1. Immunology/Inflammation NF-κB Metabolic Enzyme/Protease PI3K/Akt/mTOR
  2. Reactive Oxygen Species (ROS) Akt NO Synthase Aminotransferases (Transaminases)
  3. Ligustrazine hydrochloride

Ligustrazine hydrochloride  (Synonyms: Chuanxiongzine hydrochloride; Tetramethylpyrazine hydrochloride)

Cat. No.: HY-N0935 Purity: 99.93%
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Ligustrazine hydrochloride is an orally active, blood-brain barrier-permeable alkaloid. It can be isolated from Ligusticum striatum DC. Ligustrazine hydrochloride reduces ROS, upregulates the levels of p-Akt/Akt and p-eNOS/eNOS, and decreases ALT and AST. It inhibits glutamate excitotoxicity, calcium overload, oxidative stress, ischemia-reperfusion injury and atherosclerotic plaque progression, enhances synaptic plasticity, and improves neurological function, cerebral infarct volume and brain water content. Ligustrazine hydrochloride possesses anti-inflammatory, antioxidant, lipid-lowering, endothelial protective and hepatoprotective activities. It can be used in studies related to ischemic stroke, cerebral ischemia-reperfusion injury and atherosclerosis.

For research use only. We do not sell to patients.

CAS No. : 76494-51-4

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Customer Review

Based on 11 publication(s) in Google Scholar

Other Forms of Ligustrazine hydrochloride:

Top Publications Citing Use of Products

    Ligustrazine hydrochloride purchased from MedChemExpress. Usage Cited in: Biochem Pharmacol. 2025 Jul 26:241:117193.  [Abstract]

    Ligustrazine (TMP, 25-100 mg/kg; i.p.; once daily for 7 days) can ameliorate liver injury in septic mice: Pathological changes in liver tissues of mice in each group, yellow arrows: hepatic cords; black arrows: hepatocytes. H&E staining results showed that in the Sham group, the liver tissues were structurally intact and morphologically normal, with no cell necrosis; in the CLP group, hepatocytes were swollen and necrotic, and hepatic cords were disorganized, accompanied by extensive inflammatory cell infiltration; compared with the CLP group, liver tissue damage in the CLP + XBJ, CLP + TMP L (25 mg/kg), CLP + TMP M (50 mg/kg), and CLP + TMP H (100 mg/kg) groups was significantly improved, hepatic cord structure was restored, and inflammatory cell infiltration was reduced, with the most significant improvement in the CLP + XBJ and CLP + TMP H groups.

    Ligustrazine hydrochloride purchased from MedChemExpress. Usage Cited in: Biochem Pharmacol. 2025 Jul 26:241:117193.  [Abstract]

    Effects of Ligustrazine (TMP, 25-100 mg/kg; i.p.; once daily for 7 days) on serum levels of IL-6, TNF-α, and IL-10 in septic mice.

    Ligustrazine hydrochloride purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2025 Sep 17:178180.  [Abstract]

    Representative M-mode echocardiograms. Echocardiographic analysis revealed that Ligustrazine (TMP, 60 mg/kg; i.p.; once daily for 10 days) treatment significantly improved 5-FU (20 mg/kg; i.p.; once daily for 10 days)-induced cardiac dysfunction in BALB/c mice.

    Ligustrazine hydrochloride purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2025 Sep 17:178180.  [Abstract]

    Morphological analysis showed that Ligustrazine (TMP, 60 mg/kg; i.p.; once daily for 10 days) attenuated 5-FU (20 mg/kg; i.p.; once daily for 10 days)-induced reductions in heart size, and significantly restored HW/TL ratio in BALB/c mice.

    Ligustrazine hydrochloride purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2025 Sep 17:178180.  [Abstract]

    Representative images of cardiac tissue with HE staining. Images were taken at 40 × and 400 ×. HE staining revealed that Ligustrazine (TMP, 60 mg/kg; i.p.; once daily for 10 days) significantly ameliorated 5-FU (20 mg/kg; i.p.; once daily for 10 days)-induced cardiomyocyte disarray, inflammatory cell infiltration, and histological disruptions in BALB/c mice.

    Ligustrazine hydrochloride purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2025 Sep 17:178180.  [Abstract]

    Representative micrographs were taken at 100 × magnification with a scale bar of 100 μm. Ligustrazine (TMP, 12.5 μM; 48 h) treatment significantly reversed the reduction in cell density induced by 5-FU (10 μM; 48 h).

    Ligustrazine hydrochloride purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2025 Sep 17:178180.  [Abstract]

    Ligustrazine (TMP) (6.25-100 μM; 48 h) alone exhibited no cytotoxic effects on H9C2 cells. Co-treatment with TMP (12.5–50 μM; 48 h) significantly reversed the suppression of​ cell viability induced by​ 10 μM 5-FU.

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    Description

    Ligustrazine hydrochloride is an orally active, blood-brain barrier-permeable alkaloid. It can be isolated from Ligusticum striatum DC. Ligustrazine hydrochloride reduces ROS, upregulates the levels of p-Akt/Akt and p-eNOS/eNOS, and decreases ALT and AST. It inhibits glutamate excitotoxicity, calcium overload, oxidative stress, ischemia-reperfusion injury and atherosclerotic plaque progression, enhances synaptic plasticity, and improves neurological function, cerebral infarct volume and brain water content. Ligustrazine hydrochloride possesses anti-inflammatory, antioxidant, lipid-lowering, endothelial protective and hepatoprotective activities. It can be used in studies related to ischemic stroke, cerebral ischemia-reperfusion injury and atherosclerosis[1][2][3].

    IC50 & Target[2]

    eNOS

     

    In Vitro

    Ligustrazine (1-100 μM) hydrochloride dose-dependently increases NO production in OGD-treated human amniotic epithelial cells by activating the PI3K/Akt pathway, with no significant effect on NO production in normal HAECs[2].
    Ligustrazine (0.1-10 μM) hydrochloride dose-dependently increases p-Akt/Akt and p-eNOS/eNOS in OGD-treated human amniotic epithelial cells by activating the PI3K/Akt pathway, with no significant effect on these factors in normal HAECs[2].
    Ligustrazine hydrochloride protects endothelial cells against LDL-induced damage in an in vitro cell-based system[3].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    In Vivo

    Ligustrazine (10-120 mg/kg; intraperitoneal injection; intravenous injection; oral administration) hydrochloride exerts protective effects on rat models of ischemic stroke, significantly improves neurological function, reduces the levels of brain injury markers, regulates inflammatory and oxidative stress pathways, inhibits cell apoptosis, and repairs blood-brain barrier permeability[1].
    Ligustrazine (20 mg/kg; i.p.; 15 min after model establishment) hydrochloride improves neurological function in male C57BL/6 mouse models of ischemic stroke[1].
    Ligustrazine (1-10 mg/kg; i.p.; administered once at 2 h and 12 h post-operation) hydrochloride protects Wistar rats against cerebral ischemia-reperfusion injury in a dose-dependent manner by activating the PI3K/Akt pathway, which increases the levels of p-Akt and p-eNOS, improves neurological function, and alleviates brain tissue damage[2].
    Ligustrazine (20-80 mg/kg; p.o.; 6 weeks) hydrochloride dose-dependently inhibits the progression of atherosclerosis and hepatic lipid accumulation in Sprague-Dawley rats, with the daily oral dose of 80 mg/kg reducing the aortic lesion area by 49.0% compared with the untreated atherosclerotic control group[3].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Model: Wistar rats[2]
    Dosage: 1 mg/kg; 3 mg/kg; 10 mg/kg
    Administration: i.p.; twice (at 2 hours and 12 hours after operation)
    Result: Increased brain tissue levels of p-Akt (normalized to Akt) in a dose-dependent manner.
    Increased brain tissue levels of p-eNOS (normalized to eNOS) in a dose-dependent manner.
    Significantly improved neurological deficits compared to I/R-only rats.
    Dose-dependently alleviated brain cell shrinkage, nuclear deep staining, edema, and necrosis induced by I/R injury.
    Had its protective effects reversed by pre-treatment with the PI3K inhibitor wortmannin.
    Animal Model: Sprague-Dawley (male, SPF grade, ~200 g at study start, induced via vitamin D3 injection and atherogenic diet)[3]
    Dosage: 20 mg/kg; 80 mg/kg
    Administration: p.o.; daily; 6 weeks
    Result: Decreased total cholesterol by 65.2%, triglycerides by 53.2%, LDL by 71.2%, and slightly increased HDL at 20 mg/kg dose.
    Decreased total cholesterol by 76.7%, triglycerides by 77.9%, LDL by 79.0%, and slightly increased HDL at 80 mg/kg dose.
    Decreased circulating endothelial cells by 42.2% at 20 mg/kg dose.
    Decreased circulating endothelial cells by 60.0% at 80 mg/kg dose.
    Decreased ALT by 13.0% and AST by 10.7% at 20 mg/kg dose.
    Decreased ALT by 49.7% and AST by 14.3% at 80 mg/kg dose.
    Restored total antioxidant capacity and SOD1 activity at both doses.
    Decreased MDA generation by 12.8% at 20 mg/kg dose.
    Decreased MDA generation by 23.8% at 80 mg/kg dose.
    Reduced thoracic aorta lesion area by 18.9% relative to atherosclerotic controls at 20 mg/kg dose.
    Reduced thoracic aorta lesion area by 49.0% relative to atherosclerotic controls at 80 mg/kg dose.
    Reduced hepatic lipid accumulation, reversed elevated hepatic TG and LDL levels, and restored reduced hepatic HDL levels at both doses.
    Dose-dependently inhibited the induction of antioxidant genes (pgc-1α, sod1, catalase, gpx-1) in the aorta and liver, and suppressed mRNA expression of hepatic fatty acid oxidation genes (pgc-1α, pparα, cpt1a) at both doses.
    Formula

    C8H12N2.xHCl

    CAS No.
    Appearance

    Solid

    Color

    White to off-white

    SMILES

    CC1=C(C)N=C(C)C(C)=N1.[x HCl]

    Structure Classification
    Initial Source
    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage

    4°C, sealed storage, away from moisture

    *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

    Solvent & Solubility
    In Vitro: 

    DMSO : 100 mg/mL (Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

    H2O : 100 mg/mL (Need ultrasonic)

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    Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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    This equation is commonly abbreviated as: C1V1 = C2V2

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    In Vivo:

    Select the appropriate dissolution method based on your experimental animal and administration route.

    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.

    • Protocol 1

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% Saline

      Solubility: ≥ 2.5 mg/mL; 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 μL DMSO 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; 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 μL DMSO 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.

    For the following dissolution methods, please prepare the working solution directly. It is recommended to prepare fresh solutions and use them promptly within a short period of time.
    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.

    • Protocol 1

      Add each solvent one by one:  PBS

      Solubility: 100 mg/mL; Clear solution; Need ultrasonic

    In Vivo Dissolution Calculator
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    Working solution concentration: mg/mL
    This product has good water solubility, please refer to the measured solubility data in water/PBS/Saline for details.
    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).
    Purity & Documentation

    Purity: 99.93%

    References
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      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.

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    Product Name:
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