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| Targets |
P-glycoprotein (IC₅₀ = 15.62 μg/mL against SH-SY5Y cells; 9.1-fold inhibition at 100 μg/mL) [1]
Matrix metalloproteinase 2 (MMP-2) [2] Matrix metalloproteinase 9 (MMP-9) [2] Caspase-3 [3] Caspase-7 [4] Poly (ADP-ribose) polymerase (PARP) [4] Mitogen-activated protein kinase (MAPK) signaling pathway (Erk1/2) [4] Long noncoding RNA NEAT1_2 (lncNEAT1_2) [4] Long noncoding RNA PINT (lncPINT) [4] |
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| ln Vitro |
In the G2/M phase, solamargine (15 μg/ml; 72 hours) primarily induces cell death [3]. In a dose- and time-dependent way, solamargine (72 hours) strongly suppressed the growth of HepG2 and SMMC-7721 cells. 9.21 and 19.88 μg/ml, respectively, are the IC50 values[3].
Solamargine exhibited non-selective cytotoxicity against various cell lines, with an IC₅₀ of 15.62 μg/mL against SH-SY5Y neuroblastoma cells. [1] Solamargine showed dose-dependent P-glycoprotein inhibition (9.1-fold at 100 μg/mL) against SH-SY5Y cells, and its combination with doxorubicin produced additive effects on SH-SY5Y cells. [1] Solamargine reduced HepG2 cell viability in a concentration-dependent manner; at 7.5 μM, it decreased cell viability by less than 20%, and significantly inhibited migration (more than 70% reduction at the highest dose) and invasion (more than 72% reduction at the highest dose) of HepG2 cells. [2] Solamargine down-regulated the expression and activity of MMP-2 and MMP-9 in HepG2 cells, as demonstrated by Western blotting and gelatin zymography. [2] Solamargine significantly inhibited the growth of SMMC-7721 and HepG2 hepatoma cells, induced cell apoptosis, caused G2/M phase cell cycle arrest, and up-regulated caspase-3 expression. [3] Solamargine suppressed the viability of five gastric cancer (GC) cell lines (AGS, BGC823, SGC7901, HGC27, MGC803) in a dose-dependent manner (concentrations: 0, 2.5, 5, 10 μM) and induced notable morphological changes. [4] Solamargine promoted apoptosis of GC cells (SGC7901, HGC27, BGC823) at concentrations of 7.5 or 10 μM (treatment duration: 12, 24, 16, 48 h), enhanced cleavage of caspase-7 and PARP, and affected cell cycle distribution. [4] Solamargine inhibited phosphorylation of Erk1/2 MAPK, increased the expression of lncPINT and lncNEAT1_2 in GC cells (concentrations: 0, 5, 10 μM; treatment duration: 24, 48 h); knockdown of lncNEAT1_2 attenuated its inhibitory effect on GC cells. [4] Solamargine exhibited antitumor activity in primary GC cells from patients, with detectable IC₅₀ values after 72 h of treatment. [4] |
| ln Vivo |
In vivo, solanargine (10 mg/kg; gavage; once daily for 8 days) induces GC apoptosis and has anti-tumor actions [4].
In a xenograft mouse model of gastric cancer, Solamargine significantly suppressed tumor growth (P<0.05). [4] Solamargine induced apoptosis of cancer cells in tumor tissue of xenograft mice, as confirmed by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) and H&E staining (P<0.05). [4] |
| Enzyme Assay |
Gelatin zymography assay for MMP-2 and MMP-9 activity: HepG2 cells were treated with Solamargine, and cell lysates were prepared. The samples were subjected to gelatin zymography to separate MMP-2 and MMP-9, followed by incubation and staining to analyze their enzymatic activity. [2]
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| Cell Assay |
Cell viability assay [3]
Cell Types: SMMC-7721 Cell Tested Concentrations: 15 μg/ml Incubation Duration: 72 hrs (hours) Experimental Results: demonstrated a significant increase in sub-G1. Sulforhodamine B assay for cytotoxicity: Cancerous and non-cancerous cell lines (including SH-SY5Y) were treated with Solamargine at different concentrations, and the sulforhodamine B assay was performed to assess cell viability and calculate IC₅₀ values. [1] Rhodamine-123 assay for P-glycoprotein inhibition: SH-SY5Y cells were treated with Solamargine at various concentrations, and rhodamine-123 was used to evaluate the inhibitory effect on P-glycoprotein. [1] MTT assay for cell viability: HepG2 and SMMC-7721 cells were treated with Solamargine, and the MTT assay was conducted to measure cell viability and determine the concentration-dependent effect. [2][3] Wound healing migration assay: HepG2 cells were treated with Solamargine, and a scratch was made on the cell monolayer. The migration of cells into the scratch area was observed and quantified to assess migration ability. [2] Boyden chamber invasion assay: HepG2 cells were seeded in the upper chamber of Boyden chambers with Solamargine treatment, and the number of cells invading through the membrane to the lower chamber was counted to evaluate invasion ability. [2] Western blotting assay: HepG2, SMMC-7721, and GC cells were treated with Solamargine, and cell lysates were prepared. Proteins (MMP-2, MMP-9, caspase-3, caspase-7, PARP, cleaved PARP, cleaved caspase-7, Erk1/2, pErk1/2) were separated by electrophoresis, transferred to membranes, and detected with specific antibodies to analyze their expression levels. [2][3][4] Flow cytometry assay: SMMC-7721 cells were treated with Solamargine, and cell cycle distribution was analyzed by PI staining; GC cells were stained with Annexin V-FITC/PI to detect apoptosis rate via flow cytometry. [3][4] Colorimetric assay for caspase-3 expression: SMMC-7721 cells were treated with Solamargine, and a colorimetric assay was used to measure the expression level of caspase-3. [3] IncuCyte ZOOM Live-Cell Analysis: GC cells were treated with Solamargine at different concentrations, and cell viability was monitored every 8 h using the IncuCyte ZOOM Live-Cell Analysis System to calculate IC₅₀ values. [4] |
| Animal Protocol |
Animal/Disease Models: Female specific pathogen-free BALB/c nude mice, weighing 18-20 g (6-8 weeks old) [4]
Doses: 10 mg/kg Route of Administration: gavage; one time/day for 8 days Experimental Results: Tumor Growth was Dramatically inhibited. Xenograft mouse model of gastric cancer: Mice were implanted with gastric cancer cells to establish the xenograft model. Solamargine was administered to the model mice. After the experiment, mice were sacrificed, tumors were collected, and tumor growth was measured. TUNEL staining and H&E staining were performed on tumor tissue to detect cell apoptosis and necrotic areas. [4] |
| Toxicity/Toxicokinetics |
Solanine exhibits non-selective cytotoxicity, which may hinder drug development; P-glycoprotein inhibitory activity is only present at concentrations above the cytotoxic induction level. [1]
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| References |
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| Additional Infomation |
Solamargine is an azaspirocyclic compound, a steroidal compound, and an oxaspirocyclic compound. Solamargine has been used in research trials for the treatment of actinic keratosis. Solamargine has been reported to be found in Solanum carolinense, Solanum pittosporifolium, and other organisms with relevant data. Solamargine is a bioactive steroidal alkaloid glycoside isolated from Solanum aculeastrum (fruit) and Solanum nigrum L. [1][3] Solamargine exerts its anticancer effects through a variety of mechanisms, including inducing apoptosis, inhibiting cell migration and invasion, regulating the cell cycle, downregulating the expression and activity of MMPs, regulating the MAPK signaling pathway, and regulating the expression of lncRNAs (lncNEAT1_2, lncPINT). [2][3][4] Black nightshade (Solanum nigrum L.) is a traditional Chinese medicine with diuretic, antipyretic and hepatoprotective effects, and is widely used in folk anticancer prescriptions in China. [3] Solamargine is a derivative of solanine, a steroidal compound found in plants of the Solanum genus. Its role in gastric cancer has been elucidated, namely, inhibiting tumor progression by regulating lncNEAT1_2 through the MAPK pathway. [4]
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| Molecular Formula |
C45H73NO15
|
|---|---|
| Molecular Weight |
868.0588
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| Exact Mass |
867.498
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| CAS # |
20311-51-7
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| PubChem CID |
73611
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| Appearance |
White to off-white solid powder
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| Density |
1.4±0.1 g/cm3
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| Index of Refraction |
1.619
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| LogP |
7.18
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| Hydrogen Bond Donor Count |
9
|
| Hydrogen Bond Acceptor Count |
16
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| Rotatable Bond Count |
7
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| Heavy Atom Count |
61
|
| Complexity |
1610
|
| Defined Atom Stereocenter Count |
26
|
| SMILES |
C[C@@H]1CC[C@@]2([C@H]([C@H]3[C@@H](O2)C[C@@H]4[C@@]3(CC[C@H]5[C@H]4CC=C6[C@@]5(CC[C@@H](C6)O[C@H]7[C@@H]([C@H]([C@@H]([C@H](O7)CO)O[C@H]8[C@@H]([C@@H]([C@H]([C@@H](O8)C)O)O)O)O)O[C@H]9[C@@H]([C@@H]([C@H]([C@@H](O9)C)O)O)O)C)C)C)NC1
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| InChi Key |
MBWUSSKCCUMJHO-ZGXDEBHDSA-N
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| InChi Code |
InChI=1S/C45H73NO15/c1-19-9-14-45(46-17-19)20(2)30-28(61-45)16-27-25-8-7-23-15-24(10-12-43(23,5)26(25)11-13-44(27,30)6)57-42-39(60-41-36(53)34(51)32(49)22(4)56-41)37(54)38(29(18-47)58-42)59-40-35(52)33(50)31(48)21(3)55-40/h7,19-22,24-42,46-54H,8-18H2,1-6H3/t19-,20+,21+,22+,24+,25-,26+,27+,28+,29-,30+,31+,32+,33-,34-,35-,36-,37+,38-,39-,40+,41+,42-,43+,44+,45-/m1/s1
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| Chemical Name |
(2S,3R,4R,5R,6S)-2-[(2R,3S,4S,5R,6R)-4-hydroxy-2-(hydroxymethyl)-6-[(1S,2S,4S,5'R,6R,7S,8R,9S,12S,13R,16S)-5',7,9,13-tetramethylspiro[5-oxapentacyclo[10.8.0.02,9.04,8.013,18]icos-18-ene-6,2'-piperidine]-16-yl]oxy-5-[(2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxyoxan-3-yl]oxy-6-methyloxane-3,4,5-triol
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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) |
DMSO : ~100 mg/mL (~115.20 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (2.88 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (2.88 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (2.88 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.1520 mL | 5.7600 mL | 11.5199 mL | |
| 5 mM | 0.2304 mL | 1.1520 mL | 2.3040 mL | |
| 10 mM | 0.1152 mL | 0.5760 mL | 1.1520 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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