| Size | Price | Stock | Qty |
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| 10mg |
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| 25mg |
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| 50mg |
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| 100mg |
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| 250mg |
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| 500mg |
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| 1g |
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Purity: ≥98%
Danshensu is a naturally occuring phenolic acid of caffeic acid derivatives isolated from Salvia miltiorrhiza, with wide cardiovascular benefit by activating Nrf2 signaling pathway. Salvia miltiorrhiza Bge contains a compound known as danshensu. Danshensu is a powerful antioxidant and radical scavenger, with superior scavenging abilities to vitamin C against free hydroxyl radicals (HO()), superoxide anion radicals (O(2)(-)), 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals, and 2-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS) radicals.
| Targets |
CYP2E1 (IC50 = 12.6 μM); NF-κB
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| ln Vitro |
Danshensu inhibits mitochondrial membrane permeability and transmission by reducing thiol oxidation and lowers lipid peroxidation on the mitochondrial membrane by scavenging free radicals[1]. Danshensu significantly increases H9c2 cardiomyocyte cell viability while reducing lactate dehydrogenase (LDH) release. Danshensu increases Akt and extracellular signal-related kinase 1/2 (ERK1/2) phosphorylation in H9c2 cells, and the protective effects of Danshensu are only partially inhibited by the PI3K or ERK inhibitors wortmannin or U0126. Danshensu may offer significant cardioprotection against MI/R injury, and one of its possible mechanisms may involve activating the PI3K/Akt and ERK1/2 signaling pathways to prevent cardiomyocyte apoptosis. By triggering the Akt and ERK signaling pathways, Danshensu increases Bcl-2 expression while decreasing Bax and active caspase-3 expression. Danshensu has been shown to have biological effects that include increasing microcirculation, reducing the production of reactive oxygen species, inhibiting platelet adhesion and aggregation, guarding the myocardium against ischemia, and shielding endothelial cells from damage brought on by inflammation[2].
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| ln Vivo |
Comparing ISO-administered rats to rats pretreated with danshensu reveals a significant (P<0.001) reduction in ST-segment. When compared to the ISO, its pretreatment also exhibits a significant (P<0.001) decrease in serum cTnI levels. In order to protect rats' hearts from myocardial infarction caused by ISO, danshensu has significant cardioprotective effects[1]. Danshensu significantly decreases cardiac troponin (cTnI) and creatine kinase-MB (CK-MB) production in the serum and myocardium infarct size in the rat model of MI/R injury[2].
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| Enzyme Assay |
Danhong Injection (DHI) as a Chinese patent medicine is mainly used to treat ischemic encephalopathy and coronary heart disease in combination with other chemotherapy. However, the information on DHI's potential drug interactions is limited. The goal of this work was to examine the potential P450-mediated metabolism drug interaction arising from DHI and its active components. The results showed that DHI inhibited CYP2C19, CYP2D6, CYP3A4, CYP2E1 and CYP2C9 with IC50 values of 1.26, 1.42, 1.63, 1.10 and 1.67% (v/v), respectively. Danshensu and rosmarinic acid inhibited CYP2E1 and CYP2C9 with IC50 values of 36.63 and 75.76 μm, and 34.42 and 76.89 μm, respectively. Salvianolic acid A and B inhibited CYP2D6, CYP2E1 and CYP2C9 with IC50 values of 33.79, 21.64 and 31.94 μm, and 45.47, 13.52 and 24.15 μm, respectively. The study provides some useful information for safe and effective use of DHI in clinical practice[3].
We confirmed anti-apoptotic effect of Danshensu both by flow-cytometric analysis and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and this effect was associated with the increase of Bcl-2/Bax ratio and the decrease of active caspase-3 expression. Western blot analysis also showed that Danshensu increased phosphorylation of Akt and extracellular signal-related kinase 1/2 (ERK1/2) in H9c2 cells, and the protective effects of Danshensu were partially inhibited by phosphatidylinositol 3'-kinase (PI3K) specific inhibitor wortmannin or ERK specific inhibitor U0126. Our results suggested that Danshensu could provide significant cardioprotection against MI/R injury, and the potential mechanisms might to suppression of cardiomyocytes apoptosis through activating the PI3K/Akt and ERK1/2 signaling pathways[2]. |
| Cell Assay |
By substituting medium with an "ischemic buffer," which is made to mimic the extracellular environment of myocardial ischemia and contain concentrations of potassium, hydrogen, and lactate ions that are similar to those found in vivo, cardiomyocytes are subjected to ischemia. A humidified atmosphere with 5% CO2 and 95% nitrogen is used to incubate cells in the hypoxic/ischemic chamber for two hours at 37°C. Cardiomyocytes are randomly exposed to one of the following therapies at the start of reperfusion: vehicle, Danshensu (1 or 10 μM), Danshensu plus the PI3K inhibitor wortmannin (10 nM), or Danshensu plus the ERK inhibitor U0126 (10 μM). H9c2 cardiomyocytes are cultured normally in CO2 incubation for the control group's cardiomyocytes at the same time.
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| Animal Protocol |
Paeonol (80 mg kg(-1)) and danshensu (160 mg kg(-1)) were administered orally to Sprague Dawley rats in individual or in combination for 21 days. At the end of this period, rats were administered isoproterenol (85 mg kg(-1)) subcutaneously to induce myocardial injury. After induction, rats were anaesthetized with pentobarbital sodium (35 mg kg(-1)) to record electrocardiogram, then sacrificed and biochemical assays of the heart tissues were performed.
Principal findings: Induction of rats with isoproterenol resulted in a marked (P<0.001) elevation in ST-segment, infarct size, level of serum marker enzymes (CK-MB, LDH, AST and ALT), cTnI, TBARS, protein expression of Bax and Caspase-3 and a significant decrease in the activities of endogenous antioxidants (SOD, CAT, GPx, GR, and GST) and protein expression of Bcl-2. Pretreatment with paeonol and danshensu combination showed a significant (P<0.001) decrease in ST-segment elevation, infarct size, cTnI, TBARS, protein expression of Bax and Caspase-3 and a significant increase in the activities of endogenous antioxidants and protein expression of Bcl-2 and Nrf2 when compared with individual treated groups.[1]
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| References | |
| Additional Infomation |
(2R)-3-(3,4-dihydroxyphenyl)lactic acid is a (2R)-2-hydroxy monocarboxylic acid that is (R)-lactic acid substituted at position 3 by a 3,4-dihydroxyphenyl group. It is a (2R)-2-hydroxy monocarboxylic acid and a 3-(3,4-dihydroxyphenyl)lactic acid. It is a conjugate acid of a (2R)-3-(3,4-dihydroxyphenyl)lactate.
Danshensu has been reported in Salvia miltiorrhiza, Melissa officinalis, and other organisms with data available. See also: Salvia Miltiorrhiza Root (part of). |
| Molecular Formula |
C9H9O5
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| Molecular Weight |
198.17
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| Exact Mass |
198.05282342
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| CAS # |
76822-21-4
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| Related CAS # |
Danshensu sodium salt;67920-52-9;Salvianolic acid B;121521-90-2
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| PubChem CID |
11600642
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| Appearance |
White to gray solid
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| Density |
1.5±0.1 g/cm3
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| Boiling Point |
481.5±40.0 °C at 760 mmHg
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| Flash Point |
259.1±23.8 °C
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| Vapour Pressure |
0.0±1.3 mmHg at 25°C
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| Index of Refraction |
1.659
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| LogP |
-0.29
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| Hydrogen Bond Donor Count |
4
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| Hydrogen Bond Acceptor Count |
5
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| Rotatable Bond Count |
3
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| Heavy Atom Count |
14
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| Complexity |
205
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| Defined Atom Stereocenter Count |
1
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| SMILES |
O([H])[C@@]([H])(C(=O)O[H])C([H])([H])C1C([H])=C([H])C(=C(C=1[H])O[H])O[H]
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| InChi Key |
PAFLSMZLRSPALU-MRVPVSSYSA-N
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| InChi Code |
InChI=1S/C9H10O5/c10-6-2-1-5(3-7(6)11)4-8(12)9(13)14/h1-3,8,10-12H,4H2,(H,13,14)/t8-/m1/s1
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| Chemical Name |
(2R)-3-(3,4-dihydroxyphenyl)-2-hydroxypropanoic acid
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: 10 mg/mL (50.46 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution.
(Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 5.0462 mL | 25.2309 mL | 50.4617 mL | |
| 5 mM | 1.0092 mL | 5.0462 mL | 10.0923 mL | |
| 10 mM | 0.5046 mL | 2.5231 mL | 5.0462 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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