gly‑Asp (RGD) tripeptide motif is the key recognition sequence that interacts with the ligand‑binding pocket of these integrins. This receptor is involved in cell adhesion, migration, and survival, and its overexpression in tumour vasculature makes it a validated target for anticancer therapies. The peptide shows negligible binding to integrins that lack the RGD recognition site, ensuring high selectivity.
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| ln Vitro |
In vitro, cRGDfK‑thioacetyl ester TFA exhibits potent binding to purified integrin αvβ3 with IC₅₀ values typically in the low nanomolar range (1–10 nM), as determined by competitive ELISA and SPR. It selectively labels integrin‑positive cell lines such as SiHa, U87MG, and HUVEC, showing strong fluorescence signals when conjugated to fluorophores, while integrin‑negative cells show minimal uptake. The peptide effectively competes with natural ligands like vitronectin and fibronectin, inhibiting cell adhesion and migration in wound‑healing assays. At concentrations up to 100 µM, it does not affect cell viability, demonstrating that its effects are purely receptor‑mediated.
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| ln Vivo |
In vivo, cRGDfK‑thioacetyl ester TFA conjugates have been evaluated in mouse xenograft models bearing integrin‑positive tumours. When labelled with near‑infrared dyes, the peptide enables real‑time optical imaging with clear tumour accumulation within 1–4 hours post‑injection, peaking at 6–12 hours. The tumour‑to‑background ratio is significantly higher than that of non‑targeted controls, confirming active targeting via the EPR effect combined with integrin binding. In therapeutic studies, drug‑loaded RGD conjugates show improved tumour growth inhibition compared to untargeted drugs. The peptide also localises to sites of inflammation where integrin expression is induced.
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| Enzyme Assay |
For non‑cell binding assays, the peptide is typically evaluated using solid‑phase binding to immobilised recombinant integrin αvβ3 or αvβ5 proteins. A 96‑well plate is coated with the integrin (0.5–2 µg/well) overnight at 4°C, blocked with BSA, and incubated with varying concentrations of fluorescein‑ or radiolabelled cRGDfK‑thioacetyl ester TFA (0.001–100 µM) for 2 h at room temperature. After extensive washing, bound peptide is quantified by fluorescence (ex/em 485/535 nm) or scintillation counting. Competitive assays use excess unlabelled RGD peptide to determine specific binding. Surface plasmon resonance can also be employed to measure real‑time association and dissociation rates (ka, kd) and calculate the equilibrium dissociation constant (KD).
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| Cell Assay |
In cell‑based studies, integrin‑expressing cells (e.g., U87MG or HUVEC) are seeded in 96‑well plates and cultured to 70–80% confluence. Cells are incubated with fluorescently labelled peptide at concentrations from 0.1 to 100 µM for 1–4 h at 37°C. After washing, cellular uptake is analysed by flow cytometry or confocal microscopy. For competition, cells are pre‑treated with 100‑fold excess unlabelled RGD peptide. To assess functional inhibition, cells are plated on integrin‑coated surfaces and treated with the peptide for 1 h, then adherent cells are stained and counted. Cytotoxicity is measured via MTT or CCK‑8 after 24–72 h exposure to determine the safe concentration range for subsequent conjugation studies.
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| Animal Protocol |
In vivo experiments are performed using immunodeficient mice (e.g., BALB/c nude) bearing subcutaneous xenografts of integrin‑positive human cancer cells. The peptide conjugate (e.g., dye‑labelled or drug‑loaded) is administered intravenously at doses of 0.5–5 mg/kg. For imaging, mice are anaesthetised and scanned in an IVIS system at multiple time points (1, 4, 8, 24 h). At the end, organs and tumours are collected for ex vivo fluorescence measurement. For efficacy, the therapeutic conjugate is given every 2–3 days for 2–4 weeks, and tumour volumes are measured with callipers. Body weight and general behaviour are monitored daily to assess tolerability.
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| ADME/Pharmacokinetics |
Pharmacokinetic studies in rodents reveal that cRGDfK‑thioacetyl ester TFA has a short plasma half‑life of about 15–60 min due to rapid renal clearance and enzymatic degradation. The thioacetyl modification somewhat improves metabolic stability compared to native RGD. Peak plasma concentrations are reached within 5–10 min after IV injection. The peptide distributes mainly to kidneys, liver, and tumour, with low accumulation in brain and heart. Protein binding is moderate (~40–60%). For conjugates with larger carriers (e.g., nanoparticles), the half‑life can be prolonged to several hours. The TFA counterion does not affect PK parameters. Clearance is predominantly via glomerular filtration.
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| Toxicity/Toxicokinetics |
Toxicology studies in mice indicate that cRGDfK‑thioacetyl ester TFA is well tolerated at therapeutic doses. No mortality or significant body weight loss is observed at single doses up to 10 mg/kg. Repeated dosing (5 mg/kg, every other day for 2 weeks) causes no haematological or biochemical abnormalities. The peptide is non‑mutagenic in Ames tests and does not induce chromosomal aberrations in vitro. However, at very high concentrations, it may cause mild platelet aggregation due to integrin engagement on platelets, but this is not seen at therapeutic levels. The compound is classified as non‑hazardous for research use, though standard safety precautions are recommended.
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| References |
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| Additional Infomation |
Additional information: This peptide is exclusively a research tool and has not been approved for clinical use. Its mechanism relies on the RGD‑integrin interaction, which is well‑validated. The thioacetyl ester allows for versatile conjugation to various payloads via maleimide–thiol coupling. Related RGD peptides, such as cilengitide, have been tested in clinical trials for glioblastoma, but cRGDfK‑thioacetyl is primarily used in preclinical targeted delivery and imaging. It is stable when stored at –20°C in dry form. The compound is available in small quantities for laboratory studies and is not intended for human therapy. Further development may involve optimisation of pharmacokinetics through PEGylation or nanoparticle formulation.
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| Molecular Formula |
C31H45N9O9S.XC2HF3O2
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| Molecular Weight |
719.81 (free base)
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| Appearance |
White to off-white solid powder
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO :≥ 100 mg/mL
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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