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Synonym name: Ginkgolic Acid C17:1
Catalogue No.: BP0645
Cas No.: 111047-30-4
Formula: C24H38O3
Mol Weight: 374.565
Botanical Source: Knema elegans and Ginkgo biloba (ginkgo)
Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
Can be supplied from milligrams to grams.
For Reference Standard and R&D, Not for Human Use Directly.
Inquire for bulk scale.
HPLC of Ginkgolic Acid C17:1
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
57.5300
8.6969
5.9581
.0123
4.2996
1.2528
Low
95.5296
2.3273
No
Yes
No
No
No
No
0.0
No
No
No
No
Ginkgolic acid C17:1 is a class of natural hydroxybenzoic acid derivatives derived from ginkgo leaves and seeds. Due to its unique chemical structure and diverse biological activities, it has attracted widespread attention in the field of natural product pharmacology in recent years. As an important member of the ginoic acid family, Ginknaric acid C17:1 not only plays a role in plant defense mechanisms, but its potential pharmacological activity also opens up possibilities for the development of novel therapeutic drugs. The structure of Gink Cindic C17:1 has certain functional correlations with salicylic acid, providing a theoretical basis for studying its multiple biological effects such as anti-inflammatory, antibacterial, and anti-tumor effects.
This paper will systematically review the chemical structure and physicochemical properties of Gink Cinic Acid C17:1, plant origin, and extraction methods, with a focus on its pharmacological activity and mechanism of action. Combining druggability parameters and pharmacokinetic characteristics, it will explore its clinical application prospects and future research directions, aiming to provide scientific basis and theoretical support for the drug development of this natural product.
The chemical name of Ginkhonic Acid C17:1 is hydroxybenzoic acid derivative, with the molecular formula C24H38O3 and a molecular weight of 374.5650. Its structural features include a hydroxyl-substituted benzene ring and a fatty acid side chain containing 17 carbon atoms and an unsaturated double bond. This structure gives it both lipophilicity and certain polarity, with a LogP value as high as 8.6969, indicating high hydrophobicity. This high hydrophobicity has a significant impact on its cell membrane penetration ability and biological distribution.
The topological surface area (TPSA) of Gink Acid C17:1 is 57.53 Ų, reflecting moderate molecular polarity, which may affect its binding ability to biomacromolecules. Its water solubility is extremely low (0.0123 mg/mL), limiting its solubility and bioavailability in the aqueous phase. The blood-brain barrier penetration ability is low, indicating limited function in the central nervous system. The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity. The Ames test result was 0.0, indicating no significant genotoxicity.
In summary, the physicochemical properties of Gink Cinic Acid C17:1 suggest that its solubility and bioavailability need to be optimized in drug design, but its safety indicators are good, indicating potential for further development.
Ginkgo biloba (Ginkgo biloba) is mainly found in leaves, seeds, and fruits, with particularly abundant content in ginkgo leaf extracts. As an ancient gymnosperm, ginkgo's leaves contain various bioactive components, including flavonoids, terpenes, and ginkgo acid compounds.
Common methods for extracting Ginkgo Acid C17:1 include solvent extraction, ultrasound-assisted extraction, and liquid chromatography separation. Traditional solvent extraction mostly uses organic solvents such as ethanol, methanol, or ethyl acetate, combined with heating reflux or ultrasonic assistance to improve extraction efficiency. The extract is purified by liquid-liquid separation, silica gel column chromatography, or high-performance liquid chromatography (HPLC), ultimately yielding high-purity Gink Cinic Acid C17:1.
In recent years, green extraction technologies such as supercritical CO2 extraction and microwave-assisted extraction have gradually been applied to the separation of ginkgo acid compounds, offering advantages such as high extraction efficiency, environmental friendliness, and minimal solvent residue. Optimizing the extraction process is of great significance for ensuring the yield and activity of Ginkgo Acid C17:1.
Gink Cinic Acid C17:1 exhibits multiple pharmacological activities, mainly including anti-inflammatory, antibacterial, antitumor, and neuroprotective aspects.
Gink Acid C17:1 exhibits significant anti-inflammatory effects by inhibiting the production and release of inflammatory mediators. In vitro studies have shown that it can downregulate the expression of pro-inflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and cyclooxygenase-2 (COX-2), thereby reducing inflammatory responses. In animal models, Ginknaric Acid C17:1 significantly alleviates edema and cellular infiltration in inflamed tissues, suggesting its potential application value in inflammatory diseases.
Gink Acid C17:1 exhibits inhibitory effects against various Gram-positive and Gram-negative bacteria, especially showing strong antibacterial effects against resistant strains such as Staphylococcus aureus and Escherichia coli. Its antibacterial mechanisms may involve cell membrane destruction, inhibition of protein synthesis, and interference in energy metabolism. The antibacterial activity of Ginkura C17:1 provides a theoretical basis for its role as a natural antibiotic substitute.
In recent years, the antiproliferative and pro-apoptotic effects of Ginknaric Acid C17:1 in tumor cells have gradually been revealed. In vitro experiments have shown that GinkCinic Acid C17:1 can induce cell cycle arrest and apoptosis in various tumor cell lines (such as breast cancer, lung cancer, and colon cancer cells). Its mechanism involves mitochondrial pathway activation, reactive oxygen species (ROS) generation, and regulation of apoptosis-related protein expression. Additionally, Ginknaric Acid C17:1 can inhibit tumor cell migration and invasion, demonstrating its anti-metastatic potential.
Although Ginolate C17:1 has a lower blood-brain barrier penetration ability, some studies suggest it has some protective effects in neuroinflammation and oxidative stress models. By regulating neuroinflammatory factors and antioxidant enzyme activity, Gink Cinate C17:1 may play an adjunctive therapeutic role in neurodegenerative diseases such as Alzheimer's and Parkinson's.
The multiple pharmacological effects of Gink Cinic Acid C17:1 are attributed to its regulation of multiple signaling pathways and molecular targets.
Ginknaric acid C17:1 reduces the transcriptional activity of pro-inflammatory genes and lowers the production of inflammatory mediators by inhibiting the nuclear factor κB (NF-κB) signaling pathway. Additionally, it affects the MAPK (mitogen-activated protein kinase) pathway, regulating cellular stress and inflammatory responses.
Ginkgo acid C17:1 damages the integrity of bacterial cell membranes, leading to leakage of cellular contents and metabolic disorders. At the same time, it also inhibits bacterial protein synthesis and DNA replication, enhancing antibacterial effects.
Ginknaric acid C17:1 activates mitochondrial-dependent apoptosis pathways, promotes cytochrome C release, and activates the caspase family, triggering apoptosis. It also promotes apoptosis signaling by regulating the expression of Bcl-2 family proteins. Additionally, Ginknaric acid C17:1 induces ROS production, leading to increased oxidative stress and further promoting tumor cell death.
Gink Acid C17:1 reduces nerve cell damage by inhibiting neuroinflammatory factor expression and enhancing the antioxidant defense system. It inhibits the activation of microglial cells and reduces neuroinflammatory responses.
The druggability parameters of Ginknaric Acid C17:1 indicate that it faces certain challenges in drug development. A high LogP value (8.6969) indicates extremely high hydrophobicity, resulting in extremely low water solubility (0.0123 mg/mL), which limits oral absorption and bioavailability. Its TPSA value was 57.53, indicating moderate molecular polarity that facilitates cell membrane penetration, but overall strong hydrophobicity may limit distribution in vivo.
The blood-brain barrier has a low penetration capacity, limiting its direct application in central nervous system diseases. The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity and good safety. The Ames test is non-mutagenic, further supporting its safety.
Pharmacokinetic studies are limited. Preliminary data show that Gink Cinic Acid C17:1 is metabolized rapidly in the body and mainly through hepatic metabolic enzyme systems; the activity and toxicity of these metabolites still require further study. To improve druggability, future research may consider strategies such as structural modification, nanocarrier encapsulation, or liposome delivery to improve solubility and bioavailability.
Ginknaric acid C17:1 has broad clinical application potential due to its multiple pharmacological activities. Their anti-inflammatory and antibacterial properties give them value in treating infectious and inflammatory diseases, especially in the context of increasingly severe antibiotic resistance, making the development of natural antimicrobial agents particularly important.
Its antitumor activity offers the potential of Ginkhonic Acid C17:1 as an adjuvant anticancer drug, especially in combination chemotherapy or targeted therapy, where it may exert synergistic effects. Although neuroprotective effects are limited by blood-brain barrier penetration, optimization of drug delivery systems is expected to expand its application in neurodegenerative diseases.
Future research should focus on optimizing the pharmacokinetic properties of Gink Cinic Acid C17:1, precise resolution of its therapeutic targets, and preclinical safety evaluation. Additionally, designing and synthesizing derivatives based on their structural characteristics will help enhance their efficacy and druggability, driving their clinical adaptation.
Ginkhonic acid C17:1, as a naturally occurring hydroxybenzoic acid compound with rich bioactivity, demonstrates broad pharmacological potential in anti-inflammatory, antibacterial, antitumor, and neuroprotective properties. Its unique chemical structure provides multi-target regulation capability and good safety, providing a solid foundation for drug development. However, high hydrophobicity and low water solubility limit their broad clinical application and urgently need to be overcome through drug design and delivery technologies.
Based on existing research, Ginkhonic acid C17:1 has the potential to become a novel natural drug candidate molecule. Future research on its pharmacokinetics and mechanisms needs to be strengthened to promote clinical application. With the development of natural product pharmacology and medicinal chemistry, Ginknaric Acid C17:1 is expected to play an important role in the treatment of various diseases and become one of the key directions for natural drug development.
Shenshuai
Wenjing
Hedandan
