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| Targets |
The exact molecular target is not explicitly defined, but the compound modulates ROS and RNS production in stimulated human neutrophils. It also affects hsp72 synthesis via distinct signaling pathways: in unstimulated neutrophils, the stimulation of hsp72 is dependent on protein kinase C (PKC) (inhibited by H-7), while in unstimulated monocytes, the stimulation of hsp72 is dependent on calcium-calmodulin (inhibited by W-13). [1]
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| ln Vitro |
Taraxasteryl acetate inhibited ROS production in stimulated human neutrophils. For ROS induced by PMA, the inhibition at 1 μM was 5.2±3.9%, at 10 μM was 31.6±4.3%, and at 100 μM was 87.6±3.1%. For ROS induced by FMLP, inhibition at 1 μM was 0.5±3.8%, at 10 μM was 36.0±3.6%, and at 100 μM was 70.3±5.8%. For ROS induced by H₂O₂, inhibition at 1 μM was -8.2±4.3%, at 10 μM was 12.6±5.1%, and at 100 μM was 40.0±2.1%. The IC50 for inhibition of PMA-induced ROS was approximately 43 μM (≈20 μg/ml).
It inhibited RNS production in stimulated human neutrophils. For RNS induced by SNP, inhibition at 1 μM was -5.1±4.3%, at 10 μM was 45.3±4.2%, and at 100 μM was 58.8±3.5%. At 46 μg/ml (100 μM), it produced 50.4% inhibition of SNP-induced RNS. For RNS induced by PMA+W-13, inhibition at 1 μM was -0.2±3.8%, at 10 μM was 24.7±4.8%, and at 100 μM was 49.7±4.1%. It inhibited hsp72 production in stimulated human neutrophils. For hsp72 induced by heat, inhibition at 1 μM was 5.4±6.0%, at 10 μM was 44.3±6.8%, and at 100 μM was 55.8±6.4%. For hsp72 induced by H₂O₂, inhibition at 1 μM was 10.0±7.3%, at 10 μM was 38.9±4.8%, and at 100 μM was 64.5±6.3%. For hsp72 induced by PMA, inhibition at 1 μM was 9.7±4.3%, at 10 μM was 48.9±5.9%, and at 100 μM was 67.8±5.0%. For hsp72 induced by SNP, inhibition at 1 μM was -5.4±5.9%, at 10 μM was 30.4±5.5%, and at 100 μM was 48.0±5.0%. At 10 μM (≈4.6 μg/ml), it produced similar inhibition (35.4%-50.7%) as the crude extract at 100 μg/ml. It stimulated hsp72 production in unstimulated human neutrophils. At 100 μM (46 μg/ml), it increased hsp72 by 95% after 1 hour. This stimulation was inhibited by H-7 (a PKC inhibitor) but not by W-13 (calcium-calmodulin inhibitor) or genistein (tyrosine kinase inhibitor). It stimulated hsp72 production in unstimulated human monocytes. At 100 μM (46 μg/ml), it increased hsp72 by 568% after 1 hour. This stimulation was inhibited by W-13 but not by H-7 or genistein. Cell viability was measured by propidium iodide exclusion and was above 95% in all experiments at the tested concentrations (0.3-100 μM). [1] |
| ln Vivo |
Taraxasteryl acetate showed topical anti-inflammatory activity in the mouse ear edema model. At a dose of 100 μmol/ear (approximately 46 μg/ear), it inhibited arachidonic acid-induced edema by 63.5% (inflammation reduced from 95.1±5.6% in control to 34.7±3.2% with compound), croton oil-induced edema by 47.1% (inflammation reduced from 111.3±4.2% to 58.9±5.3%), and PMA-induced edema by 60.0% (inflammation reduced from 99.5±6.0% to 39.8±5.1%). The reference drug indomethacin (0.2 μmol/ear) showed 42.1%, 37.0%, and 51.2% inhibition respectively. The compound exhibited the same level of activity as the crude dichloromethane extract but at 1/20 of the dose (extract active at 1000 μg/ear). [1]
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| Cell Assay |
For ROS and RNS measurements, human neutrophils were isolated from buffy coats of healthy donors. The fluorescent probe 2',7'-dichlorofluorescin diacetate (DCFH-DA) was used. Neutrophils were stimulated with various agents: H₂O₂, PMA, FMLP (for ROS); SNP, or PMA plus the calmodulin inhibitor W-13 (for RNS). Taraxasteryl acetate was tested at concentrations ranging from 0.3-100 μM. Flow cytometry was used to evaluate fluorescence. Cell viability was simultaneously measured by propidium iodide exclusion and was above 95%.
For hsp72 measurements, human neutrophils or monocytes were incubated with stimulants (heat at 42°C for 120 min, PMA at 10 μM for 120 min, H₂O₂ at 100 μM for 120 min, or SNP at 10 μM for 120 min) to induce hsp72 production. For inhibition studies, taraxasteryl acetate (1-100 μM) was added. For stimulation studies, unstimulated cells were treated with taraxasteryl acetate (100 μM) for 0-5 hours, and hsp72 production was measured by flow cytometry using a monoclonal antibody anti-hsp72. To study mechanisms, unstimulated cells were treated with taraxasteryl acetate (100 μM) plus genistein (10 μM), W-13 (10 μM), or H-7 (10 μM). Viability was >95% in all experiments. [1] |
| Animal Protocol |
For the mouse ear edema test, male Swiss CD-1 albino mice (20-25 g) were used. Inflammation was induced by topical application of arachidonic acid, croton oil, or phorbol-12-myristate-13-acetate (PMA) to the ear. Taraxasteryl acetate was administered topically at a dose of 100 μmol/ear (≈46 μg/ear). Indomethacin (0.2 μmol/ear) was used as a reference drug. Inflammation was evaluated by measuring the weight of a 7 mm diameter ear punch at a prescribed time after induction. The inhibition percentage was calculated based on control inflammation. [1]
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| Toxicity/Toxicokinetics |
In all cell-based experiments (ROS, RNS, and hsp72 assays), cell viability was simultaneously measured by propidium iodide exclusion. Viability was above 95% for all tested concentrations of taraxasteryl acetate (0.3-100 μM), indicating no significant cytotoxicity at these concentrations. [1]
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| References | |
| Additional Infomation |
Taraxacum sterol acetate is a triterpenoid compound that acts as a metabolite. It has been reported to exist in Bejaranoa balansae, Sonchus asper, and other organisms with relevant data.
Taraxasteryl acetate was isolated from Pluchea sagittalis (Lam.) Cabrera (Asteraceae), a plant used in Argentine and Uruguayan folk medicine as a digestive tea and poultice for headache. The compound exhibited a dual effect on hsp72 synthesis: inhibition in stimulated cells and stimulation in unstimulated cells. This is the first report of a natural product with such dual activity on the heat shock protein response. The anti-inflammatory activity of taraxasteryl acetate may be related to its ability to reduce induced ROS and RNS and to modulate hsp72 production. The stimulation of hsp72 in unstimulated neutrophils appears to involve a PKC-dependent pathway (inhibited by H-7), while in unstimulated monocytes it involves a calcium-calmodulin-dependent pathway (inhibited by W-13). The compound showed topical anti-inflammatory activity at 1/20 the dose of the crude extract in ear edema models. [1] |
| Molecular Formula |
C32H52O2
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|---|---|
| Molecular Weight |
468.7541
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| Exact Mass |
468.396
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| Elemental Analysis |
C, 81.99; H, 11.18; O, 6.83
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| CAS # |
6426-43-3
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| PubChem CID |
13889352
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| Appearance |
White to off-white solid powder
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| Density |
1.0±0.1 g/cm3
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| Boiling Point |
502.8±19.0 °C at 760 mmHg
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| Flash Point |
254.8±9.0 °C
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| Vapour Pressure |
0.0±1.3 mmHg at 25°C
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| Index of Refraction |
1.525
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| LogP |
11.96
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| Hydrogen Bond Donor Count |
0
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| Hydrogen Bond Acceptor Count |
2
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| Rotatable Bond Count |
2
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| Heavy Atom Count |
34
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| Complexity |
872
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| Defined Atom Stereocenter Count |
10
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| SMILES |
O(C(C([H])([H])[H])=O)[C@@]1([H])C([H])([H])C([H])([H])[C@@]2(C([H])([H])[H])[C@]([H])(C1(C([H])([H])[H])C([H])([H])[H])C([H])([H])C([H])([H])C1(C([H])([H])[H])[C@]2([H])C([H])([H])C([H])([H])[C@]2([H])[C@@]3([H])[C@]([H])(C([H])([H])[H])C(=C([H])[H])C([H])([H])C([H])([H])[C@]3(C([H])([H])[H])C([H])([H])C([H])([H])[C@@]12C([H])([H])[H]
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| InChi Key |
SFEUTIOWNUGQMZ-ZHLOSDGBSA-N
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| InChi Code |
InChI=1S/C32H52O2/c1-20-12-15-29(6)18-19-31(8)23(27(29)21(20)2)10-11-25-30(7)16-14-26(34-22(3)33)28(4,5)24(30)13-17-32(25,31)9/h21,23-27H,1,10-19H2,2-9H3/t21-,23-,24+,25-,26+,27-,29-,30+,31-,32-/m1/s1
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| Chemical Name |
[(3S,4aR,6aR,6aR,6bR,8aR,12S,12aR,14aR,14bR)-4,4,6a,6b,8a,12,14b-heptamethyl-11-methylidene-1,2,3,4a,5,6,6a,7,8,9,10,12,12a,13,14,14a-hexadecahydropicen-3-yl] acetate
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| Synonyms |
NSC 401400; NSC401400; Taraxasterol Acetate; Taraxasteryl Acetate; NSC-401400
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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 Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| 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) |
H2O : < 0.1 mg/mL
DMSO :< 1 mg/mL |
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.1333 mL | 10.6667 mL | 21.3333 mL | |
| 5 mM | 0.4267 mL | 2.1333 mL | 4.2667 mL | |
| 10 mM | 0.2133 mL | 1.0667 mL | 2.1333 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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