VUF11207
Based on 4 publication(s) in Google Scholar
VUF11207 is a potent, selective, and orally active CXCR7/ACKR3 agonist (pKi = 8.1). VUF11207 specifically activates CXCR7/ACKR3, recruits β-arrestin, and induces receptor internalization, while downregulating the pro-inflammatory, pro-osteoclastogenic, and tumor immunosuppressive signaling mediated by the CXCL12-CXCR4 axis. VUF11207 can be used for research on glioblastoma, hypertension, and venous thrombosis.
For research use only. We do not sell to patients.
- Purity : 94.56%
- CAS No.: 1378524-41-4
- Formula: C27H35FN2O4
- Molecular Weight:470.58
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Storage:Pure form -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Publications Citing Use of MedChemExpress (MCE) VUF11207
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Biological Activity
Description
IC50 & Target
[1]|
CXCR7 8.1 (pKi) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| HEK293 | EC50 |
14.1 nM
Compound: 29, VUF11207
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Agonist activity at human CXCR7 expressed in HEK293 cells assessed as reduction of receptor surface expression after 1 hr by ELISA based internalization assay
Agonist activity at human CXCR7 expressed in HEK293 cells assessed as reduction of receptor surface expression after 1 hr by ELISA based internalization assay
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[PMID: 22424612] |
| HEK-293T | EC50 |
1.6 nM
Compound: 29, VUF11207
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Agonist activity at human CXCR7 expressed in HEK293T cells co-expressing beta-arrestin2-YFP assessed as beta-arrestin2 recruitment after 1 hr by BRET assay
Agonist activity at human CXCR7 expressed in HEK293T cells co-expressing beta-arrestin2-YFP assessed as beta-arrestin2 recruitment after 1 hr by BRET assay
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[PMID: 22424612] |
In Vitro
VUF11207 reduces CXCL12 mRNA expression in human U87MG and Pt#3 cells and mouse GL261 glioblastoma cells[2].
VUF11207 (500 nM) partially reverses CXCL12-induced ERK phosphorylation in glioblastoma cells, while it does not affect ERK phosphorylation by itself[2].
VUF11207 (500 nM; 48 h) eliminates the promoting effect of GAMs on tumor cell growth in the co-culture system of glioblastoma cells and GAMs, and restores the cytotoxic killing activity of CD8+ T cells[2].
VUF11207 (100 ng/mL; 5 days) inhibits RANKL (HY-P73388) and TNF-α (HY-P7090)-induced osteoclastogenesis in mouse bone marrow-derived osteoclast precursor cells in the presence of CXCL12[1].
VUF11207 (100 ng/mL; 15-30 min) reduced CXCL12-enhanced Erk phosphorylation in mouse bone marrow-derived osteoclast precursors treated with RANKL or TNF-α[1].
VUF11207 (0.5 μg/mL) promotes AngII (HY-13948)-induced expression of pro-inflammatory and pro-fibrotic factors in rat aortic adventitial fibroblasts (AFs) and exacerbates cell proliferation and migration[3].
VUF11207 competitively displaces the fluorescent ligand in HEK293G cells overexpressing NLuc-ACKR3, specifically binding to the ACKR3 receptor[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Mouse bone marrow-derived osteoclast precursors
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Concentration:100 ng/mL
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Incubation Time:5 days
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Result:Decreased the number of TRAP-positive multinucleated osteoclasts and attenuated CXCL12-enhanced p-ERK levels without altering p38 or JNK.
In Vivo
VUF11207 (5 mg/kg/d; i.g.; once daily; 14 days) significantly enhanced AngII-induced adventitial thickening and fibrosis in an AngII-induced hypertensive mouse model[3].
VUF11207 (100 µg/day; s.c.; once daily; 5 days) significantly inhibited LPS (HY-D1056)-induced osteoclastogenesis and bone resorption in a mouse model, and reduced LPS-induced RANKL and TNF-α mRNA expression[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (male, 8-10 weeks old, 20-25 g, LPS-induced osteoclastogenesis and bone resorption model)[1]
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Dosage:100 µg/day
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Administration:s.c.; once daily; 5 days
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Result:Significantly reduced osteoclastogenesis compared with LPS alone.
Significantly lowered the number of TRAP-positive osteoclasts.
Significantly decreased TRAP and Cathepsin K mRNA expression levels.
Significantly reduced bone resorption area.
Significantly lowered RANKL and TNF-α mRNA levels.
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Animal Model:C57BL/6NCrlBltw (female, 8-12 weeks old)[2]
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Dosage:10 mg/kg
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Administration:i.p.; twice weekly; from post-implantation day 7
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Result:Prolonged survival with median survival of 28 days for the VUF11207-anti-PD-L1 combination, compared to 18 days for VUF monotherapy, 20 days for anti-PD-L1 monotherapy, and 19 days for control.
Reduced tumor size on post-implantation day 20.
Decreased CXCL12 and PD-L1 expression, particularly PD-L1 in glioblastoma-associated macrophages (GAMs).
Attenuated phosphorylated ERK expression.
Increased proportion of CD8+ T cells in tumor tissues.
Achieved long-term survival in 4 of 9 mice when combined with anti-PD-L1 and control antibody, whereas all mice succumbed within 27 days when combined with anti-PD-L1 and anti-CD8β antibody.
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Animal Model:C57/B6 wild-type (WT) (male, ten weeks old, AngII-induced hypertension)[3]
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Dosage:5 mg/kg/d
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Administration:i.g.; once daily; 14 days
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Result:Strikingly aggravated aortic adventitial thickness, fibrosis, and collagen deposition in AngII-induced hypertensive mice.
Chemical Information
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CAS No. 1378524-41-4
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Appearance Oil
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Molecular Weight 470.58
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Formula C27H35FN2O4
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Color Colorless to light yellow
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SMILES
CN(CCC1)C1CCN(C/C(C)=C/C2=C(C=CC=C2)F)C(C3=CC(OC)=C(C(OC)=C3)OC)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Pure form -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Publications (4)
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Journal Impact Factor
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Most Recent
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Immunity
Spatiotemporal dynamics of CXCL10 encode contextual immune information revealed by the genetically encoded fluorescent sensor. [Abstract]2025 Sep 9;58(9):2320-2335.e9. PMID: 40818452 -
Cell Death Dis
CXCR7 activation evokes the anti-PD-L1 antibody against glioblastoma by remodeling CXCL12-mediated immunity. [Abstract]2024 Jun 19;15(6):434. PMID: 38898023 -
Cell Mol Life Sci
Crosstalk between purinergic receptor P2Y11 and chemokine receptor CXCR7 is regulated by CXCR4 in human macrophages. [Abstract]2024 Mar 13;81(1):132. PMID: 38472446 -
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (212.50 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
H2O : ≥ 100 mg/mL (212.50 mM)
* "≥" means soluble, but saturation unknown.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.5 mg/mL (5.31 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (5.31 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Working solution concentration: 0.22 mg/mL
This product has good water solubility, please refer to the measured solubility data in water/PBS/Saline for details.
Protocols
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
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Data Sheet (298 KB)
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SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
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Handling Instructions (2659 KB)
References
[1]. Nugraha AP, et al. C‑X‑C receptor 7 agonist acts as a C‑X‑C motif chemokine ligand 12 inhibitor to ameliorate osteoclastogenesis and bone resorption. Molecular medicine reports. 2022 Mar;25(3):78. [Content Brief]
[2]. Liu CC, et al. CXCR7 activation evokes the anti-PD-L1 antibody against glioblastoma by remodeling CXCL12-mediated immunity. Cell death & disease. 2024 Jun 19;15(6):434. [Content Brief]
[5]. Aslan JE. A platelet lipid switch that slows clotting. Blood. 2026 Sep 10;148(11):1379-80.
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO / H2O | 1 mM | 2.1250 mL | 10.6252 mL | 21.2504 mL | 53.1259 mL |
| 5 mM | 0.4250 mL | 2.1250 mL | 4.2501 mL | 10.6252 mL | |
| 10 mM | 0.2125 mL | 1.0625 mL | 2.1250 mL | 5.3126 mL | |
| 15 mM | 0.1417 mL | 0.7083 mL | 1.4167 mL | 3.5417 mL | |
| 20 mM | 0.1063 mL | 0.5313 mL | 1.0625 mL | 2.6563 mL | |
| 25 mM | 0.0850 mL | 0.4250 mL | 0.8500 mL | 2.1250 mL | |
| 30 mM | 0.0708 mL | 0.3542 mL | 0.7083 mL | 1.7709 mL | |
| 40 mM | 0.0531 mL | 0.2656 mL | 0.5313 mL | 1.3281 mL | |
| 50 mM | 0.0425 mL | 0.2125 mL | 0.4250 mL | 1.0625 mL | |
| 60 mM | 0.0354 mL | 0.1771 mL | 0.3542 mL | 0.8854 mL | |
| 80 mM | 0.0266 mL | 0.1328 mL | 0.2656 mL | 0.6641 mL | |
| 100 mM | 0.0213 mL | 0.1063 mL | 0.2125 mL | 0.5313 mL |
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
VUF11207 Related Classifications
HY-100677 Related Classifications
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