1. NF-κB Immunology/Inflammation TGF-beta/Smad Stem Cell/Wnt Neuronal Signaling Membrane Transporter/Ion Channel
  2. NF-κB Interleukin Related TGF-beta/Smad Calcium Channel
  3. Breviscapine

Breviscapine  (Synonyms: Breviscapinun)

Cat. No.: HY-107802 Purity: 95.59%
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Breviscapine (Breviscapinun) is a flavonoid compound with antioxidant, anti-inflammatory, anti-fibrotic, and neuroprotective activities. Breviscapine ameliorates cerebral ischemia/reperfusion injury and vascular dementia, and inhibits the formation of postoperative abdominal adhesions. The mechanism of action of Breviscapine involves the regulation of oxidative stress, inflammatory cytokines, signaling pathways such as TGF-β/Smad, and cellular calcium overload. Breviscapine is used for research on diseases including cardiovascular and cerebrovascular diseases.

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

Breviscapine

Breviscapine Chemical Structure

CAS No. : 116122-36-2

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Based on 2 publication(s) in Google Scholar

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Description

Breviscapine (Breviscapinun) is a flavonoid compound with antioxidant, anti-inflammatory, anti-fibrotic, and neuroprotective activities. Breviscapine ameliorates cerebral ischemia/reperfusion injury and vascular dementia, and inhibits the formation of postoperative abdominal adhesions. The mechanism of action of Breviscapine involves the regulation of oxidative stress, inflammatory cytokines, signaling pathways such as TGF-β/Smad, and cellular calcium overload. Breviscapine is used for research on diseases including cardiovascular and cerebrovascular diseases[1][2][3].

In Vitro

Breviscapine (6.25-100 μg/L; 24 h) protects primary cortical neurons against H2O2-induced cytotoxicity[1].
Breviscapine (50 μg/L; 24 h) reduces H2O2-induced intracellular calcium overload in primary cortical neurons[1].

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

In Vivo

Breviscapine (2 mg/kg; i.p.; 14 days) significantly improves learning and memory function, restores antioxidant balance, and alleviates neuronal histopathological damage in rats with vascular dementia induced by permanent bilateral common carotid artery ligation[1].
Breviscapine (10-40 mg/kg; i.p.; 10 days) significantly inhibits the formation of postoperative intra-abdominal adhesions in Wistar rats by suppressing inflammatory responses, upregulating peritoneal fibrinolytic activity, and regulating the TGF-β/Smad signaling pathway[2].
Breviscapine (20-100 mg/kg; i.p.; administration starts 7 days before MCAO and continues until sacrifice) dose-dependently alleviates cerebral ischemia/reperfusion injury in Sprague-Dawley rats. Among all regimens, the 100 mg/kg daily i.p. dose initiated 7 days prior to surgery exerts the optimal efficacy, including reducing cerebral infarct volume by approximately 55%, and significantly improving neurological function, levels of inflammatory markers, oxidative stress status, and apoptotic signaling pathways[3].

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

Animal Model: Wistar rats (both sexes, 9-10 weeks old, 200-250 g, cecum scraped + transient ischemia after midline laparotomy)[2]
Dosage: 10 mg/kg; 20 mg/kg; 40 mg/kg
Administration: i.p.; daily; 10 days post-surgery
Result: Decreased the levels of IL-18, IL-6, and tumor necrosis factor-a in blood serum and TGF-b1, connective tissue growth factor, PAI-1 in peritoneal
fluid. But the levels of tPA and the ratio of tPA and PAI-1 in peritoneal fluid were increased.
Significantly inhibited the expression of TGF-b1 and increased the level of Smad7 in the rat cecum tissue.
Animal Model: Wistar (male, 6 weeks old, 230 ± 10 g, permanent occlusion of bilateral common carotid arteries)[1]
Dosage: 2 mg/kg
Administration: i.p.; once daily; 14 days
Result: Improved the performance of learning and memory of VD rats in Morris water maze.
Decreased the level of lipid peroxidation and free radicals, and attenuated the pathological alterations, such as nuclear shrink, cellular edema and irregular arrangement of pyramidal layer in the hippocampal CA 1 area.
Clinical Trial
CAS No.
Appearance

Solid

Color

Light yellow to yellow

SMILES

O=C(C=C(C1=CC=C(O)C=C1)OC2=CC(O[C@@H]([C@@H]([C@@H](O)[C@@H]3O)O)O[C@@H]3C(O)=O)=C4O)C2=C4O.O[C@H]([C@H]([C@@H]([C@@H](C(O)=O)O5)O)O)[C@@H]5OC6=CC(O)=C7C(C=C(C8=CC=C(O)C=C8)OC7=C6)=O

Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Solvent & Solubility
In Vitro: 

DMSO : 100 mg/mL (ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

H2O : < 0.1 mg/mL (insoluble)

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  • Do most proteins show cross-species activity?

    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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