| Identification | Back Directory | [Name]
Notoginsenoside Ft1 | [CAS]
155683-00-4 | [Synonyms]
product/153944
Notoginsenoside Ft1
β-D-Glucopyranoside, (3β,12β,20R)-12,20-dihydroxydammar-24-en-3-yl O-β-D-xylopyranosyl-(1→2)-O-β-D-glucopyranosyl-(1→2)-
(3beta,12beta,20R)-12,20-Dihydroxydammar-24-en-3-yl O-beta-D-xylopyranosyl-(1- 2)-O-beta-D-glucopyranosyl-(1-2)-beta-D-glucopyranoside | [Molecular Formula]
C47H80O17 | [MDL Number]
MFCD22125013 | [MOL File]
155683-00-4.mol | [Molecular Weight]
917.13 |
| Chemical Properties | Back Directory | [Boiling point ]
997.8±65.0 °C(Predicted) | [density ]
1.36±0.1 g/cm3(Predicted) | [solubility ]
DMF: 20 mg/ml; DMF:PBS(pH 7.2)(1:1): 0.5 mg/ml; DMSO: 15 mg/ml; Ethanol: 5 mg/ml | [form ]
A crystalline solid | [pka]
12.84±0.70(Predicted) | [color ]
White to off-white |
| Hazard Information | Back Directory | [Description]
Notoginsenoside Ft1 is a saponin originally isolated from P. notoginseng with diverse biological activities.1,2,3,4,5 It induces proliferation, migration, and tube formation of human umbilical vein endothelial cells (HUVECs) via nuclear translocation of hypoxia-inducible factor-1α (HIF-1α) and activation of the PI3K/AKT and Raf/MEK/ERK signaling pathways in a manner dependent on mammalian target of rapamycin (mTOR).1 Notoginsenoside Ft1 (45 μM) induces cell cycle arrest at the S and G2/M phases and promotes apoptosis of SH-SY5Y cells.2 It increases cGMP levels and induces relaxation of isolated precontracted rat mesenteric arteries, effects that are reversed by the nitric oxide synthase inhibitor L-NAME (Item No. 80210) and ODQ (Item No. 81410), an inhibitor of soluble guanylyl cyclase.3 In vivo, notoginsenoside Ft1 (0.25, 2.5, and 25 mg/kg) promotes angiogenesis and decreases wound diameter in a mouse model of punched-hole ear injury.1 Notoginsenoside Ft1 (1.25 mg/kg) decreases tail bleeding time and increases thrombus weight in a rat tail bleeding assay.4 Topical administration of notoginsenoside Ft1 increases mRNA expression of the collagen expression, fibroblast proliferation, and scar formation genes COL1A1, COL3A1, TGF-β1, TGF-β3, and fibronectin, promotes neovascularization, reduces monocyte infiltration, and shortens wound closure time in a db/db mouse model of diabetic foot ulcers.5 |
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