From 11:00 pm to 12:00 pm EST ( 8:00 pm to 9:00 pm PST ) on January 6th, the website will be under maintenance. We are sorry for the inconvenience. Please arrange your schedule properly.
NotoginsenosideFt1 is a saponin found in Panax notoginseng. Notoginsenoside Ft1 inhibits the PI3K/AKT/mTOR signaling pathway, activates the p38 MAPK and ERK1/2 signaling pathways, and increases the proportion of CD8+ T cells, thereby inducing apoptosis and lysosomal cell death in various cancer cells, and promoting angiogenesis. Notoginsenoside Ft1 causes vasodilation by activating glucocorticoid receptors (GR) and estrogen receptor beta (ERβ) in endothelial cells. Notoginsenoside Ft1 increases intracellular Ca2+ accumulation, reduces cAMP levels by activating a signaling network mediated through P2Y12 receptors, and promotes platelet aggregation, thereby exerting a procoagulant effect. Notoginsenoside Ft1 inhibits ferroptosis (ferroptosis) in renal tubular epithelial cells by activating the TGR5 receptor, thereby demonstrating a renal protective effect. Notoginsenoside Ft1 acts as a TGR5 agonist and an FXR antagonist to combat obesity and insulin resistance.
For research use only. We do not sell to patients.
NotoginsenosideFt1 is a saponin found in Panax notoginseng. Notoginsenoside Ft1 inhibits the PI3K/AKT/mTOR signaling pathway, activates the p38 MAPK and ERK1/2 signaling pathways, and increases the proportion of CD8+ T cells, thereby inducing apoptosis and lysosomal cell death in various cancer cells, and promoting angiogenesis. Notoginsenoside Ft1 causes vasodilation by activating glucocorticoid receptors (GR) and estrogen receptor beta (ERβ) in endothelial cells. Notoginsenoside Ft1 increases intracellular Ca2+ accumulation, reduces cAMP levels by activating a signaling network mediated through P2Y12 receptors, and promotes platelet aggregation, thereby exerting a procoagulant effect. Notoginsenoside Ft1 inhibits ferroptosis (ferroptosis) in renal tubular epithelial cells by activating the TGR5 receptor, thereby demonstrating a renal protective effect. Notoginsenoside Ft1 acts as a TGR5 agonist and an FXR antagonist to combat obesity and insulin resistance[1][2][3][4][5][6][7][8].
In Vitro
Notoginsenoside Ft1 (0-10 μM, 0-48 h) significantly promotes HUVECs proliferation and migration, promotes the transition of the cell cycle from G1 to S phase, significantly promotes the formation of tubular structures of HUVECs, and promotes VEGF expression and secretion by inhibiting the PI3K/AKT/mTOR pathway and the Raf/MEK/ERK pathway[1].
Notoginsenoside Ft1 (0-250 μM) promotes platelet aggregation in a dose-dependent manner in Wistar rats (EC50 = 56.42 μM) and exhibits comprehensive procoagulant effects in both human (240 μg/mL, 5 min) and rat plasma (80 μg/mL, 5 min), affecting extrinsic and common coagulation pathways[2].
Notoginsenoside Ft1 (56.4 μM) induces an increase in intracellular Ca²⁺ in platelets and P2Y12-HEK293 cells, significantly inhibits the production of cAMP and induces the phosphorylation of PI3K and Akt[2].
Notoginsenoside Ft1 (1 nM-10 mM, 30 min) stimulates endothelial GRs and ERbs with subsequent activation of the PI3K/Akt and ERK1/2 pathways in rat mesenteric arteries, resulting in phosphorylation of eNOS and the release of NO, which activates soluble guanylyl cyclase in the vascular smooth muscle cells leading to vasodilatation[3].
Notoginsenoside Ft1 (0.1-100 μM, 24 h) inhibits the proliferation of SH-SY5Y cells (IC50 = 45 μM), causes cell cycle arrest and induces apoptosis involving regulating the p38 MAPK and ERK1/2 pathways[4].
Notoginsenoside Ft1 (0.1-10 μM, 0.5-24 h) significantly activates the luciferase activity of TGR5 and increases the level of cAMP in Tgr5-HEK293 cells and promotes the secretion of GLP-1 in NCI-H716 cells[5].
Notoginsenoside Ft1 (10 μM, 24 h) significantly inhibits the FXR target genes in Caco-2 cells and inhibits the FXR activity induced by GW4064 (HY-50108) in HEK293T cells[5].
Notoginsenoside Ft1 (10 μM, 24 h) has inhibitory effects on HepG2 (IC50 = 46.3 μM), Huh7 (IC50 = 35.2 μM),
and PLC/PRF/5 (IC50 = 58.9 μM) cells, but not on THLE-2 (IC50 = 82.2 μM) cells[6].
Notoginsenoside Ft1 (12.5-50 μM, 12-24 h) induces apoptosis by inhibiting the PI3K/AKT/mTOR pathway and promotes lysosomal cell death by activating TFEB in HepG2 cells[6].
Notoginsenoside Ft1 (0-100 μM, 24 h-14 d) inhibits the growth of MC38, CT26, HT29 cell with IC50 of 32.87, 30.75 and 27.59 μM, inhibits clone formation of MC38 cells and significantly inhibits the migration ability of MC38 and CT26 cells and inhibits colony number[7].
Notoginsenoside Ft1 (5 μM, 24 h) successfully inhibits the ferroptosis model in HK2 cells, as demonstrated by increased cell viability, suppressed ROS accumulation, improved mitochondrial dysfunction, and altered expression of ferroptosis marker proteins[8].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Promoted PI3K, AKT, mTOR, c-Raf, MEK1/2 and ERK1/2 phosphorylation.
Promoted HIF-1α translocation from the cytoplasm to the nucleus in a time-dependent manner.
Significantly increased p-eNOS, but no significant change in total eNOS expression; eNOS expression was almost undetectable in the endothelial removal group.
Increased Akt phosphorylation and ERK1/2 phosphorylation.
Increased the levels of p-GR (Ser211) and p-ERβ (Ser87) in the endothelial layer.
Increased significantly the proportion of early and late apoptotic cells.
Increased expression of cleaved PARP, caspase-9, caspase-8, and caspase-3.
In Vivo
Notoginsenoside Ft1 (1-25 μM for Matrigel plug assay and 0.25-25 mg/kg for ear wound healing assay, i.p., single dose and every other day for 28 days, respectively) promotes the formation of blood vessels in Matrigel plug and wound healing in mice[1].
Notoginsenoside Ft1 (1.25 mg/kg, i.v., single dose) significantly increases thrombosis and shortens the bleeding time in Wistar rats[2].
Notoginsenoside Ft1 (50-100 mg/100 g diet, p.o., for 6 weeks) ameliorates obesity, improves glucose disorder in high fat diet (HFD) mice by activating Tgr5 and enhances hepatic bile acids (BA) synthesis by antagonizing FXR[5].
Notoginsenoside Ft1 (25-50 mg/kg, p.o., once daily for 3 weeks) shows anti-cancer effects in HepG2 xenograft tumor mice model[6].
Notoginsenoside Ft1 (10-30 mg/kg, i.p., once daily for 24 days) markedly inhibits subcutaneous tumor formation in colorectal cancer (CRC) and enhances the proportion of CD8+ T cells in tumor-bearing mice, thus restraining tumor growth[7].
Notoginsenoside Ft1 controls blood sugar in mice, reduces renal tubular damage, and intervenes in the occurrence of renal ferroptosis by activating the JUN signaling pathway[8].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Matrigel plug assay established in Balb/c nude mice (8 weeks old)[1]
Dosage:
1, 5 and 25 μM with Heparin (HY-17567) in Matrigel
Administration:
Intraperitoneal injection (i.p.), single dose
Result:
Formed of a functional vasculature inside the Matrigel.
Increased the hemoglobin content in a dose-dependent manner.
Revealed a dose-dependent increase in staining with the blood vessel endothelial cell marker CD-31 Matrigels with more enlarged and more blood vessels.
Animal Model:
Ear wound healing assay established in Balb/c nude mice (8 weeks old)[1]
Dosage:
0.25 mg/kg, 2.5 mg/kg or 25 mg/kg
Administration:
Intraperitoneal injection (i.p.), every other day for 28 days
Result:
Significantly reduced the diameter of the wound, and more new blood vessels could be observed at the wound edge.
Significantly upregulated the expression of VEGF mRNA.
No significant difference in the weight changes of the mice in each group.
Animal Model:
Diet-induced obesity model established in Tgr5 -/- mice, Cyp27a1-/- mice and wild-type mice[5]
Dosage:
50 and 100 mg/100 g diet
Administration:
Oral administration (p.o.) with diet, for 6 weeks
Result:
Reduced the weight gain of mice, significantly decreased the diameter of fat cells, and reduced the deposition of lipid droplets in the liver.
Reduced fasting metabolic parameters, lowered blood sugar, improved insulin resistance index (HOMA-IR) and enhanced insulin sensitivity.
Increased energy digestion and improved cold tolerance.
Upregulated Cyp7a1 and Cyp27a1 mRNA in the liver and downregulated Fgf15 mRNA in the ileum.
Increased Ucp1 expression in BAT and iWAT, and upregulated genes such as Pgc1a and Prdm16.
Increased PKA substrate phosphorylation, HSL phosphorylation, and serum glycerol levels.
Animal Model:
HepG2 xenograft tumor model established in adult male mice[6]
Dosage:
25 and 50 mg/kg
Administration:
Oral administration (p.o.), once daily for 3 weeks
Result:
Significantly reduced tumor volume and weight.
No significant weight loss caused, and no obvious pathological changes found in major organs.
Reduced KRAS, ERK1/2, c-Fos, and JUND proteins levels.
Animal Model:
MC38 or CT26 -induced CRC model established in C57BL/6J and Balb/c mice, male, SPF grade, aged 6-8 weeks, and weighing 18 g[7]
Dosage:
10 and 30 mg/kg
Administration:
Intraperitoneal injection (i.p.), once daily for 24 days
Result:
Significantly inhibited tumor growth at 30 mg/kg.
No obvious weight loss, no obvious pathological changes in major organs such as liver and kidney.
Significantly increased the proportion of CD8+ T cells in tumors.
DMSO : 100 mg/mL (109.04 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
1.0904 mL
5.4518 mL
10.9036 mL
5 mM
0.2181 mL
1.0904 mL
2.1807 mL
10 mM
0.1090 mL
0.5452 mL
1.0904 mL
View the Complete Stock Solution Preparation Table
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (stored under nitrogen). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Protocol 2
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (2.73 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
Protocol 3
Add each solvent one by one: 10% DMSO 90% Corn Oil
This protocol yields a clear solution of ≥ 0.67 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (6.7 mg/mL) to 900 μLCorn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO,
. All of co-solvents are available by MedChemExpress (MCE).
, Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration:
mg/mL
Method for preparing stock solution:
mg
drug dissolved in
μL
DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take
μL DMSO stock solution, add
μL .
μL , mix evenly, next add
μL Tween 80, mix evenly, then add
μL Saline.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (stored under nitrogen). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
Powered by Bioz
