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Notoginsenoside Ft1

HY-N0910
MedChem Express
CAS Number155683-00-4
Product group Chemicals
Estimated Purity98.0
Molecular Weight917.13
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Overview

  • Supplier
    MedChem Express
  • Product Name
    Notoginsenoside Ft1 [155683-00-4]
  • Delivery Days Customer
    10
  • CAS Number
    155683-00-4
  • Certification
    Research Use Only
  • Estimated Purity
    98.0
  • Molecular Formula
    C47H80O17
  • Molecular Weight
    917.13
  • Scientific Description
    Notoginsenoside Ft1 is a saponin isolated from Panax notoginseng; stimulator of angiogenesis. IC50 value: Target: angiogenesis stimulator in vitro: Ft1 increases translocalization of hypoxia-inducible factor-1alpha (HIF-1alpha) from cytoplasm to nuclei, where it binds to the vascular endothelial growth factor (VEGF) promoter, increasing the expression of VEGF mRNA and the subsequent secretion of the growth factor. Ft1 induces the activation of PI3K/AKT and Raf/MEK/ERK signaling pathways [1]. Among the saponins examined, Ft1 was the most potent procoagulant and induced dose-dependent platelet aggregation. Ft1 reduced plasma coagulation indexes, decreased tail bleeding time and increased thrombogenesis. Moreover, it potentiated ADP-induced platelet aggregation and increased cytosolic Ca(2+) accumulation, effects that were attenuated by clopidogrel. Ft1 binds to platelet P2Y12 receptors. The increase in intracellular Ca(2+) evoked by Ft1 in HEK293 cells overexpressing P2Y12 receptors could be blocked by ticagrelor [2]. Ft1 caused endothelium-dependent relaxations, which were abolished by l-NAME (inhibitor of nitric oxide synthases) and ODQ (inhibitor of soluble guanylyl cyclase). Ft1 increased the cGMP level in rat mesenteric arteries. GR and ER were present in the endothelial layer and their antagonism by RU486 and PHTPP, respectively, inhibited Ft1-induced endothelium-dependent relaxations and phosphorylations of eNOS, Akt and ERK1/2 [3]. Ft1 showed the best inhibitory effect on cell proliferation of SH-SY5Y cells with IC50 of 45microM. Ft1 not only arrested the cell cycle at S, G2/M stages, but also promoted cell apoptosis. Ft1 up-regulated the protein expressions of cleaved caspase 3, phospho-p53, p21, and cyclin B1, but down-regulated that of Bcl-2. Moreover, Ft1 enhanced the phosphorylation of ERK1/2, JNK and p38 MAPK [4]. in vivo: Ft1 promotes the formation of blood vessels in Matrigel plug and wound healing in mice [1].
  • SMILES
    C[C@@]([C@@]12C)(CC[C@@]3([H])C4(C)C)[C@@](C[C@@H](O)[C@]1([H])[C@]([C@](C)(O)CC/C=C(C)/C)([H])CC2)([H])[C@]3(CC[C@@H]4O[C@@](O[C@H](CO)[C@@H](O)[C@@H]5O)([H])[C@@H]5O[C@@](O[C@H](CO)[C@@H](O)[C@@H]6O)([H])[C@@H]6O[C@@](OC[C@@H](O)[C@@H]7O)([H])[C@@H]7O)C
  • Storage Instruction
    2°C to 8°C
  • UNSPSC
    12352200

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