VUF11207

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^{[1][2][3][4][5]}. In Vitro:VUF11207 reduces CXCL12 mRNA expression in human U87MG and Pt#3 cells and in mouse GL261 glioblastoma cells^[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 (60 min) specifically binds NLuc-ACKR3 in HEK293G cells with a pK_d of 7.89^[4].
VUF11207 (500 nM) partially reverses CXCL12-induced ERK phosphorylation in glioblastoma cells, while it does not affect ERK phosphorylation by itself^[2]. In Vivo:VUF11207 (10 mg/kg; i.p.; twice weekly; starting on day 7 after implantation) prolonged the survival of glioblastoma-bearing mice and enhanced the antitumor effect of anti-PD-L1 therapy, with a median survival of 28 days for the combination treatment^[2].
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].