Product name: Scutellarein
Synonym name: 6-Hydroxyapigenin
Catalogue No.: BP1277
Cas No.: 529-53-3
Formula: C₁₅H₁₀O₆
Mol Weight: 286.239
Botanical Source: Scutellariae radix
Physical Description:
Type of Compound: Flavonoids

Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle

Storage: Store in a well closed container, protected from air and light. Put into refrigerate or freeze for long term storage.
Whenever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20℃. Generally, these will be useable for up to two weeks.

The product could be supplied from milligrams to grams
Inquire for bulk scale.

Description:

Scutellarein has antioxidant, antitumor, anti-adipogenic, antiviral and anti-inflammatory activities, it can improve neuronal injury, has better protective effect in rat cerebral ischemia. Scutellarein may serve as a SARS-CoV chemical inhibitor, it also exerts strong inhibition towards the tested UDP-glucuronosyltransferase isoforms.

References:

Chin J Physiol. 2014 Aug 31;57(4):182-7.    

Inhibitory effects of scutellarein on proliferation of human lung cancer A549 cells through ERK and NFκB mediated by the EGFR pathway.    

High expression levels of cyclooxygenase-2 (COX-2) contribute a strong proliferative ability to human lung cancer cells, and this function is link to the epidermal growth factor receptor (EGFR) pathway, which was mediated by extracellular-signal-regulated kinase (ERK) and nuclear factor kappa B (NFκB).

METHODS AND RESULTS:

In this study, Scutellarein, a flavonoid compound, was screened for proliferation inhibition at different concentrations (0, 5, 25 and 50 μM) at 24 h or 48 h in human lung cancer cell line A549. Results showed that A549 cell proliferation was inhibited by 50 μM Scutellarein treatment in 24 h and 48 h of treatment. The expression levels of phosphorylated EGFR, phosphorylated ERK, phosphorylated NFκB and COX-2 were reduced in a dose-dependent manner after 24 h Scutellarein treatments at different concentrations. Further, ERK inhibitor U0126 and NFκB inhibitor MG132 also inhibited A549 cell proliferation similar to 50 κM Scutellarein treatment from 24 h to 48 h. 

CONCLUSIONS:

The experimental results showed that Scutellarein could inhibit proliferation of the human lung cancer cell line A549 through ERK and NFκB mediated by the EGFR pathway.    

Pharmacol Biochem Behav. 2014 Mar;118:51-9.    

Neuroprotective effects of scutellarin and scutellarein on repeatedly cerebral ischemia-reperfusion in rats.    

Scutellarin had protective effects against neuronal injury, however, there are few studies on the protective effect of Scutellarein, which is the main metabolite of scutellarin in vivo. 

METHODS AND RESULTS:

This study investigated whether the neural injury by ischemia/reperfusion would be influenced by different doses of scutellarin and Scutellarein. Male Wistar rats were orally administered with scutellarin and Scutellarein at the doses of 0.09, 0.17, 0.35, 0.70, 1.40 mmol/kg, respectively; then after six consecutive days, they were subjected to global ischemia by occlusion of the bilateral common carotid arteries (BCCAO). After reperfusion for about 21 h, neurological and histological examinations were performed. The present results showed that Scutellarein attenuated neuronal cell damage, reduced cerebral water content, regulated the expression of glutamic acid (Glu), aspartic acid (Asp), glycine (Gly), γ-aminobutyric acid (GABA) and taurine (Tau), and improved the Ca(2+)-ATPase and Na(+),K(+)-ATPase activity. Meanwhile, significant difference was found among various doses of scutellarin and Scutellarein. 

CONCLUSIONS:

Our studies indicated that scutellarin and Scutellarein could improve neuronal injury, and Scutellarein had better protective effect than scutellarin in rat cerebral ischemia.    

Int J Mol Med. 2015 Jan;35(1):31-8.    

Scutellarein inhibits cancer cell metastasis in vitro and attenuates the development of fibrosarcoma in vivo.    

Fibrosarcoma is an aggressive and highly metastatic cancer of the connective tissue, for which effective therapeutic methods are limited. Recently, there has been a renewed interest in small molecular compounds from natural products in the treatment of cancer. 

METHODS AND RESULTS:

In the present study, we investigated the compound, Scutellarein, extracted from the perennial herb Scutellaria lateriflora, and it was found to possess anticancer potential. Cell proliferation assay and cell cycle analysis revealed that the proliferation rate of HT1080 human fibrosarcoma cells was significantly suppressed by treatment with Scutellarein through the induction of apoptosis. Moreover, an in vivo experiment using Balb/c nude mice revealed that the volume and weight of the tumors were markedly reduced following treatment with Scutellarein. We also analyzed the effects of Scutellarein on the markers of metastasis, using the HT1080 cells. The results indicated that Scutellarein potently inhibited cell migration, invasion and the expression and activity of matrix metalloproteinase (MMP)-2, -9 and -14. Furthermore, MMP activation and cell survival were suppressed due to the Scutellarein-mediated downregulation of nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) activation. 

CONCLUSIONS:

In conclusion, our data suggest that Scutellarein has the ability to attenuate the development of fibrosarcoma and inhibit cancer cell metastasis.    

HPLC of Scutellarein

NMR of Scutellarein

Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃

Introduction/Overview

Scutellarein (CAS No.: 529-53-3) is a natural flavonoid compound that has attracted widespread attention in the field of natural product pharmacology in recent years due to its remarkable biological activity and potential medicinal value. As a metabolite of baicalein, wild baicalein is replaced by hydroxyl groups at positions C-4', 5, 6, and 7, giving it unique chemical properties and biological activity. Its structure is closely related to apigenin and is also a conjugate acid of scutellarin. Numerous studies have shown that wild baicalin possesses significant anti-inflammatory, antioxidant, antitumor, and neuroprotective pharmacological activities, especially showing good potential in regulating oxidative stress-related diseases.

This review aims to systematically summarize the chemical structure and physicochemical properties of wild baicalin extraction, plant origins and extraction methods, explore its pharmacological activity and mechanism of action in depth, evaluate its druggability and pharmacokinetic characteristics, look ahead to its clinical application prospects, and provide theoretical basis and practical guidance for subsequent research and drug development.

Chemical structure and physicochemical properties

Wild baicalin belongs to the flavonoid class of compounds, with the chemical formula C15H10O6 and a molecular weight of 286.2390. Its basic framework consists of a flavonoid structure, specifically 2-phenyl-4H-1benzopyran-4 ketone, with hydroxyl groups located at C-4', 5, 6, and 7, forming a multi-hydroxyl-substituted flavonoid structure. This structure endows Wild Scutellaria with strong free radical scavenging and metal ion chelation abilities, forming the basis of its antioxidant activity.

In terms of physicochemical properties, the LogP value of wild baicalin is about 2.0096, indicating moderate lipid solubility that facilitates cell membrane penetration. The polarized surface area (TPSA) is 111.13 Ų, indicating high polarity, affecting its bioavailability and ability to penetrate the blood-brain barrier. Low water solubility (0.0332 mg/mL) suggests limited solubility in the aqueous phase and may affect oral absorption. Low blood-brain barrier penetration suggests limited distribution in the central nervous system. The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity. The Ames test result was 0.6, indicating a low genotoxicity risk and good safety.

Plant Origins and Extraction Methods

Wild Scutellaria is mainly found in the genus Scutellaria in the Lamiaceae family, with Scutellaria baicalensis being the primary source. The roots of wild Scutellaria baicalensis are rich in flavonoids, among which wild baicalin is one of the important active ingredients, widely distributed in the roots, stems, leaves, and other parts of the plant.

Traditional extraction methods mainly use solvent extraction techniques, such as ethanol, methanol, or water-alcohol mixed solvents. The extraction process typically includes crushing plant material, soaking, reflux extraction, or ultrasound-assisted extraction, followed by filtration and concentration to obtain the crude extract. To improve purity, column chromatography (such as silica gel columns, C18 reversed phase columns) or high-performance liquid chromatography (HPLC) are commonly used for separation and purification.

In recent years, green and efficient technologies such as supercritical CO2 extraction and microwave-assisted extraction have gradually been applied to the extraction of wild baicalin, significantly improving extraction efficiency and purity, and reducing solvent usage and environmental pollution. In addition, enzyme-assisted extraction technology has also been explored to improve the extraction rate of wild baicalin.

Pharmacological activity research

Anti-inflammatory effects

Wild baicalin demonstrates significant anti-inflammatory activity. Multiple in vitro and in vivo studies have shown that wild baicalin can inhibit the expression and release of inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), nitric oxide (NO), and cyclooxygenase-2 (COX-2). Its anti-inflammatory mechanism mainly regulates the nuclear factor κB (NF-κB) signaling pathway, inhibits the transcription of inflammatory genes, and alleviates inflammatory responses.

Antioxidant effects

Wild baicalin is a polyhydroxyflavonoid with a powerful free radical scavenging ability. It can directly eliminate reactive oxygen species (ROS) and reactive nitrogen (RNS), reducing oxidative damage. Additionally, wild baicalin activates the intracellular antioxidant defense system, regulating key antioxidant enzymes such as superoxide dismutase (SOD1, SOD2), catalase peroxide (CAT), glutathione peroxidase (GPX1), and heme oxygenase-1 (HMOX1), enhancing cells' resistance to oxidative stress.

Neuroprotective effects

Due to its antioxidant and anti-inflammatory properties, wild baicalin shows potential in the field of neuroprotection. Research shows that wild baicalin can reduce damage to nerve cells caused by oxidative stress and inflammation, improve cognitive function, and slow the progression of neurodegenerative diseases such as Alzheimer's and Parkinson's.

Antitumor effects

Wild baicalin exhibits effects in various tumor cell lines by inhibiting proliferation, inducing apoptosis, and blocking the cell cycle. Its anti-tumor mechanism involves regulating multiple signaling pathways, including PI3K/Akt, MAPK, Wnt/β-catenin, etc., affecting tumor cell growth, migration, and invasion capabilities.

Other activities

In addition, wild baicalin exhibits multiple biological activities including antibacterial, antiviral, cardiovascular protection, and liver protection, demonstrating its potential as a multi-target drug.

Mechanism of action and molecular targets

The pharmacological effects of wild baicalin mainly work by regulating oxidative stress and inflammation-related signaling pathways. Its key molecular targets include:

• NFE2L2/NRF2: Wild baicalin can activate NRF2 transcription factors, promote their intranuclear translocation, and induce the expression of downstream antioxidant enzyme genes (such as SOD1, SOD2, CAT, GPX1, HMOX1), enhancing cellular antioxidant defenses and reducing oxidative damage.

• SOD1, SOD2, CAT, GPX1, HMOX1: These antioxidant enzymes are key enzymes for clearing ROS in cells. Wild baicalin promotes redox balance by upregulating their expression.

• NF-κB signaling pathway: Wild Scutellaria inhibits NF-κB activation, reduces the expression of inflammatory factors, and alleviates inflammatory responses.

• Signaling pathways such as MAPK and PI3K/Akt: Involved in regulating cell proliferation, apoptosis, and metabolism, wild baicalin exerts antitumor and neuroprotective effects by modulating these pathways.

Additionally, wild baicalin as a conjugate acid of lamp flower hormone may regulate its bioactivity and pharmacokinetic properties through metabolic transformation.

Druggability evaluation and pharmacokinetics

Druggability evaluation of wild baicalin shows certain advantages and limitations. Its molecular weight of 286.24 conforms to the Lipinski rule, with a moderate LogP value, indicating good cell membrane permeability. TPSA is relatively high, which may limit its oral bioavailability. Low water solubility suggests that its absorption and distribution in the body may be limited.

The low penetration capacity of the blood-brain barrier limits its direct application in central nervous system diseases, but it also reduces the risk of central side effects. The hERG inhibitory test was negative, indicating low cardiotoxicity and good safety. Ames test results show that it carries a low risk of genotoxicity.

Pharmacokinetic studies show that wild baicalin is absorbed orally slowly, has limited bioavailability, and metabolism in the body mainly occurs through hepatic enzyme systems, producing various metabolites. Its metabolites may exhibit different bioactive and pharmacokinetic characteristics. To improve its pharmacokinetic properties, strategies such as nanoformulations, liposome encapsulation, and structural modification have been widely explored.

Prospects and outlooks for clinical applications

With its multi-target and multi-mechanism pharmacological activity, Wild Scutellaria shows broad clinical application prospects. Its potential in anti-inflammatory, antioxidant, neuroprotection, and antitumor areas offers new approaches for the treatment of related diseases.

In the treatment of neurodegenerative diseases, cardiovascular diseases, chronic inflammatory diseases, and tumors, wild baicalin is expected to play an adjunctive therapeutic role as a single drug or in combination therapy. However, clinical research on wild baicalin is still in its early stages and lacks systematic clinical trial data. Its low water solubility and limited bioavailability are the main bottlenecks restricting its clinical application.

Future research should focus on optimizing its pharmacokinetic characteristics, developing efficient delivery systems, deeply analyzing its mechanism of action and safety assessment, and promoting clinical translation. In addition, the design and synthesis of derivatives based on the structure of wild baicalin also provide broad opportunities for new drug development.

Conclusion

Wild baicalin is, as an important natural flavonoid compound, has become a hot topic in natural product pharmacology research due to its remarkable anti-inflammatory, antioxidant, and various pharmacological activities. Systematic studies in chemistry, pharmacology, and druggability have laid a solid foundation for its clinical application. Despite challenges such as water solubility and bioavailability, with the development of modern drug delivery technologies and structural modification strategies, wild baicalin is expected to become a novel natural drug candidate molecule for treating various diseases. In the future, it is necessary to strengthen preclinical and clinical research to comprehensively evaluate efficacy and safety, promote clinical application, and benefit human health.