VUF11207 TFA
Based on 4 publication(s) in Google Scholar
VUF11207 TFA is a potent, selective, and orally active CXCR7/ACKR3 agonist (pKi = 8.1). VUF11207 TFA 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 TFA can be used for research on glioblastoma, hypertension, and venous thrombosis.
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- No. CAS: 1492153-74-8
- Fòrmula: C29H36F4N2O6
- Peso molecular:584.60
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Almacenamiento:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Other In-stock Forms of VUF11207 TFA
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Actividad biológica
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Chemical Information
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Publications Citing Use of MedChemExpress (MCE) VUF11207 TFA
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Actividad biológica
Descripciòn
IC50 & Target
[1]|
CXCR7 8.1 (pKi) |
In Vitro
VUF11207 (500 nM) TFA partially reverses CXCL12-induced ERK phosphorylation in glioblastoma cells, while it does not affect ERK phosphorylation by itself[2].
VUF11207 (100 ng/mL; 15-30 min) TFA reduced CXCL12-enhanced Erk phosphorylation in mouse bone marrow-derived osteoclast precursors treated with RANKL or TNF-α[1].
VUF11207 (0.5 μg/mL) TFA 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 TFA 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.
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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
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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No. CAS 1492153-74-8
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Peso molecular 584.60
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Fòrmula C29H36F4N2O6
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SMILES
O=C(N(C/C(C)=C/C1=CC=CC=C1F)CCC2N(C)CCC2)C3=CC(OC)=C(OC)C(OC)=C3.FC(C(O)=O)(F)F
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
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 -
Pureza y Documentación
Referencias
[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.
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
VUF11207 TFA Related Classifications
HY-115615 Related Classifications
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