Product name: Salvianolic acid A
Synonym name:
Catalogue No.: BP1247
Cas No.: 96574-01-5
Formula: C₂₆H₂₂O₁₀
Mol Weight: 494.452
Botanical Source: Salviae Miltiorrhizae Radix et Rhizoma
Physical Description:
Type of Compound: Stibene glucosides

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:

Salvianolic acid A has antioxidant, hepatoprotective, antithrombotic effect, and antiplatelet actions. it also has a significant protective effect against isoproterenol-induced myocardial infarction; it activates the Nrf2/HO-1 axis in RPE cells and protects against oxidative stress via activation of Akt/mTORC1 signaling. Salvianolic acid A (oral) can significantly improve glucose metabolism and inhibit oxidative injury as well as protect against impaired vascular responsiveness in STZ-induced diabetic rats. It is a novel matrix metalloproteinase-9 inhibitor, can prevents cardiac remodeling in spontaneously hypertensive rats.

References:

Phytomedicine. 2014 Oct 15;21(12):1725-32.    

Salvianolic acid A reverses paclitaxel resistance in human breast cancer MCF-7 cells via targeting the expression of transgelin 2 and attenuating PI3 K/Akt pathway.    

Chemotherapy resistance represents a major problem for the treatment of patients with breast cancer and greatly restricts the use of first-line chemotherapeutics paclitaxel. 

METHODS AND RESULTS:

The purpose of this study was to investigate the role of transgelin 2 in human breast cancer paclitaxel resistance cell line (MCF-7/PTX) and the reversal mechanism of Salvianolic acid A (SAA), a phenolic active compound extracted from Salvia miltiorrhiza. Western blotting and real-time quantitative polymerase chain reaction (qRT-PCR) indicated that transgelin 2 may mediate paclitaxel resistance by activating the phosphatidylinositol 3-kinase (PI3 K)/Akt signaling pathway to suppress MCF-7/PTX cells apoptosis. The reversal ability of SAA was confirmed by MTT assay and flow cytometry, with a superior 9.1-fold reversal index and enhancement of the apoptotic cytotoxicity induced by paclitaxel. In addition, SAA effectively prevented transgelin 2 and adenosine-triphosphate binding cassette transporter (ABC transporter) including P-glycoprotein (P-gp), multidrug resistance associated protein 1 (MRP1), and breast cancer resistance protein (BCRP) up-regulation and exhibited inhibitory effect on PI3 K/Akt signaling pathway in MCF-7/PTX cells. Taken together, SAA can reverse paclitaxel resistance through suppressing transgelin 2 expression by mechanisms involving attenuation of PI3 K/Akt pathway activation and ABC transporter up-regulation. 

CONCLUSIONS:

These results not only provide insight into the potential application of SAA in reversing paclitaxel resistance, thus facilitating the sensitivity of breast cancer chemotherapy, but also highlight a potential role of transgelin 2 in the development of paclitaxel resistance in breast cancer.    

J Ethnopharmacol. 2014 Sep 29;155(3):1589-96.Prevention of pulmonary fibrosis with salvianolic acid a by inducing fibroblast cell cycle arrest and promoting apoptosis.

Danshen (Salvia miltiorrhiza Bunge) is widely used in traditional Chinese medicine (TCM), often in combination with other herbs, to treat a diversity of ailments. More recent studies have focused on its possible roles in the treatment of respiratory diseases (pneumonia and pulmonary fibrosis) and found that it has pharmacological activity that protects pulmonary morphology and function. However, the mechanism underlying this activity has not yet been clarified. 

METHODS AND RESULTS:

The purpose of this study was to investigate the anti-pulmonary fibrosis effects exerted by Salvianolic acid A (SAA), the ingredient responsible for the pharmacological activity of Danshen, and the underlying mechanisms. Bleomycin (BLM)-induced rat pulmonary fibrosis was used to evaluate the antifibrotic role of SAA, and fibroblast cells were used to study the mechanism involved. BLM-treated rats exhibited increased alveolar wall thickness and collagen deposition in lung tissues, but these pathologies were greatly attenuated by daily administration of SAA. We also found that SAA significantly inhibited the proliferation, adhesion and migration of fibroblasts in vitro. This was partly due to a strong induction of cell cycle arrest and apoptosis upon SAA treatment. Consistent with these phenotypes, we observed decreased expression of the cell cycle-related proteins cyclin D1, cyclin E1, and cyclin B1, and increased expression of p53 and p21 in SAA-treated cells. In addition, the anti-apoptotic Bcl-2 protein decreased in a dose-dependent manner, while cleaved caspase-3 protein increased upon SAA treatment. 

CONCLUSIONS:

These results suggest that the alleviation of rat pulmonary fibrosis by SAA is due to the inhibition of fibroblast proliferation and induction of apoptosis, which occurs mainly through p53-dependent growth arrest and apoptosis. We suggest that SAA should be considered as a potential novel therapeutic agent for the treatment of fibrotic lung diseases.

HPLC of Salvianolic acid A

HNMR of Salvianolic acid A

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

Introduction/Overview

Salvianolic acid A (CAS No.: 96574-01-5) is a typical natural polyphenolic compound, mainly found in the traditional Chinese medicinal material Salvia miltiorrhiza. As one of the most important water-soluble active components in Danshen, Danphenic Acid A has attracted widespread attention in recent years in the field of cardiovascular and cerebrovascular disease prevention and treatment due to its remarkable antioxidant, anti-inflammatory, and vascular protective effects. Numerous studies have shown that Danphenol A not only protects the blood-brain barrier (BBB) by inhibiting matrix metalloproteinase 9 (MMP-9), but also exerts cardiovascular protective effects by regulating various molecular targets. This paper will systematically review the chemical structure and physicochemical properties of Danphenolic Acid A, plant origin and extraction methods, pharmacological activity and mechanism of action, druggability evaluation, and pharmacokinetic characteristics, thereby exploring its clinical application prospects and future development directions.

Chemical structure and physicochemical properties

Danphenol Acid A is a water-soluble phenolic acid compound with a molecular formula of C_27H_22O_11 and a molecular weight of 494.4520. Its structural feature is the presence of multiple phenolic hydroxyl and carboxyl groups, which impart excellent antioxidant activity. The LogP value of tanphenol acid A is 2.8617, indicating moderate lipid solubility and beneficial cell membrane permeability, but its topological pole surface area (TPSA) reaches 184.98 Ų, indicating strong polarity and low water solubility (0.0737 mg/mL), which somewhat limits its oral bioavailability. Tanphenol A has no inhibitory effect on hERG channels; the Ames test result is 0.0, indicating low genotoxicity risk and good safety. Its blood-brain barrier penetration capacity is relatively low, which aligns with its pharmacological properties of protecting the blood-brain barrier function.

Plant Origins and Extraction Methods

Danphenol A is mainly found in Salvia miltiorrhiza, a plant in the Lamiaceae family, especially concentrated in the roots. As a traditional Chinese medicine, Danshen has long been used to treat cardiovascular and cerebrovascular diseases, and the extraction and purification techniques for its active ingredient, Danphenolic Acid A, are becoming increasingly sophisticated.

Common extraction methods include water extraction, alcohol extraction, and ultrasound-assisted extraction. Water extraction is simple and aligns with traditional Chinese medicine techniques, but its extraction efficiency is relatively low. Alcohol extraction methods (such as ethanol or methanol) are widely used because they can effectively dissolve polyphenols. In recent years, the introduction of ultrasound-assisted extraction and microwave-assisted extraction technologies has significantly improved the extraction rate and purity of Danphenic Acid A.

During purification, liquid chromatography (such as high-performance liquid chromatography (HPLC) is commonly used for separation, combined with preparative column chromatography to obtain high-purity tanphenolic acid A. In addition, supercritical fluid extraction technology has also been explored for the green and efficient extraction of danphenic acid A.

Pharmacological activity research

Danphenol A possesses multiple pharmacological activities, mainly including antioxidant, anti-inflammatory, antithrombotic, and blood-brain barrier protection.

Antioxidant effects

Danphenolic acid A contains abundant phenolic hydroxyl groups, which can effectively eliminate free radicals and reduce oxidative stress damage. In vitro studies have shown that Danphenolic acid A can inhibit the production of reactive oxygen species (ROS), protecting cells from oxidative damage. Its antioxidant capacity is superior to other Danshin phenolic acid components, such as Danheolic acid B.

Anti-inflammatory effects

Inflammatory responses play a key role in the pathogenesis of various cardiovascular and cerebrovascular diseases. Tanphenic acid A exerts significant anti-inflammatory effects by inhibiting the nuclear factor κB (NF-κB) signaling pathway, reducing the expression of pro-inflammatory factors such as TNF-α, IL-1β, IL-6. In addition, tanphenolic acid A can inhibit white blood cell adhesion induced by inflammatory mediators, reducing vascular endothelial damage.

Blood-brain barrier protection

The integrity of the blood-brain barrier is crucial for maintaining homeostasis in the central nervous system. Research has found that tanphenic acid A protects nerve function by inhibiting matrix metalloproteinase 9 (MMP-9) activity, reducing the permeability of the blood-brain barrier, and preventing inflammatory cells and harmful substances from entering brain tissue. In addition, the anti-inflammatory effect of tanphenic acid A further reinforces its protective effect against the blood-brain barrier.

Cardiovascular protection

Danphenic acid A exhibits multi-target, multi-mechanism protective effects in the cardiovascular system. It can regulate vasoconstriction and dilation, inhibit platelet aggregation, inhibit inflammation and apoptosis of vascular endothelial cells, promote angiogenesis, and improve myocardial ischemia-reperfusion injury. Animal model studies have shown that Danphenol A significantly reduces the area of myocardial infarction and improves cardiac function.

Mechanism of action and molecular targets

The pharmacological effects of tanphenic acid A involve multiple signaling pathways and several key targets, mainly including:

• Matrix metalloproteinase 9 (MMP-9): Danphenol acid A directly or indirectly inhibits MMP-9 activity, reduces extracellular matrix degradation, and maintains the integrity of the blood-brain barrier.

• Selectin P (SELP): Danphenol acid A regulates SELP expression, reduces adhesion between white blood cells and endothelial cells, and inhibits infiltration of inflammatory cells.

• Peroxisome proliferator-activated receptor γ (PPARG): Danphenol A activates PPARG, regulates lipid metabolism and inflammatory responses, and exerts anti-atherosclerotic effects.

• Angiotensin-converting enzyme (ACE): Danphenic acid A inhibits ACE activity, reduces the formation of vasoconstrictor substances, and improves blood pressure regulation.

• Protein kinase B (AKT1): Danphenolic acid A activates the AKT1 signaling pathway, promoting cell survival and angiogenesis.

• β2 adrenergic receptor (ADRB2): Danphenic acid A regulates ADRB2-mediated myocardial function and improves cardiac contractility.

• Voltage-Gated Potassium Channel (KCNH2): Danphenol A affects the function of the KCNH2 channel, regulates the action potential of myocardial cells, and reduces the risk of arrhythmias.

• Endothelial nitric oxide synthase (NOS3): Danphenic acid A promotes NOS3 expression and activity, enhances nitric oxide (NO) production, and improves vasodilatory function.

• Intercellular Adhesion Molecule 1 (ICAM1) and Vascular Cell Adhesion Molecule 1 (VCAM1): Tanphenol A inhibits the expression of ICAM1 and VCAM1, reducing vascular endothelial inflammatory responses.

• Sodium-calcium exchange protein (SLC8A1): Danphenic acid A regulates SLC8A1 function and maintains calcium homeostasis in myocardial cells.

In summary, Danphenic Acid A regulates inflammation, oxidative stress, apoptosis, and vascular function in the cardiovascular and cerebrovascular systems through multi-target synergistic effects, demonstrating good pharmacological activity.

Druggability evaluation and pharmacokinetics

The druggability parameters of tanphenic acid A indicate that it has certain development potential, but there are also challenges. Its molecular weight is close to 500, meeting the upper limit of Lipinski's rule. The LogP value is moderate, which facilitates cell membrane penetration, but its high TPSA and low water solubility limit its oral absorption. Danphenol A has relatively low blood-brain barrier permeability, which aligns with its pharmacological protective effect on the blood-brain barrier, but it may be limiting in treating central nervous system diseases.

Tanphenol A does not inhibit hERG channels, suggesting good cardiac safety. Ames test negative, low genotoxicity risk, and relatively high safety.

Pharmacokinetics, anthanolic acid A has low oral bioavailability, mainly due to its high polarity and first-pass effect. Its distribution in the body is mainly concentrated in the liver, kidneys, and heart-brain tissues. The metabolic pathway mainly involves the metabolism of phenolic hydroxyl groups in liver enzyme systems and glucuronic acid binding. Excretion is mainly carried out through the kidneys.

To overcome bioavailability limitations, researchers have recently attempted to optimize the pharmacokinetic performance of tanphenic acid A through strategies such as nanocarriers, liposome encapsulation, and structural modification.

Prospects and outlooks for clinical applications

Tanphenic acid A has significant potential value in cardiovascular and cerebrovascular diseases. Its multi-target, multi-mechanism mode of action, especially its protection of the blood-brain barrier and its anti-inflammatory and antioxidant capacity, provide new therapeutic approaches for cerebrovascular diseases such as ischemic stroke and secondary injury after cerebral hemorrhage. At the same time, tanphenol acid A also shows good therapeutic potential for cardiovascular diseases such as myocardial ischemia, atherosclerosis, and hypertension.

Currently, Danphenic acid A is still in basic research and preclinical stages, lacking systematic clinical trial data. In the future, pharmacokinetic optimization should be strengthened, safety evaluations and multicenter clinical trials should be conducted to verify efficacy and safety. In addition, by combining modern drug design with nanotechnology, developing tanphenol acid A as a novel therapeutic drug for cardiovascular and cerebrovascular diseases holds broad prospects.

Conclusion

As an important active ingredient in Danshen, Danshen A demonstrates great potential in the prevention and treatment of cardiovascular and cerebrovascular diseases due to its unique chemical structure and diverse pharmacological activities. By regulating various molecular targets, it exerts multiple mechanisms of anti-inflammatory, antioxidant, and blood-brain barrier protection, making it a hot topic in natural product pharmacology research. Despite challenges such as low bioavailability and druggability, advances in drug delivery technology and structural optimization are expected to make Danphenol A an important candidate for future cardiovascular and cerebrovascular disease treatments. Future research should focus on its clinical translation and in-depth analysis of its mechanisms, aiming to advance its clinical application and achieve successful transformation of natural products into clinical drugs.