•Astragaloside IV

Inhibitors

Product Data Sheet

Screening Libraries

CAS No.:84687-43-4

Molecular Formula:

C41H68O14

Molecular Weight:

784.97

Target:

MMP; ERK; JNK

Pathway:

Metabolic Enzyme/Protease; MAPK/ERK Pathway; Stem Cell/Wnt

Storage:

PowderIn solvent-20°C

3 years

4°C

2 years-80°C

6 months-20°C

1 monthProteins

HY-N0431•Cat. No.:SOLVENT & SOLUBILITY
In Vitro

DMSO : ≥ 100 mg/mL (127.39 mM)* "≥" means soluble, but saturation unknown.

Solvent

Mass
1 mg

5 mg

10 mg

1 mM

1.2739 mL

6.3697 mL

12.7393 mL

5 mM

0.2548 mL

1.2739 mL

2.5479 mL

10 mM

0.1274 mL

0.6370 mL

1.2739 mL

Concentration
Preparing
Stock Solutions

Please refer to the solubility information to select the appropriate solvent.
In Vivo

1. Add each solvent one by one: 10% DMSO >> 40% PEG300 >> 5% Tween-80 >> 45% saline
Solubility: 2.5 mg/mL (3.18 mM); Suspended solution; Need ultrasonic
2. Add each solvent one by one: 10% DMSO >> 90% (20% SBE-β-CD in saline)
Solubility: ≥ 2.5 mg/mL (3.18 mM); Clear solution
3. Add each solvent one by one: 10% DMSO >> 90% corn oil
Solubility: ≥ 2.5 mg/mL (3.18 mM); Clear solution

BIOLOGICAL ACTIVITY
Description

Astragaloside IV, an active component isolated from Astragalus membranaceus, suppresses the activation of ERK1/2 andJNK, and downregulates matrix metalloproteases (MMP)-2, (MMP)-9 in MDA-MB-231 breast cancer cells.

IC₅₀ & Target

MMP-2

MMP-9

ERK1

ERK2

JNK

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In Vitro

Astragaloside IV (10, 20, 40 ng/mL) inhibits NSCLC cell growth, whereas low concentrations of astragaloside IV (1, 2.5, 5ng/mL) has no obvious cytotoxicity on cell viability. Moreover, combined treatment with astragaloside IV significantly
increases chemosensitivity to cisplatin in NSCLC cells. On the molecular level, astragaloside IV co-treatment significantlyinhibits the mRNA and protein levels of B7-H3 in the presence of cisplatin[2]. Astragaloside IV inhibits the viability andinvasive potential of MDA-MB-231 breast cancer cells, suppresses the activation of the mitogen activated protein kinase(MAPK) family members ERK1/2 and JNK, and downregulates matrix metalloproteases (MMP)-2 and -9[4].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Astragaloside IV (10, 20 mg/kg, p.o.) exhibits a potent ability to prevent cognitive deficits induced by transient cerebral
ischemia and reperfusion. Astragaloside IV (10 mg/kg) and Astragaloside IV (20 mg/kg) can significantly decrease the levelsof these cytokines compared to the Model group. Astragaloside IV significantly inhibits the level of TLR4 and its downstreamproteins, suggesting that both MyD88-dependent and -independent pathways play important roles in the anti-inflammatory
effects of Astragaloside IV. Astragaloside IV attenuates NLRP3 and cleaved-caspase-1 expression, and reduces Iba1 protein
expression[1].
In the mice model, the high-dose astragaloside IV group has a significant increase in the 48-hour survival rate [60% (9/15) vs13.3% (2/15), P < 0.05], significant reductions in the serum ALT and AST levels (P < 0.01), and significant reductions in liver
histopathological indices and the degree of apoptosis of hepatocytes (P < 0.01), as well as a significant reduction in thecontent of MDA in liver homogenate (P < 0.01) and a significant increase in the activity of SOD[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.

PROTOCOL
Kinase Assay [4]Briefly, MDA-MB-231 cells treated as indicated or tumor tissues are harvested and lysed in Mg2+ lysis buffer containing 50
mM Tris (pH 7.5), 10 mM MgCl2, 0.5 M NaCl, and protease inhibitor cocktail. Equal amounts of lysates are incubated with
PAK-PBD beads at 4°C for 1 h. PAK-PBD beads are pelleted by centrifugation and washed with ish buffer containing 25 mM
Tris (pH 7.5), 30 mM MgCl2, 40 mM NaCl. Active Rac1 is detected by western blotting.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Assay [2]Cell viability is determined by CCK-8 assay. To be brief, cultured NSCLC cells are seeded into 96-well plates at the density of
4×104 (cells/well). Then 10 µL⁄well CCK8 solution is added and incubated in dark at 37°C for another 2 h. The absorbance isdetermined with the wavelength of 490 nm.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.

AnimalTransient cerebral ischemia and reperfusion is prepared by BCCAO, as BCCAO is considered an ideal model to study

Administration [1]transient cerebral ischemia and reperfusion injury-mediated inflammatory response. Mice are randomLy divided into theSham, Model, Astragaloside IV (10 mg/kg) and Astragaloside IV (20 mg/kg) treatment groups. The Astragaloside IV treatmentgroups are intragastrically administered 7 days before the surgery and terminated on the day of sacrifice. On the day of thesurgery, Astragaloside IV is administrated 2 h prior to ischemia. The Sham-operated and Model groups are treated with
distilled water. After the mice are anesthetized with an intraperitoneal injection of chloral hydrate (350 mg/kg), the bilateralcommon carotid arteries are exposed and carefully separated with a small ventral neck incision and occluded twice (20 mineach) with ligated surgical silk as described previously with minor modifications. There is a 10 min reperfusion period
between the two occlusion periods (ischemia 20 min − reperfusion 10 min − ischemia 20 min). Sham-operated mice aresubjected to the same surgical operation without the surgical silk ligation. Mouse body temperature is maintained at
37±0.5°C during the surgery with heating equipment until recovery from the anesthesia.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.

CUSTOMER VALIDATION• Biomed Pharmacother. 2024 Jun 19:177:117008.

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• Int Immunopharmacol. 2020 Dec;89(Pt A):107169.
• Front Pharmacol. 2018 Apr 16;9:345.
• Eur J Pharmacol. 2020 Oct 15;885:173399.
• Bioengineered. 2022 Apr;13(4):8240-8254.
See more customer validations on www.MedChemExpress.com

REFERENCES[1]. Li M, et al. Astragaloside IV attenuates cognitive impairments induced by transient cerebral ischemia and reperfusion in mice via anti-inflammatory mechanisms.
Neurosci Lett. 2016 Dec 20. pii: S0304-3940(16)30994[2]. He CS, et al. Astragaloside IV Enhances Cisplatin Chemosensitivity in Non-Small Cell Lung Cancer Cells Through Inhibition of B7-H3. Cell Physiol Biochem.
2016;40(5):1221-1229. Epub 2016 Dec 14.
[3]. Liu L, et al. [Protective effect of astragaloside IV against acute liver failure in experimental mice]. Zhonghua Gan Zang Bing Za Zhi. 2016 Oct 20;24(10):772-777[4]. Jiang K, et al. Astragaloside IV inhibits breast cancer cell invasion by suppressing Vav3 mediated Rac1/MAPK signaling. Int Immunopharmacol. 2016 Dec 5;42:195-20

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Caution: Product has not been fully validated for medical applications. For research use only.
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