Schizandrin BCAS# 61281-37-6 |
- Gomisin N
Catalog No.:BCN2271
CAS No.:69176-52-9
Quality Control & MSDS
3D structure
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Number of papers citing our products
| Cas No. | 61281-37-6 | SDF | Download SDF |
| PubChem ID | 108130 | Appearance | White powder |
| Formula | C23H28O6 | M.Wt | 400.47 |
| Type of Compound | Lignans | Storage | Desiccate at -20°C |
| Synonyms | Schizandrin-B; Wuweizisu-B; gamma-Schisandrin | ||
| Solubility | DMSO : 14.29 mg/mL (35.68 mM; Need ultrasonic) H2O : < 0.1 mg/mL (insoluble) | ||
| SMILES | CC1CC2=CC3=C(C(=C2C4=C(C(=C(C=C4CC1C)OC)OC)OC)OC)OCO3 | ||
| Standard InChIKey | RTZKSTLPRTWFEV-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C23H28O6/c1-12-7-14-9-16(24-3)20(25-4)22(26-5)18(14)19-15(8-13(12)2)10-17-21(23(19)27-6)29-11-28-17/h9-10,12-13H,7-8,11H2,1-6H3 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Schisandrin B, a kind of ATR and P-gp inhibitor with high safety, has been shown to produce antioxidant effect on rodent liver and heart. It also has anti-photoaging, and presents promising activities for future development of protective agents against CisPt nephrotoxicity. Combination of schizandrin B and paclitaxel(PTX) can enhance anti-tumor effects and relieve side effects of PTX on rats with mammary carcinoma. |
| Targets | Wnt/β-catenin | Caspase | p53 | P21 | P450 (e.g. CYP17) | P-gp | Fas | ATR |
| In vitro | Protective effects of schizandrin and schizandrin B towards cisplatin nephrotoxicity in vitro.[Pubmed: 24155209]J Appl Toxicol. 2014 Dec;34(12):1311-9.Renal proximal tubular epithelial cells are the main targets of toxic drugs such as cisplatin (CisPt), an alkylating agent indicated for the treatment of solid organ tumors. Current techniques aiming at reducing nephrotoxicity in patients receiving CisPt are still not satisfactory as they can only partially prevent acute kidney injury. New nephroprotective strategies remain to be developed.
Action of schizandrin B, an antioxidant, on lipid peroxidation in primary cultured hepatocytes.[Pubmed: 2624122]Zhongguo Yao Li Xue Bao. 1989 Jul;10(4):353-6.
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| In vivo | Experimental research on Schizandrin B enhancing sensitivity to paclitaxel on rats with mammary carcinoma.[Reference: WebLink]J. Pract. Med., 2012, 28(15):2506-9.To investigate the effects of Schizandrin B (Sch B) on enhancing sensitivity to paclitaxel (PTX) on rats with mammary carcinoma. |
| Kinase Assay | [Effect of schizandrin B on H(2)O(2)-induced apoptosis of human hepatocytes in vitro: role of Fas pathway].[Pubmed: 22543149]Nan Fang Yi Ke Da Xue Xue Bao. 2012 Apr;32(4):583-5, 592.To investigate the role of Fas pathway in H(2)O(2)-induced apoptosis of L02 human hepatocytes and the effect of schisandrin B on Fas pathway.
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| Cell Research | Protective effect of schizandrin B against oxidative damage of UVB irradiated HaCaT cells and its molecular mechanism.[Reference: WebLink]Chinese Pharmacological Bulletin, 2014, 30(4):523-7.To investigate the inhibitory effect of Schizandrin B (SchB) on ultraviolet radiation b (UVB) radiation-induced apoptosis of HaCaT cells. |
Schizandrin B Dilution Calculator
Schizandrin B Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.4971 mL | 12.4853 mL | 24.9707 mL | 49.9413 mL | 62.4266 mL |
| 5 mM | 0.4994 mL | 2.4971 mL | 4.9941 mL | 9.9883 mL | 12.4853 mL |
| 10 mM | 0.2497 mL | 1.2485 mL | 2.4971 mL | 4.9941 mL | 6.2427 mL |
| 50 mM | 0.0499 mL | 0.2497 mL | 0.4994 mL | 0.9988 mL | 1.2485 mL |
| 100 mM | 0.025 mL | 0.1249 mL | 0.2497 mL | 0.4994 mL | 0.6243 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Schisandrin B(Wuweizisu-B) is a dibenzocyclooctadiene derivative isolated from Fructus Schisandrae, has been shown to produce antioxidant effect on rodent liver and heart. IC50 value: Target: in vitro: Schisandrin B exhibits anti-inflammatory activity through modulation of the redox-sensitive transcription factors Nrf2 and NF-κB. SB inhibited mitogen-induced proliferation and cytokine secretion by lymphocytes [1]. Sch B can protect neuronal cells against oxidative challenge, presumably by functioning as a hormetic agent to sustain cellular redox homeostasis and mitoenergetic capacity in neuronal cells [2]. Sch B exerted significant neuroprotective effects against microglial-mediated inflammatory injury in microglia-neuron co-cultures. Sch B significantly downregulated pro-inflammatory cytokines, including nitrite oxide (NO), tumor necrosis factor (TNF)-α, prostaglandin E(2) (PGE(2)), interleukin (IL)-1β and IL-6 [3]. Sch B could inhibit TGF-β induced EMT of 4T1 cells and of primary human breast cancer cells [4]. in vivo: Similar anti-inflammatory effects of SB on lymphocyte proliferation and cytokine secretion were also observed in vivo [1]. Treatment with Sch B in CsA-treated mice significantly suppressed the elevation of blood urea nitrogen (BUN) and serum creatinine levels and attenuated the histopathological changes. Additionally, Sch B also decreased renal MDA levels and increased GSH levels in CsA-treated mice [5].
References:
[1]. Checker R, et al. Schisandrin B exhibits anti-inflammatory activity through modulation of the redox-sensitive transcription factors Nrf2 and NF-κB. Free Radic Biol Med. 2012 Oct 1;53(7):1421-30.
[2]. Lam PY, et al. Schisandrin B as a hormetic agent for preventing age-related neurodegenerative diseases. Oxid Med Cell Longev. 2012;2012:250825.
[3]. Zeng KW, et al. Schisandrin B exerts anti-neuroinflammatory activity by inhibiting the Toll-like receptor 4-dependent MyD88/IKK/NF-κB signaling pathway in lipopolysaccharide-induced microglia. Eur J Pharmacol. 2012 Oct 5;692(1-3):29-37.
[4]. Liu Z, et al. Schisandrin B attenuates cancer invasion and metastasis via inhibiting epithelial-mesenchymal transition. PLoS One. 2012;7(7):e40480.
[5]. Zhu S, et al. Protective effect of schisandrin B against cyclosporine A-induced nephrotoxicity in vitro and in vivo. Am J Chin Med. 2012;40(3):551-66.
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Protective effects of schizandrin and schizandrin B towards cisplatin nephrotoxicity in vitro.[Pubmed:24155209]
J Appl Toxicol. 2014 Dec;34(12):1311-9.
Renal proximal tubular epithelial cells are the main targets of toxic drugs such as cisplatin (CisPt), an alkylating agent indicated for the treatment of solid organ tumors. Current techniques aiming at reducing nephrotoxicity in patients receiving CisPt are still not satisfactory as they can only partially prevent acute kidney injury. New nephroprotective strategies remain to be developed. In the present in vitro study, schizandrin (Schi) and Schizandrin B (Schi B), major phytochemicals from Schisandra chinensis (Turcz.) Baill. fruits, were tested on HK-2 cells along four processes that could help alleviate CisPt toxicity. Results indicated that: (i) both Schi and Schi B enhanced cell survival via reducing apoptosis rate; (ii) only Schi showed moderate effects towards modulation of regeneration capacities of healthy cells; (iii) both Schi and Schi B limited extracellular matrix deposition; and (iv) both compounds could help preventing dedifferentiation processes via the beta-catenin pathway. Schi and Schi B present promising activities for future development of protective agents against CisPt nephrotoxicity.
[Effect of schizandrin B on H(2)O(2)-induced apoptosis of human hepatocytes in vitro: role of Fas pathway].[Pubmed:22543149]
Nan Fang Yi Ke Da Xue Xue Bao. 2012 Apr;32(4):583-5, 592.
OBJECTIVE: To investigate the role of Fas pathway in H(2)O(2)-induced apoptosis of L02 human hepatocytes and the effect of schisandrin B on Fas pathway. METHODS: Real-time quantitative PCR was used to detect the expressions of FAS, fas associated death domain protein (FADD) and caspase-8 mRNA in L02 cells exposed to H(2)O(2). Flow cytometry was employed to assess the cell apoptosis. ELISA, Western blotting and spectrophotometric assay were performed to determine the expressions of FAS protein, FADD protein and caspase-8 activity. RESULTS: Within the dose range of 5-15 mol/L, schisandrin B dose-dependently inhibited FAS and FADD expressions and caspase-8 activation. CONCLUSION: Schisandrin B can partially inhibit H(2)O(2)-induced L02 cell apoptosis possibly by affecting the FAS-FADD-caspase-8 pathway.
[Action of schizandrin B, an antioxidant, on lipid peroxidation in primary cultured hepatocytes].[Pubmed:2624122]
Zhongguo Yao Li Xue Bao. 1989 Jul;10(4):353-6.
The action of Schizandrin B (Sin B) was observed in freshly isolated hepatocytes damaged by FeSO4/cysteine and CCl4. Two types of free radicals, .OH and .CCl3, generated from FeSO4/cysteine and CCl4, respectively, induced lipid peroxidation in hepatocytes. It was found that the speed of lipid peroxidation (MDA production) and the degree of alteration in hepatocyte morphology were closely related to the type of free radicals. MDA production and membrane protrusion of hepatocytes injuries by FeSO4/cysteine were faster and more severe than those observed with CCl4. Sin B was shown to decrease the production of MDA and the release of GPT and LDH, and to increase hepatocyte viability as well as maintaining the integrity of the hepatocyte membrane surface. These actions of Sin B were stronger than vitamin E at the same concentration. It was observed that no inhibitory effect of phenobarbital, a typical inducer of cytochrome P-450, as Sin B induced liver cytochrome P-450, on MDA production in hepatocytes damaged by FeSO4/cysteine. The results suggest that Sin B possesses antioxidant activity.
