| Size | Price | |
|---|---|---|
| Other Sizes |
| Targets |
Natural flavone; anti-inflammatory, anti-tumor, anti-oxidant, neuroprotective, anti-fungal activities
Breviscapine targets multiple pathways including PI3K/AKT, where it decreases the levels of p-PI3K and p-AKT in a concentration-dependent manner. It also modulates RANKL-mediated MAPK and NF-κB signaling pathways in osteoclasts and downregulates STAT3/Girdin/Akt signaling in HCC cells. The compound regulates the proliferation and apoptosis of colorectal cancer (CRC) cells through the PI3K/AKT pathway. |
|---|---|
| ln Vitro |
Breviscapine is a crude extract of several flavonoids of Erigeron breviscapus (Vant.) Hand.-Mazz., containing more than 85% of scutellarin, which has been traditionally used in China as an activating blood circulation medicine to improve cerebral blood supply. Accumulating evidence from various in vivo and in vitro studies has shown that breviscapine exerts a broad range of cardiovascular pharmacological effects, including vasodilation, protection against ischaemia/reperfusion (I/R), anti-inflammation, anticoagulation, antithrombosis, endothelial protection, myocardial protection, reduction of smooth muscle cell migration and proliferation, anticardiac remodeling, antiarrhythmia, blood lipid reduction, and improvement of erectile dysfunction. In addition, several clinical studies have reported that breviscapine could be used in conjunction with Western medicine for cardiovascular diseases (CVDs) including coronary heart disease, myocardial infarction, hypertension, atrial fibrillation, hyperlipidaemia, viral myocarditis, chronic heart failure, and pulmonary heart disease. However, the protective effects of breviscapine on CVDs based on experimental studies along with its underlying mechanisms have not been reviewed systematically. This paper reviewed the underlying pharmacological mechanisms in the cardioprotective effects of breviscapine and elucidated its clinical applications[1].
In vitro studies demonstrate that breviscapine (25-100 μM) attenuates the migration and invasion abilities of CRC cells in Transwell assays. It regulates cell proliferation and apoptosis through the PI3K/AKT pathway, with decreased p-PI3K and p-AKT levels observed with increasing breviscapine concentrations. The reduced cell proliferation and increased apoptosis triggered by breviscapine can be reversed by treatment with the PI3K/AKT activator 740Y-P. Breviscapine also suppresses cell migration, invasion, and EMT progress through the PI3K/AKT pathway. |
| ln Vivo |
Breviscapine is one of the extracts of several flavonoids of Erigeron breviscapus. Scutellarin is the main active component of breviscapine, and the qualitative or quantitative criteria as well. Scutellarin and its analogs share a similar skeleton of the flavonoids. Breviscapine has been widely used in the treatment of cerebral infarction and its sequelae, cerebral thrombus, coronary heart disease (CHD), and angina pectoris. Breviscapine has a broad spectrum of pharmacological activities, such as increasing blood flow, improving microcirculation, dilating blood vessels, decreasing blood viscosity, promoting fibrinolysis, inhibiting platelet aggregation, and thrombosis formation, etc. In addition, breviscapine and its analogs have significant value for drug research and development because of the superiority of those significant bioactivities. Furthermore, an increasing number of pharmacokinetic studies have explored the mechanism of scutellarin and its analogs. To provide a comprehensive understanding of the current research on breviscapine, scutellarin, and the analogs, the structural features, distribution situation, preparation method, content determination method, clinical applications, pharmacological action as well as pharmacokinetics are summarized in the present review[2].
In vivo studies in a rat model of middle cerebral artery occlusion showed that breviscapine treatment significantly reduced infarct volume, brain water content, and neurological deficits. In a CRC xenograft model, breviscapine (40 mg/kg) significantly decreased tumor weight and volume. IHC assay revealed lower expression of the cell proliferation marker Ki-67 in the breviscapine-treated group. Breviscapine also reduces cisplatin-induced renal toxicity in mice. |
| Enzyme Assay |
Non-cellular enzyme/receptor binding assays for breviscapine typically involve measuring its effects on PI3K/AKT phosphorylation levels using Western blotting with specific antibodies against p-PI3K, PI3K, p-AKT, and AKT in cell lysates. Cytochrome P450 inhibition can be assessed using standard fluorogenic substrates. The compound's antioxidant activity can be measured using DPPH or ABTS radical scavenging assays. These cell-free systems allow for characterization of the compound's direct biochemical interactions.
|
| Cell Assay |
Cellular assays for breviscapine are conducted using cancer cell lines such as HCT116 and SW480 colorectal cancer cells. Cells are treated with varying concentrations of breviscapine (0, 25, 50, 100 μM), and cell proliferation is measured using MTT or CCK-8 assays. Apoptosis is evaluated by flow cytometry with Annexin V/PI staining. Cell migration and invasion are assessed using Transwell assays. Western blotting is used to measure protein expression of p-PI3K, PI3K, p-AKT, AKT, and EMT markers.
|
| Animal Protocol |
In vivo animal experiments for breviscapine typically use rodent models. In a rat model of middle cerebral artery occlusion, breviscapine is administered and infarct volume, brain water content, and neurological deficits are assessed. In CRC xenograft studies, mice bearing tumor xenografts are treated with breviscapine (40 mg/kg), and tumor weight and volume are measured. IHC analysis of tumor tissues is performed to assess Ki-67 expression.
|
| ADME/Pharmacokinetics |
Pharmacokinetic properties of breviscapine have been studied in various models. As a flavonoid glycoside with molecular weight 1293.34 g/mol, it may have limited oral bioavailability. The compound is soluble in DMSO and can be formulated for in vivo administration. Its half-life, Cmax, and AUC depend on the route of administration and formulation. Breviscapine undergoes metabolism to its aglycone forms.
|
| Toxicity/Toxicokinetics |
Breviscapine has been shown to reduce cisplatin-induced renal toxicity in mice, suggesting a protective effect against chemotherapy-induced organ damage. As a natural product, it is generally considered to have a favorable safety profile. No significant systemic toxicity has been reported at therapeutic doses. However, comprehensive toxicological studies including acute and chronic toxicity assessments are limited. Standard laboratory safety precautions should be followed when handling the compound.
|
| References | |
| Additional Infomation |
Scutellarin is the 7-O-glucuronide of baicalin, belonging to the glycosyloxyflavonoid family. It possesses antitumor activity and is also a proteasome inhibitor. Scutellarin is a glycosyloxyflavonoid, glucuronic acid, trihydroxyflavonoid, and monosaccharide derivative whose function is related to baicalin; it is the conjugate acid of Scutellarin (1-). Scutellarin has been reported to exist in perilla, Indian scutellaria, and other organisms with relevant data.
Breviscapine is a natural product used primarily as a research tool in cardiovascular and neurological disease research. It has been used in the study of cerebral infarction, cerebral thrombosis, and their sequelae. The compound has also demonstrated antitumor properties in colorectal cancer. Breviscapine is not approved for clinical use in most countries and is available as a research reagent. Its mechanism of action involves modulation of PI3K/AKT, MAPK, and NF-κB signaling pathways. |
| Molecular Formula |
C54H84N16O21
|
|---|---|
| Molecular Weight |
1293.34
|
| Exact Mass |
908.164
|
| CAS # |
116122-36-2
|
| PubChem CID |
185617
|
| Appearance |
Light yellow to yellow solid
|
| Density |
1.81g/cm3
|
| Boiling Point |
891.6ºC at 760mmHg
|
| Flash Point |
314.9ºC
|
| Vapour Pressure |
3.91E-34mmHg at 25°C
|
| Index of Refraction |
1.763
|
| LogP |
0.8
|
| Hydrogen Bond Donor Count |
7
|
| Hydrogen Bond Acceptor Count |
12
|
| Rotatable Bond Count |
4
|
| Heavy Atom Count |
33
|
| Complexity |
777
|
| Defined Atom Stereocenter Count |
5
|
| SMILES |
OC1C=CC(C2=CC(=O)C3=C(C(=C(C=C3O2)O[C@@H]2O[C@H](C(=O)O)[C@@H](O)[C@H](O)[C@H]2O)O)O)=CC=1
|
| InChi Key |
DJSISFGPUUYILV-ZFORQUDYSA-N
|
| InChi Code |
InChI=1S/C21H18O12/c22-8-3-1-7(2-4-8)10-5-9(23)13-11(31-10)6-12(14(24)15(13)25)32-21-18(28)16(26)17(27)19(33-21)20(29)30/h1-6,16-19,21-22,24-28H,(H,29,30)/t16-,17-,18+,19-,21+/m0/s1
|
| Chemical Name |
(2S,3S,4S,5R,6S)-6-[5,6-dihydroxy-2-(4-hydroxyphenyl)-4-oxochromen-7-yl]oxy-3,4,5-trihydroxyoxane-2-carboxylic acid
|
| Synonyms |
Breviscapinun; Scutellarin; 27740-01-8; Breviscapin; Scutellarin B; Scutellarein-7-glucuronide; Scutellarein-7beta-D-glucuronide; Breviscapine
|
| HS Tariff Code |
2934.99.9001
|
| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
DMSO: 100 mg/mL (77.32 mM)
H2O: < 0.1 mg/mL |
|---|---|
| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 0.7732 mL | 3.8660 mL | 7.7319 mL | |
| 5 mM | 0.1546 mL | 0.7732 mL | 1.5464 mL | |
| 10 mM | 0.0773 mL | 0.3866 mL | 0.7732 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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