VSPPLTLGQLLS is a small peptide FGFR3 inhibitor, peptide P3, inhibits FGFR3 phosphorylation. VSPPLTLGQLLS inhibits 9-cisRA-induced tracheal lymphangiogenesis and blocks lymphatic endothelial cell (LEC) proliferation, migration, and tubule formation[2].In Vitro:VSPPLTLGQLLS (5 μM and 10 μM; 24 h and 48 h) inhibits human primary lymphatic endothelial cell (LEC)s proliferation, migration, and tubule formation.
VSPPLTLGQLLS shows effective inhibition in FGFR3 phosphorylation in LECs and also demonstrated to be effective in ATDC5 chondrogenic cells, 293T cells, explanted metatarsal bone cultures, and an in vivo mouse model of thanatophoric dysplasia II[2].
VSPPLTLGQLLS (10 μM; 6 h) inhibits tyrosine kinase activity of FGFR3 and its typical downstream molecules, extracellular signal-regulated kinase/mitogen-activated protein kinase[2].
VSPPLTLGQLLS (0, 1, 10, and 50 μM; 24 h and 3 or 7 days, respectively) also promotes proliferation and chondrogenic differentiation of cultured ATDC5 chondrogenic cells[2].
VSPPLTLGQLLS (10 μM; 0-60 min) inhibits the ERK/MAPK pathway in FGFR3-expressing chondrocytic cell line ATDC5[2].
In Vivo:VSPPLTLGQLLS (1 mM; intranasal dropping; onced daily for 7 d) blocks 9-cisRA-induced lymphangiogenesis in vivo, while 9-cisRA is an isoform of vitamin A involving in AIDS-related Kaposi Sarcoma.
VSPPLTLGQLLS alleviates the bone growth retardation in bone rudiments from mice mimicking human thanatophoric dysplasia type II (TDII), reversed the neonatal lethality of TDII mice[2].