| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| 10mg |
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| Other Sizes |
| Targets |
Solasodine targets multiple cellular pathways involved in cancer progression and inflammation. It decreases RAD51 expression while increasing γH2AX and p53 levels, indicating its role in DNA damage response and cell cycle regulation. The compound has been found to inhibit the activity of the ABCB1 transporter, which is responsible for the efflux of chemotherapeutic agents from cancer cells. In the context of inflammation, solasodine demonstrates anti-inflammatory activity by inhibiting the production of pro-inflammatory mediators and suppressing key signaling pathways including NF-κB, ERK1/2, Akt, and STAT1. It also exhibits anti-tumor effects on LLC tumors and lung cancer models.
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| ln Vitro |
In vitro, solasodine exhibits potent antiproliferative activity across various human tumor cell lines, including HT-29 colon cancer and HepG2 hepatocellular carcinoma cells, with GI50 values in the low micromolar range. The compound induces DNA damage as evidenced by increased γH2AX foci formation and decreased RAD51 expression. It promotes p53 activation, leading to cell cycle arrest and apoptosis in cancer cells. Solasodine has also been shown to reduce neovascularization, suggesting anti-angiogenic properties. Interestingly, the compound promotes breast cancer cell proliferation in certain contexts, indicating cell-type specific effects. Its ability to inhibit ABCB1 transporter activity may enhance the efficacy of co-administered chemotherapeutic agents.
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| ln Vivo |
In vivo studies have demonstrated the anti-tumor efficacy of solasodine in animal models. The compound exhibits anti-tumor effects on Lewis lung carcinoma (LLC) tumors and lung cancer xenografts. Oral administration of solasodine has been shown to be effective, indicating good oral bioavailability. In tumor-bearing mice, treatment with solasodine resulted in reduced tumor growth and increased survival rates. The compound's ability to modulate RAD51 and p53 expression contributes to its in vivo anti-tumor activity. Additionally, solasodine's anti-inflammatory effects may contribute to its overall therapeutic efficacy in cancer models by reducing tumor-associated inflammation.
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| Enzyme Assay |
For in vitro enzyme/receptor binding assays, solasodine can be evaluated using cell-free systems to assess its interactions with molecular targets. Binding studies may employ purified proteins such as RAD51, p53, or ABCB1 transporter to measure direct compound-protein interactions using techniques like surface plasmon resonance (SPR) or fluorescence polarization. Enzyme inhibition assays can be performed to evaluate the compound's effect on specific kinases or transporters. IC50 values for target inhibition are determined through dose-response curves using appropriate substrates. These cell-free assays help elucidate the primary molecular targets of solasodine and provide mechanistic insights into its anticancer and anti-inflammatory activities without cellular interference.
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| Cell Assay |
In vitro cellular assays for solasodine typically utilize human tumor cell lines such as HT-29 (colon), HepG2 (liver), and LLC (lung cancer) cells. Cells are cultured in standard media and treated with solasodine at concentrations ranging from 0.1 to 100 μM for 24-72 hours. Cell proliferation is assessed using MTT or SRB assays to determine GI50 values. Apoptosis is evaluated through Annexin V/PI staining, caspase activity assays, and DNA fragmentation analysis. Western blotting is performed to detect changes in RAD51, γH2AX, p53, and other signaling proteins. Transporter activity assays using fluorescent substrates can measure ABCB1 inhibition. Reactive oxygen species (ROS) generation and mitochondrial membrane potential changes can also be monitored to assess the compound's effects on cellular metabolism.
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| Animal Protocol |
In vivo animal experiments with solasodine are conducted using mouse models of cancer. For LLC tumor studies, immunocompetent mice are inoculated subcutaneously with Lewis lung carcinoma cells. After tumor establishment, solasodine is administered orally or intraperitoneally at various doses. Tumor volume is measured regularly using calipers, and tumor weights are recorded at study endpoint. For lung cancer xenograft models, immunodeficient mice are used with human lung cancer cell lines. Endpoint analyses include immunohistochemistry for RAD51, γH2AX, and p53 expression in tumor tissues. Blood samples may be collected for pharmacokinetic analysis. Body weight and general health of animals are monitored throughout the study to assess toxicity.
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| ADME/Pharmacokinetics |
Pharmacokinetic properties of solasodine have been partially characterized. The compound is orally active, indicating good absorption following oral administration. As a steroidal alkaloid with a logP of 5.592, solasodine exhibits high lipophilicity, which facilitates tissue distribution but may limit aqueous solubility. The compound is metabolized in the liver and eliminated primarily via biliary excretion. Its half-life and bioavailability are influenced by the route of administration and formulation. Detailed PK parameters such as Cmax, Tmax, AUC, and protein binding are not extensively documented, and researchers often refer to general steroidal alkaloid pharmacokinetic profiles. The compound's physicochemical properties include a melting point of 212-214°C and a boiling point of 503.1°C.
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| Toxicity/Toxicokinetics |
Solasodine exhibits a dual profile as both a potential therapeutic agent and a toxin. As a steroidal glycoalkaloid metabolite, it has been associated with teratogenic activities. The compound's toxicity is dose-dependent and may affect multiple organ systems. At high concentrations, solasodine can disrupt cell membranes and interfere with normal cellular functions. Its ability to promote breast cancer cell proliferation in some contexts raises concerns about cell-type specific effects and potential safety risks. The compound's anti-tumor effects on LLC tumors and lung cancer must be balanced against its toxicological profile. Solasodine is strictly for research use only and not intended for human therapeutic applications. Researchers should exercise caution when handling this compound and follow appropriate safety protocols.
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| References | |
| Additional Infomation |
Solanidine is a steroidal alkaloid belonging to the 3β-hydroxy-Δ5-steroid and solanidine-5-en-3-ol class of compounds. It is both a plant metabolite and a toxin. It is the conjugate base of solanidine(1+). Solanidine has been reported to be found in Veratrum taliense, potato (Solanum tuberosum), and several other organisms with relevant data.
Beyond its primary anticancer and anti-inflammatory activities, solasodine serves as a valuable tool for studying DNA damage repair mechanisms through its modulation of RAD51 and p53. The compound's ability to inhibit ABCB1 transporter activity makes it useful for investigating multidrug resistance mechanisms in cancer cells. Solasodine can be employed to study the interplay between inflammation and cancer, as it suppresses multiple inflammatory signaling pathways including NF-κB, ERK1/2, Akt, and STAT1. Its anti-angiogenic properties provide opportunities for research into tumor vascularization. The compound is also relevant for studies on plant metabolism and natural product chemistry, as it is a major alkaloid found in potato species. |
| Molecular Formula |
C27H43NO
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|---|---|
| Molecular Weight |
397.63642
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| Exact Mass |
397.334
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| CAS # |
80-78-4
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| PubChem CID |
65727
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| Appearance |
White to off-white solid
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| Density |
1.1g/cm3
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| Boiling Point |
503.1ºC at 760 mmHg
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| Melting Point |
212-214ºC
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| Flash Point |
223.5ºC
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| Index of Refraction |
1.576
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| LogP |
5.592
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
2
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| Rotatable Bond Count |
0
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| Heavy Atom Count |
29
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| Complexity |
715
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| Defined Atom Stereocenter Count |
11
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| SMILES |
C[C@]12CC[C@@H]3[C@]4(CC[C@H](O)CC4=CC[C@H]3[C@@H]1C[C@@H]1N3C[C@@H](C)CC[C@@H]3[C@H]([C@H]21)C)C
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| InChi Key |
JVKYZPBMZPJNAJ-OQFNDJACSA-N
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| InChi Code |
InChI=1S/C27H43NO/c1-16-5-8-23-17(2)25-24(28(23)15-16)14-22-20-7-6-18-13-19(29)9-11-26(18,3)21(20)10-12-27(22,25)4/h6,16-17,19-25,29H,5,7-15H2,1-4H3/t16-,17+,19-,20+,21-,22-,23+,24-,25-,26-,27-/m0/s1
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| Chemical Name |
(1S,2S,7S,10R,11S,14S,15R,16S,17R,20S,23S)-10,14,16,20-tetramethyl-22-azahexacyclo[12.10.0.02,11.05,10.015,23.017,22]tetracos-4-en-7-ol
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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) |
Ethanol : ~3.57 mg/mL (~8.98 mM)
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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 | 2.5148 mL | 12.5742 mL | 25.1484 mL | |
| 5 mM | 0.5030 mL | 2.5148 mL | 5.0297 mL | |
| 10 mM | 0.2515 mL | 1.2574 mL | 2.5148 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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