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VSPPLTLGQLLS

CAS No. : 1206896-24-3

MCE 站：VSPPLTLGQLLS

产品活性：VSPPLTLGQLLS 是小肽 FGFR3 抑制剂，是一种肽P3，能够抑制 FGFR3 的磷酸化。VSPPLTLGQLLS 抑制 9-cisRA 诱导的气管淋巴管生成，并阻止淋巴内皮细胞(LEC)增殖、迁移和小管形成。

研究领域：Protein Tyrosine Kinase/RTK

作用靶点：FGFR

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.
VSPPLTLGQLLS (10 μM; 6 h) inhibits tyrosine kinase activity of FGFR3 ａnd its typical downstream molecules, extracellular signal-regulated kinase/mitogen-activated protein kinase.
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.
VSPPLTLGQLLS (10 μM; 0-60 min) inhibits the ERK/MAPK pathway in FGFR3-expressing chondrocytic cell line ATDC5.

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.

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