耗材描述
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。
产品来源: https://www.medchemexpress.cn/vsppltlgqlls.html
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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