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| Targets |
Astragaloside VI targets the epidermal growth factor receptor (EGFR) and activates the EGFR/ERK signaling pathway. It also activates EGFR/MAPK signaling cascades. Through EGFR activation, the compound promotes cell proliferation, wound healing, and neurogenesis. The compound is a triterpenoid saponin that exerts antioxidant and anti-inflammatory effects. Its mechanism involves activation of EGFR and downstream signaling pathways including ERK and MAPK, leading to enhanced cellular proliferation and tissue repair.
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| ln Vitro |
In HaCaT cells, pretreatment with 1 μM astragaloside VI (AS-VI) boosted EGFR activation. The primary intestine metabolite of astragaloside IV, astragaloside VI, exhibits the highest activation of EGFR. It was projected that EGF would lead to 1.5 ± 0.03-fold increase in cell proliferation in positive control HaCaT cells as compared to the control. HaCaT and HDF cell proliferation can also be markedly enhanced by astragaloside VI at specific doses [1]. By triggering the EGFR/MAPK signaling cascade, astragaloside VI stimulates the growth of neural stem cells and improves neurological functional recovery following acute cerebral ischemia injury [2].
In vitro studies have demonstrated that Astragaloside VI (1 microM) enhances EGFR activation in HaCaT cells and significantly promotes cell proliferation in both HaCaT and HDF cells. Compared to control, the positive control EGF is expected to result in a 1.5-fold increase in cell proliferation. Astragaloside VI is the major intestinal metabolite of astragaloside IV and exhibits the strongest EGFR-activating effects among astragaloside metabolites. The compound's ability to activate EGFR and promote cell proliferation has been confirmed in multiple cell types. Its antioxidant and anti-inflammatory activities have also been characterized in vitro. |
| ln Vivo |
Comparing Astragaloside VI to the control, wound healing was enhanced. Astragaloside VI shortened the time needed for wound closure in mice using a basic non-infected wound model by about 2-4 days as compared to the control group. When astragaloside VI was applied topically, pus output was lower than in the control group. Astragaloside VI-treated wounds healed more quickly than those in the petroleum jelly and control groups. Wounds treated with astragaloside VI were fully closed by day 22, however wounds treated with petroleum jelly and blank materials were not fully closed until day 26. A crucial stage in the development of granulation tissue and the healing of wounds is angiogenesis. In wound models that are both infected and non-infected, astragaloside VI promotes vascularization [1]. In the brain following temporary cerebral ischemia, astragaloside VI can efficiently activate the EGFR/MAPK signaling cascade, encourage the proliferation and neurogenesis of NSCs, and enhance the restoration of neurological function in rats following ischemic stroke [2].
In vivo studies have shown that Astragaloside VI accelerates wound healing, shortening closure time by 2-4 days, reducing pus formation, and increasing angiogenesis in infected and non-infected wound models. It promotes neural stem cell proliferation and enhances neurological function recovery in transient cerebral ischemic injury via activating EGFR/MAPK signaling cascades. The compound increases blood vessel formation in both non-infected and infected wound models. In post-ischemic stroke rats, astragaloside VI promotes NSC proliferation and neurogenesis, improving the repair of neurological functions. These findings support its potential in wound healing and neuroprotection. |
| Enzyme Assay |
The in vitro cell-based assay for Astragaloside VI involves treating HaCaT (human keratinocyte) or HDF (human dermal fibroblast) cells with the compound at concentrations such as 1 microM. EGFR activation is assessed by measuring receptor phosphorylation using Western blotting with phospho-specific antibodies. Cell proliferation is measured using standard assays such as MTT, BrdU incorporation, or cell counting. Signaling pathway activation (EGFR/ERK) is confirmed by measuring phosphorylation of downstream targets including ERK. Control experiments include treatment with EGF as a positive control. Data are collected from multiple replicates and analyzed statistically.
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| Cell Assay |
In vitro cellular assays for Astragaloside VI are conducted using HaCaT and HDF cells to evaluate EGFR activation and cell proliferation. Cells are serum-starved and treated with varying concentrations of astragaloside VI. EGFR phosphorylation is measured by Western blotting or ELISA. ERK and MAPK phosphorylation are assessed to confirm downstream signaling activation. Cell proliferation is evaluated using MTT, BrdU, or EdU incorporation assays. Wound healing assays (scratch assays) can be performed to assess the compound's effects on cell migration. The positive control EGF is used to validate the assay system. All experiments include appropriate vehicle controls.
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| Animal Protocol |
In vivo animal studies for Astragaloside VI are performed in wound healing models and cerebral ischemia models. For wound healing, infected and non-infected wound models are created in rodents, and astragaloside VI is administered topically or systemically. Wound closure is monitored, and tissues are collected for histopathological analysis and angiogenesis assessment. For cerebral ischemia, transient middle cerebral artery occlusion (MCAO) models are used, and neurological function recovery is assessed. Neural stem cell proliferation and neurogenesis are evaluated by immunohistochemistry. Standard animal study designs with appropriate control groups are employed.
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| ADME/Pharmacokinetics |
Pharmacokinetic data for Astragaloside VI indicate that it is a major intestinal metabolite of astragaloside IV. The compound is a triterpenoid saponin with a molecular structure consistent with natural product metabolites. Specific pharmacokinetic parameters such as bioavailability, half-life, and tissue distribution are not extensively reported. For in vivo studies, the compound is typically administered topically for wound healing or systemically for neuroprotection studies. Its metabolic stability and clearance would be consistent with other triterpenoid saponins. The compound is for research use only.
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| Toxicity/Toxicokinetics |
Toxicology data for Astragaloside VI are not extensively reported. As a natural product-derived compound, it is expected to have a favorable safety profile. The compound has been evaluated in wound healing and neuroprotection studies without significant adverse effects reported. However, specific toxicity data, including LD50 values, organ toxicity profiles, and genotoxicity assessments, are not readily available. Standard preclinical safety evaluations would be required for therapeutic development. The compound is for research use only.
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| References |
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| Additional Infomation |
Reports indicate that astragaloside VI is present in Astragalus membranaceus, Astragalus mongholicus, and Astragalus niger, and relevant data are available for reference.
Astragaloside VI is a triterpenoid saponin and major intestinal metabolite of astragaloside IV with the strongest EGFR-activating effects among astragaloside metabolites. It accelerates wound healing by activating the EGFR/ERK signaling pathway and promotes neural stem cell proliferation and neurological function recovery in cerebral ischemia via EGFR/MAPK activation. The compound shortens wound closure time by 2-4 days and increases angiogenesis. It has antioxidant and anti-inflammatory properties. Astragaloside VI is a research compound for wound healing and neuroprotection studies. |
| Molecular Formula |
C47H78O19
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|---|---|
| Molecular Weight |
947.110820000001
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| Exact Mass |
946.514
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| CAS # |
84687-45-6
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| PubChem CID |
71448940
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| Appearance |
White to yellow solid powder
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| LogP |
-0.3
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| Hydrogen Bond Donor Count |
12
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| Hydrogen Bond Acceptor Count |
19
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| Rotatable Bond Count |
10
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| Heavy Atom Count |
66
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| Complexity |
1770
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| Defined Atom Stereocenter Count |
26
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| SMILES |
C[C@]12CC[C@@]34C[C@@]35CC[C@@H](C([C@@H]5[C@H](C[C@H]4[C@@]1(C[C@@H]([C@@H]2[C@]6(CC[C@H](O6)C(C)(C)O)C)O)C)O[C@H]7[C@@H]([C@H]([C@@H]([C@H](O7)CO)O)O)O)(C)C)O[C@H]8[C@@H]([C@H]([C@@H](CO8)O)O)O[C@H]9[C@@H]([C@H]([C@@H]([C@H](O9)CO)O)O)O
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| InChi Key |
FLPVEPQEIRRVKG-SXCMWBRFSA-N
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| InChi Code |
InChI=1S/C47H78O19/c1-41(2)26(64-40-35(28(52)21(51)18-60-40)65-39-34(58)32(56)30(54)24(17-49)63-39)9-11-47-19-46(47)13-12-43(5)36(45(7)10-8-27(66-45)42(3,4)59)20(50)15-44(43,6)25(46)14-22(37(41)47)61-38-33(57)31(55)29(53)23(16-48)62-38/h20-40,48-59H,8-19H2,1-7H3/t20-,21+,22-,23+,24+,25-,26-,27-,28-,29+,30+,31-,32-,33+,34+,35+,36-,37-,38+,39-,40-,43+,44-,45+,46-,47+/m0/s1
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| Chemical Name |
(2R,3R,4S,5S,6R)-2-[[(1S,3R,6S,8R,9S,11S,12S,14S,15R,16R)-6-[(2S,3R,4S,5R)-4,5-dihydroxy-3-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyoxan-2-yl]oxy-14-hydroxy-15-[(2R,5S)-5-(2-hydroxypropan-2-yl)-2-methyloxolan-2-yl]-7,7,12,16-tetramethyl-9-pentacyclo[9.7.0.01,3.03,8.012,16]octadecanyl]oxy]-6-(hydroxymethyl)oxane-3,4,5-triol
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~100 mg/mL (~105.58 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (2.64 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (2.64 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (2.64 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.0558 mL | 5.2792 mL | 10.5584 mL | |
| 5 mM | 0.2112 mL | 1.0558 mL | 2.1117 mL | |
| 10 mM | 0.1056 mL | 0.5279 mL | 1.0558 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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