Swertiamarin
Based on 1 publication(s) in Google Scholar
Swertiamarin is an orally active natural product with hypoglycemic, lipid-lowering, anti-rheumatic, and antioxidant activities. Swertiamarin can regulate the levels of pro-inflammatory cytokines, MMP, and NF-κB, and promote osteoblast proliferation. Swertiamarin has antioxidant and hepatoprotective effects against carbon tetrachloride induced rat liver toxicity through the Nrf2/HO-1 pathway. Swertiamarin can attenuate inflammatory mediators by regulating JAK2/STAT3 transcription factors in adjuvant induced arthritis rats. Swertiamarin can be used in the research of diabetes and arthritis.
For research use only. We do not sell to patients.
- Purity : 99.03%
- CAS No.: 17388-39-5
- Formula: C16H22O10
- Molecular Weight:374.34
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Storage:
4°C, protect from light
* In solvent : -80°C, 2 years; -20°C, 1 year (protect from light)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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Publications Citing Use of MedChemExpress (MCE) Swertiamarin
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Biological Activity
Description
In Vitro
Swertiamarin (10-50 μg/mL, 48 h) can regulate the levels of pro-inflammatory cytokines, MMP, and NF-κB and promote the proliferation of osteoblasts[3]. Swertiamarin promotes 3T3-L1 adipocyte differentiation through its active metabolite gentianine, and induces PPAR-g, GLUT-4 and adiponectin mRNA expression, thus having anti diabetes activity[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Calvarial osteoblast cells
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Concentration:10-50 μg/mL
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Incubation Time:48 h
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Result:Improved cell proliferation and ALP levels of osteoblasts.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male Sprague Dawley (SD) rats with hypercholesterolemia induced by supplementing a diet rich in cholesterol[1].
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Dosage:50, 75 mg/kg
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Administration:Oral gavage (p.o.); once daily; 7 days
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Result:Reduced serum total cholesterol, triglyceride concentration and atherosclerosis index.
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Animal Model:Male Sprague Dawley (SD) rat model of liver injury induced by CCl4[2].
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Dosage:100, 200 mg/kg
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Administration:i.g. ; once daily; 8 weeks
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Result:Reduced the levels of serum marker enzymes ALT, AST, and ALP representing liver damage, and restored antioxidant enzyme activity and GSH content in rat liver.
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Animal Model:
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Dosage:2, 5, 10 mg/kg
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Administration:Oral gavage (p.o.); once daily; 2 weeks
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Result:Reduced calcium and TRAP, ACP, and ALP levels in serum and urine of arthritis rats, and increased phosphorus and collagen levels[3]. Inhibited paw thickness, lysosomal enzyme levels, and increased body weight in rats[4].
Chemical Information
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CAS No. 17388-39-5
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Appearance Solid
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Molecular Weight 374.34
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Formula C16H22O10
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Color Off-white to light yellow
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SMILES
C=C[C@@H]([C@@H]1O[C@]([C@@H]([C@@H](O)[C@@H]2O)O)([H])O[C@@H]2CO)[C@@](C3=CO1)(CCOC3=O)O
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, protect from light
* In solvent : -80°C, 2 years; -20°C, 1 year (protect from light)
Publications (1)
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Journal Impact Factor
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Most Recent
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PLoS One
Swertiamarin fails to induce cytotoxicity in colon cancer cell lines: Evidence against a direct anticancer effect. [Abstract]2026 Mar 16;21(3):e0344653. PMID: 41838704
Solvent & Solubility
In Vitro:
DMSO : 175 mg/mL (467.49 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year (protect from light). When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year (protect from light). When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.17 mg/mL (5.80 mM); Clear solution
This protocol yields a clear solution of ≥ 2.17 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (21.7 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.17 mg/mL (5.80 mM); Clear solution
This protocol yields a clear solution of ≥ 2.17 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (21.7 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL. * In solvent : -80°C, 2 years; -20°C, 1 year (protect from light)
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocols
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Collagen-Induced Arthritis
Collagen-induced arthritis (CIA) is an autoimmune murine model of rheumatoid arthritis in which immunization with type II collagen (CII) emulsified in an adjuvant induces a T cell- and autoantibody-driven inflammatory arthritis characterized by synovial hyperplasia, immune cell infiltration, and joint destruction. The model typically relies on genetically susceptible mouse strains (e. g. , DBA/1) and reproduces key features of human rheumatoid arthritis, including anti-collagen immune responses and progressive joint inflammation. Disease onset generally occurs within ~3-4 weeks after immunization, depending on antigen/adjuvant combinations and protocol variation. The immunopathology is driven by adaptive immune activation against CII, leading to systemic and local joint inflammation mediated by pro-inflammatory cytokines and effector immune cells, making CIA a standard preclinical platform for evaluating immunomodulatory and anti-arthritic interventions.
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Mitochondrial membrane-potential fluorescent assay
Mitochondrial membrane potential fluorescent assays estimate ΔΨm in living cells using lipophilic cationic dyes such as TMRM, TMRE, rhodamine 123, and JC-1, which accumulate in mitochondria according to membrane polarization; loss of signal after FCCP or CCCP treatment is interpreted as mitochondrial depolarization. TMRM/TMRE and rhodamine 123 are commonly used for semi-quantitative live-cell microscopy or flow cytometry, while JC-1 can report a shift from red aggregate fluorescence to green monomer fluorescence during depolarization; interpretation requires controls because dye concentration, quenching mode, cell type, dye efflux, and mitochondrial mass can affect fluorescence independently of ΔΨm.
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LPS-Induced Endotoxemia/Systemic Inflammation
Lipopolysaccharide (LPS)-induced endotoxemia is a widely used in vivo model of acute systemic inflammation in which LPS, a Gram-negative bacterial endotoxin, activates innate immune signaling primarily through TLR4, leading to rapid and transient induction of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and tissues. This cytokine surge is commonly used as a measurable readout of systemic inflammatory activation and immune dysregulation, and is typically assessed within hours after intraperitoneal LPS administration in mouse models of endotoxemia. The model captures key features of systemic inflammatory response syndrome, including cytokine release, immune cell activation, and downstream tissue responses, and has been used to evaluate anti-inflammatory interventions such as cytokine modulation, lipid mediators, and immune cell-targeting therapies.
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Mitochondrial membrane-potential and mitochondrial mass staining
Mitochondrial membrane potential staining measures the electrochemical polarization across the mitochondrial inner membrane in live cells using lipophilic cationic fluorescent probes; early rhodamine-based work showed that selective mitochondrial dye accumulation is lost when the mitochondrial transmembrane potential is dissipated. JC-1 reports mitochondrial polarization by shifting from green monomer fluorescence to red J-aggregate fluorescence as dye concentration increases within energized mitochondria; therefore, the red/green fluorescence ratio is used as a relative readout of mitochondrial membrane potential. TMRE or TMRM staining provides a single-channel relative readout because these cationic rhodamine esters accumulate in polarized mitochondria, and lower fluorescence indicates reduced mitochondrial polarization when acquisition and dye-loading conditions are controlled. Mitochondrial mass staining is commonly performed with MitoTracker Green FM or related MitoTracker dyes as
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Hepatotoxicity Study
This protocol evaluates hepatotoxicity using complementary in vivo mouse APAP acute liver injury and in vitro hepatocyte-based cytotoxicity readouts. In vivo APAP injury is assessed by serum ALT/AST, liver histology, hepatic glutathione, protein adducts, necrosis, inflammation, and regeneration-related endpoints. In vitro hepatotoxicity is assessed by loss of viability, leakage of ALT/AST/LDH, oxidative-stress markers, mitochondrial function, nuclear morphology, intracellular calcium, and high-content imaging endpoints.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
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Data Sheet (284 KB)
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SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
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Handling Instructions (2659 KB)
References
[1]. Vaidya H, et al. Swertiamarin: a lead from Enicostemma littorale Blume. for anti-hyperlipidaemic effect. Eur J Pharmacol. 2009 Sep 1;617(1-3):108-12. [Content Brief]
[2]. Wu T, et al. Antioxidant and Hepatoprotective Effect of Swertiamarin on Carbon Tetrachloride-Induced Hepatotoxicity via the Nrf2/HO-1 Pathway. Cell Physiol Biochem. 2017;41(6):2242-2254. [Content Brief]
[3]. Hairul-Islam MI, et al. Swertiamarin, a natural steroid, prevent bone erosion by modulating RANKL/RANK/OPG signaling. Int Immunopharmacol. 2017 Dec;53:114-124. [Content Brief]
[4]. Saravanan S, et al. Swertiamarin attenuates inflammation mediators via modulating NF-κB/I κB and JAK2/STAT3 transcription factors in adjuvant induced arthritis. Eur J Pharm Sci. 2014 Jun 2;56:70-86. [Content Brief]
[5]. Vaidya H, et al. Anti-diabetic activity of swertiamarin is due to an active metabolite, gentianine, that upregulates PPAR-γ gene expression in 3T3-L1 cells. Phytother Res. 2013 Apr;27(4):624-7. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year (protect from light). When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 2.6714 mL | 13.3568 mL | 26.7137 mL | 66.7842 mL |
| 5 mM | 0.5343 mL | 2.6714 mL | 5.3427 mL | 13.3568 mL | |
| 10 mM | 0.2671 mL | 1.3357 mL | 2.6714 mL | 6.6784 mL | |
| 15 mM | 0.1781 mL | 0.8905 mL | 1.7809 mL | 4.4523 mL | |
| 20 mM | 0.1336 mL | 0.6678 mL | 1.3357 mL | 3.3392 mL | |
| 25 mM | 0.1069 mL | 0.5343 mL | 1.0685 mL | 2.6714 mL | |
| 30 mM | 0.0890 mL | 0.4452 mL | 0.8905 mL | 2.2261 mL | |
| 40 mM | 0.0668 mL | 0.3339 mL | 0.6678 mL | 1.6696 mL | |
| 50 mM | 0.0534 mL | 0.2671 mL | 0.5343 mL | 1.3357 mL | |
| 60 mM | 0.0445 mL | 0.2226 mL | 0.4452 mL | 1.1131 mL | |
| 80 mM | 0.0334 mL | 0.1670 mL | 0.3339 mL | 0.8348 mL | |
| 100 mM | 0.0267 mL | 0.1336 mL | 0.2671 mL | 0.6678 mL |
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