| Catalog No | Package | Original Price | Price | Inventory | Quantity | Operating |
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| BP5047-5mg | 5mg | $450.00 | Sign in |
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Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
Pterosin B (CAS No.: 34175-96-7) is a type of bracken derived from Pteridium aquilinum) natural indmenone compounds. As an oral active ingredient, fernin B has demonstrated multiple biological activities in recent pharmacological studies, especially showing significant potential in anti-inflammation, antioxidant, anti-myocardial hypertrophy, cognitive function improvement, and metabolic regulation. Its unique molecular structure gives fernin B excellent bioavailability and blood-brain barrier permeability, enabling it to demonstrate positive therapeutic effects in various disease models including neurodegenerative diseases, osteoarthritis, pathological cardiac hypertrophy, and diabetes.
This review aims to systematically summarize the chemical structure and physicochemical properties of fernin B, plant origins and extraction methods, with a focus on evaluating its pharmacological activity and mechanism of action, exploring its druggability and pharmacokinetic characteristics, and, combined with current research progress, anticipate its clinical application prospects, providing theoretical basis and research directions for subsequent drug development and clinical translation.
Frenin B is a natural product of the inmanone class, with a molecular formula of C_13H_14O_3 and a molecular weight of 218.2960. Its structural core is the indinone skeleton, which has strong chemical stability and biological activity. The LogP value of fernin B was 2.7746, indicating moderate lipid solubility, which is beneficial for cell membrane penetration and distribution in vivo. The polar surface area (TPSA) was 37.3 Ų, indicating moderate molecular polarity, which is beneficial for oral absorption and blood-brain barrier penetration. Its low water solubility (0.0645 mg/mL) indicates limited solubility in the aqueous phase, but moderate lipid solubility aids its absorption and distribution in the body.
Notably, fern B does not exhibit hERG channel inhibitory activity, suggesting a low risk of cardiotoxicity; The Ames test result was negative, indicating a low genotoxicity risk. These physicochemical and toxicological parameters provide a solid foundation for the safety and druggability of fern B.
Fern B is mainly isolated from Pteridium aquilinum. Bracken is widely distributed in temperate and subtropical regions worldwide and is a traditional medicinal and edible plant. Its above-ground parts are rich in inmanketone compounds, with fern B being relatively high.
Common extraction methods include:
In recent years, the application of ultrasound-assisted extraction and microwave-assisted extraction technologies has improved the extraction efficiency and purity of fern B, providing technical support for large-scale preparation.
Research on the pharmacological activity of fern B covers multiple disease areas, mainly including anti-inflammation, antioxidant, neuroprotection, anti-myocardial hypertrophy, anti-diabetic, and anti-osteoarthritis.
Research shows that fern B can effectively inhibit mouse chondrocyte hypertrophy and slow the progression of osteoarthritis (OA). Its mechanism involves inhibiting the expression of hypertrophy-related genes in chondrocytes, reducing the release of inflammatory mediators, protecting cartilage matrix integrity, and delaying articular cartilage degeneration.
Frenin B reduces the expression of the transcription factor Klf5 by inhibiting the Sik3 signaling pathway, thereby decreasing β-amyloid (Aβ) deposition, showing significant improvement in cognitive impairment in Alzheimer's (AD) model mice. Its excellent blood-brain barrier permeability makes it a potential candidate molecule for central nervous system drugs.
In the pathological cardiac hypertrophy model, fern B effectively inhibits myocardial cell hypertrophy and improves heart function. This effect may be achieved by regulating intracardiac signaling pathways and inhibiting the expression of hypertrophy-related genes, suggesting its potential application value in cardiovascular disease prevention and treatment.
Frenin B has shown blood sugar-lowering effects in diabetes models and may play a role in improving insulin sensitivity and regulating signaling pathways related to glycolipid metabolism, providing new approaches for the treatment of diabetes and its complications.
Frenin B exhibits certain inhibitory effects on various pathogens, with related targets including bacterial DNA gyrase (GYRA), cell membrane protein (GYPB), cell division protein (FTSZ), fatty acid synthase (FABI), and dihydrofolate reductase (DHFR). Its antibacterial spectrum covers both Gram-positive and Gram-negative bacteria, demonstrating potential anti-infective applications.
The multi-target mechanism of fernin B forms the basis of its broad pharmacological activity. The core mechanism mainly involves the following aspects:
Sik3 (salt-induced kinase 3) is an important kinase that regulates cellular metabolism and inflammatory responses. Fracken B, as an inhibitor of Sik3, regulates the expression of downstream transcription factor Klf5 by blocking its kinase activity, thereby affecting cell proliferation, differentiation, and inflammatory responses, exerting anti-inflammatory, anti-hypertrophy, and neuroprotective effects.
Klf5 (Krüppel-like factor 5) is an important transcription factor regulating cell proliferation and fibrosis. Ferrulin B reduces cell hypertrophy and fibrosis processes by inhibiting Klf5 expression, alleviating myocardial hypertrophy and cartilage degeneration.
In Alzheimer's disease models, Fern B reduces the accumulation of β-amyloid in the brain, alleviating neurotoxicity and cognitive impairment. The specific mechanism may involve promoting Aβ clearance and inhibiting the activity of enzymes that produce related enzymes.
Fracken B inhibits various key bacterial enzymes and proteins, including DNA gyrase (GYRA), fatty acid synthase (FABI), and dihydrofolate reductase (DHFR), interfering with bacterial DNA replication, lipid synthesis, and metabolism, thereby exerting antibacterial effects.
Druggability evaluation of fernin B shows it has promising potential for drug development:
Pharmacokinetics, fern B exhibits good oral absorption and blood-brain barrier crossing ability, is widely distributed in the body, metabolically stable, and excreted mainly by liver and renal excretion. In the future, further systematic research is needed on its half-life, metabolites, and drug interactions to provide data support for clinical applications.
As a multi-target natural product, fern B possesses broad pharmacological activity and good druggability, demonstrating clinical application potential across various disease fields:
Future research should focus on preclinical safety evaluation, pharmacokinetic optimization, formulation development, and clinical trial design for fern B, promoting its translation from laboratory research to clinical application. At the same time, combining modern medicinal chemistry and pharmacological technologies, structural modification and derivative design are carried out to enhance activity and selectivity, expanding application fields.
Frenin B, a natural inmanketone compound derived from bracken, demonstrates therapeutic potential in various diseases such as osteoarthritis, Alzheimer's disease, cardiac hypertrophy, and diabetes due to its unique chemical structure and multi-target pharmacological activity. Its excellent druggability parameters and safety lay the foundation for subsequent drug development. With further research, fern B is expected to become a new generation of natural medicine or lead compound, offering new drug options and therapeutic strategies for related diseases. Future research needs to strengthen molecular-level analysis of its mechanism of action, optimize pharmacokinetic characteristics, and promote clinical translational processes to fully realize its unique value in the field of natural product pharmacology.
