Levistilide A (Synonyms: (Z,Z')-Diligustilide, Z-Ligustilide Dimer) |
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Catalog No.GN10044
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Levistilide A is a natural phthalide compound extracted from the traditional Chinese medicine Ligusticum chuanxiong, possessing multiple biological activities.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 88182-33-6
Sample solution is provided at 25 µL, 10mM.
Levistilide A is a natural phthalide compound extracted from the traditional Chinese medicine Ligusticum chuanxiong, possessing multiple biological activities. Levistilide A can induce cancer cell apoptosis by activating PPARγ and inhibiting the GSK3α/β pathway, as well as promoting ROS generation. Levistilide A can be used in research related to Alzheimer's disease, tumors, and kidney diseases[1-4].
In vitro, Levistilide A (0–80μM) was used to treat MDA-MB-231 and MCF-7 breast cancer cells for 24–48 hours. Levistilide A significantly reduced cell viability and increased lactate dehydrogenase release in a dose-dependent manner, promoting cell damage and death. Levistilide A treatment significantly inhibited GPX4 protein expression while upregulating the mRNA expression of SLC7A11, SLC3A2, GCLC, GCLM, GSS, TFRC, SLC11A2, and NCOA4. Levistilide A treatment markedly increased the protein and mRNA expression levels of Nrf2 and HO-1[5]. Levistilide A (1–10μM) was co-treated with LPS (200ng/ml–1μg/ml) in BV-2 microglial cells and mouse primary microglial cells for 24 hours. Levistilide A significantly inhibited the expression of pro-inflammatory factors NO, IL-6, and TNF-α, reducing the inflammatory response[6].
In vivo, Levistilide A (3mg/kg and 6mg/kg; once daily) was intraperitoneally injected into CCl4-induced liver fibrosis Wistar rats for three weeks. Levistilide A improved the rats' serum liver function, alleviated liver fibrosis, and inhibited angiogenesis[7]. Levistilide A (20mg/kg; once daily) was administered orally to lauric acid-induced thromboangiitis obliterans Wistar rats, starting two days before surgery and continuing for 16 days. Levistilide A improved blood flow, reduced muscle inflammatory necrosis, and decreased serum levels of IL-1β, IL-6, and CRP, as well as NLRP3 expression[8].
References:
[1] Yang Y, Zhang Y, Wang L, et al. Levistolide A Induces Apoptosis via ROS-Mediated ER Stress Pathway in Colon Cancer Cells. Cell Physiol Biochem. 2017;42(3):929-938.
[2] Qu X, Guan P, Han L, et al. Levistolide A Attenuates Alzheimer's Pathology Through Activation of the PPARγ Pathway. Neurotherapeutics. 2021 Jan;18(1):326-339.
[3] Zeng W, Ren J, Li Z, et al. Levistolide A Inhibits PEDV Replication via Inducing ROS Generation. Viruses. 2022 Jan 27;14(2):258.
[4] Li S, Zhao W, Zhao Z, et al. Levistilide A reverses rat hepatic fibrosis by suppressing angiotensin II‑induced hepatic stellate cells activation. Mol Med Rep. 2020 Sep;22(3):2191-2198.
[5] Jing S, Lu Y, Zhang J, Ren Y, et al. Levistilide a Induces Ferroptosis by Activating the Nrf2/HO-1 Signaling Pathway in Breast Cancer Cells. Drug Des Devel Ther. 2022 Sep 7;16:2981-2993.
[6] Zhang M, Duan C, Lin W, et al. Levistilide A Exerts a Neuroprotective Effect by Suppressing Glucose Metabolism Reprogramming and Preventing Microglia Polarization Shift: Implications for Parkinson's Disease. Molecules. 2024 Feb 19;29(4):912.
[7] Zhao ZM, Liu HL, Sun X, et al. Levistilide A inhibits angiogenesis in liver fibrosis via vascular endothelial growth factor signaling pathway. Exp Biol Med (Maywood). 2017 May;242(9):974-985.
[8] Guo H, Sun L, Ling S, et al. Levistilide A Ameliorates NLRP3 Expression Involving the Syk-p38/JNK Pathway and Peripheral Obliterans in Rats. Mediators Inflamm. 2018 Aug 12;2018:7304096.
| Cell experiment [1]: | |
Cell lines | BV-2 cells (mouse microglial cell line) and primary microglial cells |
Preparation Method | Cells were stimulated with lipopolysaccharide (LPS) at 200ng/ml to 1μg/ml and treated with Levistilide A. |
Reaction Conditions | 1 to 10μM; 24 hours |
Applications | Levistilide A significantly inhibited the production of pro-inflammatory cytokines (NO, IL-6, TNF-α) and the expression of iNOS, IL-6, TNF-α, and IL-1β mRNA, reduced ROS production, suppressed IKB-α phosphorylation and NF-κB p65 nuclear translocation, reversed glucose metabolism reprogramming (decreased glycolysis and increased oxidative phosphorylation), inhibited glucose uptake and downregulated glycolysis enzymes (GLUT-1, PKM2, HK-1, HK-2), modulated the AMPK/mTOR pathway (increased AMPK phosphorylation and decreased mTOR phosphorylation). |
| Animal experiment [2]: | |
Animal models | Wistar rats |
Preparation Method | Rats were subcutaneously injected with CCl4 twice a week for six weeks to duplicate the liver fibrosis model and then treated with Levistilide A from the fourth week to the end of the experiment. |
Dosage form | 3mg/kg and 6mg/kg; intraperitoneal injection; daily for three weeks |
Applications | Levistilide A ameliorated serum liver function (reversed the increase of ALT and AST and the decrease of Alb), alleviated liver fibrosis (reduced collagen deposition, decreased hepatic hydroxyproline content, and downregulated the expression of collagen I and α-SMA), and inhibited angiogenesis (reduced the number of new microvessels and vWF expression, partly recovered sinusoidal fenestration, and downregulated the expression of CD31, VEGF, and VEGF-R2). |
References: | |
| Cas No. | 88182-33-6 | SDF | |
| Synonyms | (Z,Z')-Diligustilide, Z-Ligustilide Dimer | ||
| Chemical Name | (1Z,5S,5aS,8Z,10bS,10cS)-1,8-dibutylidene-5,5a,6,7-tetrahydro-1H-5,10c-ethanonaphtho[1,2-c:7,8-c']difuran-3,10(8H,10bH)-dione | ||
| Canonical SMILES | O=C(O/C1=C\CCC)C2=C1CC[C@]3([H])[C@@]2([H])[C@@]45C(C(O/C4=C\CCC)=O)=C[C@]3(CC5)[H] | ||
| Formula | C24H28O4 | M.Wt | 380 |
| Solubility | ≥ 38mg/mL in DMSO | Storage | Store at 2-8°C |
| General tips | Please select the appropriate solvent to prepare the stock solution according to the
solubility of the product in different solvents; once the solution is prepared, please store it in
separate packages to avoid product failure caused by repeated freezing and thawing.Storage method
and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored
at -20°C, please use it within 1 month. To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time. |
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| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.6316 mL | 13.1579 mL | 26.3158 mL |
| 5 mM | 526.3 μL | 2.6316 mL | 5.2632 mL |
| 10 mM | 263.2 μL | 1.3158 mL | 2.6316 mL |
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid 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 master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL saline, mix and clarify.
Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
3. All of the above co-solvents are available for purchase on the GlpBio website.
Quality Control & SDS
- View current batch:
- Purity: >98.50% Appearance: A solid
- COA (Certificate of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Average Rating: 5 (Based on Reviews and 30 reference(s) in Google Scholar.)















