| Size | Price | Stock | Qty |
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| 10mg |
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| 50mg |
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| 100mg |
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| 250mg |
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| 500mg |
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| Other Sizes |
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| Targets |
Biochemical reagent; natural alkaloid
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| ln Vitro |
In human pancreatic, gastric, liver, colon, gallbladder, and prostate cancer cells, sophoridine (0-500 μM; 48 hours) shows substantial growth inhibitory effects with IC50 values of approximately 20 μM to 200 μM[1]. From 26.23% (control) to 38.67% in Miapaca-2 cells and from 29.56% (control) to 39.16% in PANC-1 cells, sophoridine (0 – 20 μM) increases the S phase cell population in 48 hours, almost 1.5 and 1.3 times, respectively[1]. With a considerable increase in the Bax/Bcl-2 ratio, sophoridine (0-20 μM; 48 hours) considerably raises the levels of bad and bax and, in contrast, decreases the levels of bcl-2 and bcl-xl; [1].
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| ln Vivo |
Sophoridine (20 or 40 mg/kg; intraperitoneal injection; 21 days) can stop pancreatic tumor growth in xenografts[1].
Sophoridine suppressed tumor growth in vivo[1] To further validate Sophoridine can inhibit tumor growth in vivo, 2 × 106 Miapaca-2 cells were subcutaneously inoculated in Balb/c nude mice. Sophoridine treatment was administrated from the 7th day at 20 or 40 mg/kg intraperitoneally for 21 days. We found that Sophoridine showed significant inhibitory effects on tumor volume (Fig. 7a and b). The mass of tumors under 20 or 40 mg/kg Sophoridine treatment was significantly less than that of the control group (Fig. 7c). However, there was no significant changes on body weight under Sophoridine treatment (Fig. 7d). Furthermore, the activation of ERK and JNK in xenograft tumor tissues was tested by immunohistochemistry and immunoblotting. It showed that both ERK and JNK were activated in Sophoridine-treated xenograft tumor tissues (Fig. 7e and Additional file 7: Figure S5). In addition, IHC analysis of proliferating cell nuclear antigen (PCNA), cleaved caspase-3 and tunel staining showed significantly fewer proliferative cells, and more apoptotic cells in Sophoridine-treated tumors (Fig. 7e). The liver and kidney biochemical functions were monitored, and there were no obvious difference between control and Sophoridine treatment group (Fig. 7f). The liver and kidney from control and Sophoridine group were stained with H&E to further evaluate the toxicity after treatment. The histological structure of liver and kidney were observed and compared microscopically, and there were almost no histological changes after Sophoridine treatment (Fig. 7g). These results suggest that Sophoridine was an effective agent that can inhibit the growth of xenograft pancreatic tumors in vivo with well-tolerated toxicity[1]. |
| Cell Assay |
Cell viability assay [1]
Cell viability was measured with CCK-8 kit, followed the manufacturer. Briefly, cancer cells seeded in 96-well plates were either treated with Sophoridine at serial concentrations for 48 h, or were treated for various time points (0, 24, 48, or 72 h). After treatment for indicated time, CCK- 8 solution was added and incubated with cancer cells for 4 h. The percentages of cell survival was measured by SpectraMax190 microplate reader based on the absorbance. Cell cycle and apoptosis analysis [1] Propidium iodide (PI) staining assay was used to analyze the cell cycle distribution. After exposed to different concentrations of Sophoridine for 48 h, cancer cells were harvested and fixed with 70% ethanol, followed by centrifugation (3000 rpm, 5 min), incubation with 100 mg/mL RNase in PBS for 30 min at 37 °C, and then staining with 50 mg/mL PI in PBS. The cell cycle distribution were analyzed by a Cell Lab Quanta SC flow cytometer. The Annexin V–FITC Apoptosis Detection Kit (BioVision) was used for the apoptosis analysis. Cells (5 × 105) were exposed to different concentrations of Sophoridine for 48 h. After resuspended in 500 ml binding buffer, cells were incubated with Annexin V– fluorescein isothiocyanate (FITC; 5 ml) and PI (5 ml). After 30-min incubation, cells were analyzed by fluorescence-activated cell sorting (FACS) by flow cytometer. Annexin V–FITC–stained only cells which indicated early apoptosis and cells with Annexin V–FITC- and PI double positive signals were combined for analysis. Colony formation assay [1] Five hundred cancer cells per well were seeded into 6-well plates, and then treated with Sophoridine at different concentrations for 48 h. After treatment, the cells were allowed to form cell colonies for another 7 days. Then cell colonies were fixed with 4% paraformaldehyde and stained with 0.1% crystal violet. After 3 times washing and air-dried, the stained colonies were counted and photographed under microscope. |
| Animal Protocol |
Animal treatment with Sophoridine [1]
BALB/c homozygous (nu/nu) nude mice (6 weeks, 18 g) were used. The mice were maintained in pathogen-free environment for one week after arrival. 2 × 106 Miapca-2 cells in 100 μl PBS were inoculated in the right flank of nude mice. One week later, mice were randomly divided into 3 groups (7 mice/group). 3 groups received relatively an intraperitoneally (i.p.) injection of PBS as control, 20 mg/kg of Sophoridine, or 40 mg/kg of Sophoridine daily. After 3 weeks treatment, mice were sacrificed to weigh the tumors. |
| References | |
| Additional Infomation |
(+)-Matrine has been reported in Euchresta horsfieldii, Gymnospermium darwasicum, and other organisms with data available.
See also: Matrine (annotation moved to). Background: Pancreatic cancer is generally acknowledged as the most common primary malignant tumor, and it is known to be resistant to conventional chemotherapy. Novel, selective antitumor agents are pressingly needed. Methods: CCK-8 and colony formation assay were used to investigate the cell growth. Flow cytometry analysis was used to evaluate the cell cycle and cell apoptosis. The peroxide-sensitive fluorescent probe DCFH-DA was used to measure the intracellular ROS levels. Western blot assay was used to detect the levels of cell cycle and apoptosis related proteins. Xenografts in nude mice were used to evaluate the effect of Sophoridine on pancreatic cancer cell in vivo. Results: Sophoridine killed cancer cells but had low cytotoxicity to normal cells. Pancreatic cancer cells were particularly sensitive. Sophoridine inhibited the proliferation of pancreatic cancer cells and induced cell cycle arrest at S phase and mitochondrial-related apoptosis. Moreover, Sophoridine induced a sustained activation of the phosphorylation of ERK and JNK. In addition, Sophoridine provoked the generation of reactive oxygen species (ROS) in pancreatic cancer cells. Finally, in vivo, Sophoridine suppressed tumor growth in mouse xenograft models. Conclusion: These findings suggest Sophoridine is promising to be a novel, potent and selective antitumor drug candidate for pancreatic cancer.[1] |
| Molecular Formula |
C15H24N2O
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|---|---|
| Molecular Weight |
248.36
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| Exact Mass |
248.189
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| CAS # |
83148-91-8
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| Related CAS # |
Sophoridine;6882-68-4
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| PubChem CID |
285698
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| Appearance |
Typically exists as solid at room temperature
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| Density |
1.164 g/cm3
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| Boiling Point |
396.738ºC at 760 mmHg
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| Flash Point |
172.748ºC
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| LogP |
1.747
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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 |
0
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| Heavy Atom Count |
18
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| Complexity |
356
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| Defined Atom Stereocenter Count |
0
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| SMILES |
O=C1CCC[C@H]2[C@@H]3CCCN4[C@@H]3[C@@H](CCC4)CN12
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| InChi Key |
ZSBXGIUJOOQZMP-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C15H24N2O/c18-14-7-1-6-13-12-5-3-9-16-8-2-4-11(15(12)16)10-17(13)14/h11-13,15H,1-10H2
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| Chemical Name |
7,13-diazatetracyclo[7.7.1.02,7.013,17]heptadecan-6-one
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| Synonyms |
83148-91-8; Matridin-15-one; (+)-Matrine; (+)-Sophoridine; Matridin-15-one, (6b,7b,11a)- (9CI); 7,13-diazatetracyclo[7.7.1.02,7.013,17]heptadecan-6-one; .alpha.-Matrine; Matrene, (+)-;
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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 |
| 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) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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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 | 4.0264 mL | 20.1321 mL | 40.2641 mL | |
| 5 mM | 0.8053 mL | 4.0264 mL | 8.0528 mL | |
| 10 mM | 0.4026 mL | 2.0132 mL | 4.0264 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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