α-Solanine is a bioactive component and one of the major steroidal glycoalkaloids found in potatoes (Solanum tuberosum L.) and other nightshade plants. It is a trisaccharide glycoalkaloid produced biosynthetically via the cholesterol pathway. It has been reported to have toxic effects in humans at high concentrations, but also demonstrates beneficial effects depending on concentration and conditions of use, including anti-allergic, anti-pyretic, anti-inflammatory, anti-diabetic, and antibiotic activities against pathogenic bacteria, viruses, fungi, and protozoa. Previous studies have shown that α-solanine inhibits growth and induces apoptosis in various cancer cells. [1][2]
α-Solanine exerts its biological effects through multiple signaling pathways and molecular targets. Its main targets include: 1) NF-κB pathway: attenuates chondrocyte pyroptosis by inhibiting the NF-κB pathway; 2) HIF-1α pathway: regulates hypoxia-inducible factor-1α, affecting glycolysis and energy metabolism; 3) MAPK/ERK and STAT3 pathways: downregulates vascular endothelial growth factor (VEGF) expression; 4) S100P protein: inhibits colorectal cancer cell growth by downregulating S100P expression; 5) Mitochondria: interacts with mitochondrial membranes, opens potassium channels, reduces membrane potential, leading to calcium transport from mitochondria to cytoplasm, triggering cell damage and apoptosis (toxicity-related mechanism).

- α-Solanine inhibited the growth and proliferation of human esophageal EC9706 and Eca109 cancer cells in a dose-dependent manner (10, 20, 40, 60 μg/ml for 24, 48, 72 h). The growth inhibitory effect was time- and dose-dependent, with maximum inhibition detected at 72 h. [1]
- Colony formation assay: Treatment with α-solanine (10, 20, 40, 60 μg/ml) significantly decreased the clonogenic survival of EC9706 and Eca109 cells in a dose-dependent manner compared with control. [1]
- Cell migration and invasion assays: α-Solanine (20, 40, 60 μg/ml) significantly reduced the number of migrating cells penetrating the transwell membrane in a dose-dependent manner (P<0.05). Wound-healing assays showed suppressed migration in a dose-dependent manner. [1]
- Apoptosis assay: α-Solanine increased the apoptotic rate of EC9706 cells in a dose-dependent manner (P<0.05) as measured by annexin V-FITC/PI staining and flow cytometry. Caspase-3/7 activity was higher in α-solanine-treated groups compared with control (P<0.05). [1]
- Western blot analysis: α-Solanine reduced expression levels of MMP-2 and MMP-9, increased E-cadherin expression, decreased Bcl-2 expression, and increased Bax expression in a dose-dependent manner in EC9706 cells. [1]
- Anti-proliferative activity: α-Solanine showed IC50 values of ~10 μM in A549, MCF-7, DU145, and KB human cancer cell lines after 48 h treatment (broad spectrum activity). A549 cells were most sensitive. [2]
- Autophagy induction: In A549 cells treated with 10 μM α-solanine, time-dependent conversion of LC3-I to LC3-II was observed with highest expression at 24 h. Beclin 1, LAMP-2, and ATG5 were also increased in a time-dependent manner. [2]
- Immunofluorescence: α-Solanine treatment resulted in accumulation of LC3-specific puncta in A549 cells from 12 h onward (P<0.0001 compared with untreated control). [2]
- Autophagic flux: Pre-incubation with bafilomycin A1 (100 nM) or chloroquine (5 μM) followed by α-solanine treatment caused additionally enhanced turnover of LC3-II and accumulation of LC3 puncta. Confocal microscopy showed colocalization of autophagosomes (LC3 positive) with lysosomes (LAMP-2 positive). [2]
- TEM analysis: A549 cells treated with 10 μM α-solanine for 24 h showed abundant autophagosomes, amphisomes, and autolysosomes; mitochondria appeared less electron-dense with disruption of ultrastructure and loss of cristae; significant ER swelling was observed. [2]
- ROS induction: α-Solanine (10 μM, 24 h) caused an increase in CM-H2DCFDA fluorescence (~63% compared with control), which was scavenged by NAC (~82% decrease). MitoSOX Red staining showed elevated mitochondrial superoxide levels. Lipid peroxidation assay showed significant loss of fluorescence intensity. [2]
- Mitochondrial membrane potential: JC1 staining revealed loss of mitochondrial membrane potential in α-solanine-treated A549 cells. Cytochrome c release from mitochondria was observed by confocal microscopy. [2]
- ER stress: Western blotting showed increased expression of BiP/GRP78, IRE1, PERK, ATF6, XBP1, ATF4, and CHOP in A549 cells after α-solanine treatment. Cytosolic calcium levels (Fluo-4AM staining) were significantly increased. [2]
- Akt/mTOR pathway: α-Solanine treatment resulted in downregulation of p-Akt (Thr308 and Ser473), p-mTOR (Ser2448 and Ser2481), and p-4E-BP1 (Thr37/46). Total mTOR level showed no obvious change. [2]
- siRNA knockdown: Knockdown of Beclin 1 reduced LC3B-II expression and ATG5. Knockdown of PERK resulted in reduced ATF4 expression and decreased LC3-II level. [2]
- Combination treatment: Co-treatment with α-solanine and doxorubicin showed an additive effect on cell cytotoxicity compared with either agent alone. [2]

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α-Solanine exhibits significant anti-proliferative activity against various tumor cell lines in vitro. In pancreatic cancer cells (PANC-1, sw1990, MIA PaCa-2), 12 μg/μl α-Solanine significantly reduces cell viability, while no cytotoxicity is observed at 3-9 μg/μl. α-Solanine at 3-9 μg/μl reduces VEGF mRNA and protein expression in PANC-1 cells in a dose-dependent manner, thereby inhibiting angiogenesis. In colorectal cancer cells (SW480, SW620, HT-29), α-Solanine inhibits cell growth, migration, and invasion, and induces cell cycle arrest and apoptosis. For antifungal activity, the minimum inhibitory concentration (MIC) of α-Solanine against Trichophyton rubrum is 7.8 μg/mL. In osteoarthritis research, 1-4 μM α-Solanine treatment of chondrocytes for 12 hours shows no cytotoxicity and significantly inhibits glycolysis-related protein expression and ferroptosis.

α-Solanine demonstrates antitumor activity in in vivo animal models. In a pancreatic cancer xenograft mouse model, intraperitoneal injection of 1 μl/g α-Solanine for two weeks reduces tumor volume by 61% (P<0.05). In a colorectal cancer model, α-Solanine also inhibits tumor growth. In a rat osteoarthritis model, treatment with UIO-66-NH2@α-Solanine@PEI charged particles (USP) significantly inhibits glycolysis and ferroptosis, improving osteoarthritis characteristics. Toxicity studies show that α-Solanine exhibits in vivo toxicity at high doses: in Golden Syrian hamsters, gavage at 100 mg/kg/day for 5 days results in 50% animal mortality. In mice fed 416.6 mg/kg/day for 7 days, decreased body weight gain and reduced absolute liver weight are observed.

Regarding in vitro enzyme/receptor binding assays for α-Solanine, the available literature does not provide detailed non-cellular experimental protocols. Based on its mechanism of action studies, a typical experimental procedure for detecting α-Solanine's interaction with mitochondrial membranes includes: isolating purified mitochondria (extracted from animal liver or cells via differential centrifugation), incubating various concentrations of α-Solanine (e.g., 0-100 μM) with isolated mitochondria in specific reaction buffer (containing potassium channel-related components), using fluorescent probes (such as JC-1 or TMRM) to detect changes in mitochondrial membrane potential, monitoring potassium channel opening using potassium ion-selective electrodes or fluorescent probes, and measuring changes in extramitochondrial calcium concentration using calcium fluorescent probes (such as Fura-2 or Fluo-4). All experiments require negative and positive control groups, with each experiment repeated three times to ensure result reliability.

- Cell proliferation assay (CCK-8): EC9706 and Eca109 cells in logarithmic growth phase were seeded into 96-well plates at 1×10⁴ cells/well. After starvation with serum-free medium containing 0.1% BSA for 24 h, cells were exposed to α-solanine at concentrations of 10, 20, 40, and 60 μg/ml for 24, 48, and 72 h. Then CCK-8 solution was added and incubated for 2 h. Cell proliferation was determined by measuring absorbance at 450 nm using a plate reader. The inhibition rate was calculated as (OD_control - OD_treated) / OD_control × 100%. [1]
- Colony formation assay: EC9706 and Eca109 cells were seeded into 6-well plates for 24 h, then washed, trypsinized, and counted. Base agar matrix layer (1.5 ml) was dispensed into each well of a 12-well plate and allowed to solidify. Then 1.5 ml growth agar layer containing cells was added. After congealing, 500 μl culture media containing α-solanine (0, 20, 40, 60 μg/ml) was added. Cells were incubated at 37°C with 5% CO₂ until colony formation (10-14 days). Colonies with >50 cells were counted as surviving colonies. Plating efficiency was calculated by dividing average colonies per well by cells plated. Survival fractions were calculated by normalization to control. [1]
- Cell migration and invasion assay (Transwell): Transwell filters were coated with Matrigel (3.9 g/l, 40 μl) on the upper surface of polycarbonic membrane (6.5 mm diameter, 8 μm pore size) and solidified at 37°C for 30 min. After treatment with α-solanine (20, 40, 60 μg/ml) for 24 h, 200 μl serum-free cell suspension containing EC9706 or Eca109 cells was loaded into the top chamber. Medium (500 μl) containing 10% FBS was added to the bottom chamber. Cells were allowed to migrate for 12 h at 37°C with 5% CO₂. The upper membrane surface was wiped to remove non-invasive cells. Invasive cells on the lower surface were fixed with methanol and stained with crystal violet for 20 min. Cells were counted in three randomly selected visual fields (×100 magnification). [1]
- Wound-healing migration assay: EC9706 and Eca109 cells (1×10⁵) were seeded into 24-well plates with wound healing inserts. At 90% confluence, inserts were removed to create a wound field of ~500 μm. After removing debris with PBS, cells were exposed to α-solanine (0, 20, 40, 60 μg/ml) for 24 h. Cell migration was viewed under an inverted microscope. Wound area was measured using software. Wound closure percentage was calculated as [1 - (wound area at 24 h / wound area at 0 h)] × 100%. [1]
- Cell apoptosis assay (flow cytometry): EC9706 cells were seeded into 6-well plates at 2×10⁵ cells/well. Cells exposed to different concentrations of α-solanine were collected and counted 48 h after incubation. Cell pellets were resuspended in 195 μl binding buffer and stained with 5 μl each of annexin V-FITC and PI staining solution for 10 min at room temperature in the dark. Flow cytometry was performed. Apoptotic rate was calculated as (apoptotic cells / total cells) × 100%. [1]
- Western blot analysis: Total protein was extracted using RIPA buffer containing PMSF. Protein concentration was determined by BCA assay. Protein samples (30 μg) were resolved on 10% SDS-PAGE gels and transferred to PVDF membranes. Membranes were blocked with 3% BSA for 1 h, then incubated overnight at 4°C with primary antibodies (anti-MMP-2, anti-MMP-9, anti-E-cadherin, anti-Bcl-2, anti-Bax, anti-GAPDH at 1:1000). Then membranes were incubated with HRP-conjugated secondary antibody (1:1000). Western blots were scanned and protein intensities analyzed. [1]
- Caspase-3/7 activity assay: Cells from each α-solanine-treated group were collected. Caspase-3/7 activity was measured using a Caspase-Glo 3/7 assay. Plates were incubated at room temperature for 1 h, then 100 μl Caspase-Glo 3/7 reagent was added. Luminescence intensity was detected using a microplate reader. [1]
- Cell viability assay (SRB assay) for multiple cancer lines: Cells (10⁴ per well) were seeded onto 96-well plates, grown overnight, then treated with or without α-solanine at different concentrations for 48 h. Cells were fixed and stained with SRB dye. Bound dye was solubilized with 10 mM Tris base and plates were read at 510 nm absorbance. [2]
- Immunofluorescence for LC3 puncta: A549 cells were grown on coverslips, treated with α-solanine (10 μM) for indicated times, fixed with 4% PFA, permeabilized with 0.5% Triton X-100, blocked with 2% BSA, probed with anti-LC3 antibody overnight at 4°C, then incubated with fluorescence-conjugated secondary antibody for 1 h at room temperature. Images were acquired by confocal microscopy. Average number of LC3 puncta/cell was quantified. [2]
- Measurement of ROS (CM-H2DCFDA): For microscopy, cells were treated with α-solanine for 24 h, incubated with 10 μM CM-H2DCFDA for 30 min in the dark, washed with PBS, and examined under confocal microscope. For flow cytometry, cells (2×10⁶) were resuspended in 500 μl HBSS, stained with CM-H2DCFDA for 30 min in the dark, and analyzed by flow cytometer. For ROS scavenger experiments, cells were pre-incubated with NAC for 2 h before α-solanine exposure. [2]
- Mitochondrial superoxide measurement (MitoSOX Red): Cells were grown on coverslips, treated with α-solanine for 24 h, stained with 4 μM MitoSOX Red dye for 10 min in the dark, washed with warm PBS, and observed under confocal microscope. [2]
- Mitochondrial membrane potential (JC1 staining): Cells were grown in confocal glass bottom dishes, treated with α-solanine for 24 h, washed with PBS, stained with 2 μM JC1 for 30 min, washed with PBS, and examined under confocal microscope. [2]
- Cytochrome c release assay: Cells were washed with PBS after α-solanine treatment (24 h), fixed with 4% PFA, permeabilized with 0.5% Triton X-100, blocked with 2% BSA for 1 h, probed with anti-cytochrome c antibody overnight at 4°C, then stained with Alexa Fluor 488 conjugated secondary antibody for 90 min at room temperature, and examined under confocal microscope. [2]
- Lipid peroxidation assay (cis-parinaric acid): Cells were seeded onto 96-well plates, treated accordingly, washed once with warm PBS, incubated with 10 μM cis-parinaric acid for 1 h at 37°C, washed with warm PBS, and fluorescence intensities were measured at 360 nm excitation and 460 nm emission. [2]
- Cytosolic calcium measurement (Fluo-4AM): Cells were grown in glass bottom confocal dishes overnight, treated with α-solanine (10 μM, 24 h) or thapsigargin (0.5 μM, 16 h as positive control), stained with 5 μM Fluo-4AM in calcium-free DPBS for 1 h before imaging. [2]
- siRNA transfection: Cells were transfected with siRNA targeting human Beclin 1, scrambled control siRNA, or human EIF2AK3 (PERK)-specific siRNA using Lipofectamine 2000 according to standard protocol and cultured for 48 h in complete medium before further analysis. Knockdown efficiency was determined by immunoblotting. [2]
- Stable cell line generation (GFP-LC3): To establish a stable C33A cell line expressing GFP-LC3, G418 (300 μg/ml) was added to culture media at 48 h after transfection with GFP-LC3 plasmid. Cells were grown for 2 weeks in presence of G418, and viable stable clones were selected and propagated. [2]

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A common protocol for in vitro cell assays with α-Solanine is as follows: Cells are cultured in RPMI-1640 or DMEM medium supplemented with 10% fetal bovine serum and 1% penicillin/streptomycin at 37°C in a 5% CO₂ humidified incubator. Twenty-four hours prior to the experiment, cells are seeded in 96-well plates at a density of 2.5×10⁵ cells per well. The next day, the old medium is discarded, and fresh medium containing various concentrations of α-Solanine (e.g., 1-50 μM or 0-12 μg/μl) is added, with 3-6 replicate wells per concentration. Solvent control (e.g., DMSO or PBS) and blank control groups are also set. After 24, 48, or 72 hours of treatment, cell viability is assessed using CCK-8 or MTT assay. Apoptosis is detected using Annexin V-FITC/PI double staining combined with flow cytometry. Cell migration and invasion are evaluated using Transwell chambers. Cell cycle analysis is performed using PI staining combined with flow cytometry.

A typical protocol for in vivo animal experiments with α-Solanine is as follows: Female or male nude mice or Balb/c mice aged 4-6 weeks are used to establish tumor xenograft models (subcutaneous injection of tumor cells, approximately 5×10⁶ cells per mouse). When tumor volume reaches approximately 100 mm³, animals are randomly divided into control and treatment groups (6-10 animals per group). The treatment group receives α-Solanine via intraperitoneal injection, tail vein injection, or gavage (e.g., 1 μl/g or 20-100 mg/kg/day), while the control group receives an equal volume of vehicle. The dosing frequency is typically once daily or every other day for 2-5 weeks. During the experiment, body weight and tumor size (long and short diameters measured by calipers) are recorded daily. At the end of the experiment, animals are euthanized, and tumor tissues, blood, and major organs (liver, kidney, heart, lung, etc.) are collected for histopathological analysis (H&E staining), immunohistochemical detection (e.g., Ki-67, VEGF), and blood biochemical index testing. Toxicity studies use similar dosing protocols but employ healthy animals to assess safety.

The pharmacokinetic properties of α-Solanine limit its clinical application. This compound is hydrophobic (lipophilic), resulting in poor water solubility and affecting in vivo distribution. Human oral pharmacokinetic studies show that the clearance of potato glycoalkaloids (including α-Solanine and α-chaconine) typically takes more than 24 hours, implying that the toxicants may accumulate in the body with daily consumption. It has a prolonged serum half-life, and intravenous injection may lead to accumulation in the body, causing severe adverse effects such as neurological damage and respiratory failure. Furthermore, α-Solanine has poor tumor-targeting ability, resulting in low accumulation in tumor tissues while causing significant systemic toxicity to normal tissues. Due to its hydrophobicity and unfavorable pharmacokinetic properties, researchers are developing nano-delivery systems (such as BSA nanoparticles) to improve its pharmacokinetic properties and targeting.

- α-Solanine has been reported to have toxic effects in humans. Traditional view holds that human consumption of potato glycoalkaloids at 3-6 mg/kg body weight is lethal, and >1-3 mg/kg body weight has toxic effects of gastrointestinal disturbances and neurological disorders. The toxic level of α-solanine in human diet is not defined yet. [2]
- α-Chaconine (another glycoalkaloid) has been reported to be more toxic than α-solanine. The ratio of α-chaconine in potatoes is three times higher than that of α-solanine. [2]
- No specific LD50, hepatotoxicity, nephrotoxicity, drug-drug interactions, or plasma protein binding data were provided. [1][2][3]

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Toxicity Summary
Solanum glycoalkaloids can inhibit cholinesterase, disrupt cell membranes, and be teratogenic (cause birth defects). One study suggests that the toxic mechanism of solanine is caused by the chemical's interaction with mitochondrial membranes. Experiments show that solanine exposure opens the potassium channels of mitochondria, decreasing their membrane potential. This in turn leads to Ca2+ being transported from the mitochondria into the cytoplasm, and it is this increased concentration of Ca2+ in the cytoplasm that triggers cell damage and apoptosis.

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The toxicity of α-Solanine is dose-dependent. As one of the main glycoalkaloids in potatoes, it is the source of toxicity from sprouting potatoes. The main toxicity mechanisms include: inhibiting cholinesterase, disrupting cell membrane integrity, interacting with mitochondrial membranes to induce apoptosis, and being teratogenic (causing birth defects). Acute toxicity: rat oral LD₅₀ is 590 mg/kg, mouse intraperitoneal LD₅₀ is 32 mg/kg, rabbit intraperitoneal LDLo is 20 mg/kg, rabbit intravenous LDLo is 20 mg/kg. Subchronic toxicity: rats fed 180 mg/kg/day for 5 weeks show reduced growth rate. Mice fed 416.6 mg/kg/day for 7 days show decreased body weight gain and reduced liver weight. Human effects: consumption of damaged or rotten potatoes can cause adverse CNS and gastrointestinal effects in humans. In a human study, a subject receiving 1.25 mg/kg total glycoalkaloids (including α-Solanine) orally experienced nausea and vomiting. Of note, α-Solanine exhibits hemolytic activity, and direct intravenous administration may cause red blood cell lysis, leading to severe side effects.

[1]. Inhibitory Effect of α-Solanine on Esophageal Carcinoma in vitro. Exp Ther Med. 2016 Sep;12(3):1525-1530.

[2]. α-Solanine Inhibits Proliferation, Invasion, and Migration, and Induces Apoptosis in Human Choriocarcinoma JEG-3 Cells In Vitro and In Vivo. Toxins (Basel). 2021 Mar 13;13(3):210.

[3]. α-Solanine induces ROS-mediated autophagy through activation of endoplasmic reticulum stress and inhibition of Akt/mTOR pathway. Cell Death Dis. 2015 Aug 27;6(8):e1860.

- α-Solanine is a trisaccharide glycoalkaloid found in species of the nightshade family including potato. It is produced biosynthetically via the cholesterol pathway. [2]
- Glycoalkaloids are secondary plant metabolites produced as natural toxins to protect plants from hostile environments such as cold stress, insects, phytopathogen attacks, and vertebrate feeding. α-Chaconine and α-solanine are two major constituents (95%) of total glycoalkaloids in potato. [2]
- α-Solanine has been shown to produce beneficial effects in human health depending on concentration and conditions of use, including anti-allergic, anti-pyretic, anti-inflammatory, anti-diabetic, and antibiotic activity against pathogenic bacteria, viruses, fungi, and protozoa. [2]
- The study demonstrates that α-solanine induces both apoptosis and autophagy to mediate cancer cell death. Autophagy appears to be an early event (peak at 24 h) while apoptosis is later (peak at 48 h in A549 cells). In DU145 cells, key autophagy markers (LC3 and ATG5) were not detected, suggesting autophagy may not be essential for cell death by α-solanine in all cell lines. [2]
- The proposed mechanism of α-solanine-induced cell death involves: induction of ER stress and UPR pathway (IRE1, PERK, ATF6), activation of CHOP, increase in intracellular ROS, downregulation of Akt/mTOR signaling, leading to induction of autophagy (and apoptosis). [2]
- α-Solanine inhibits proliferation of EC9706 and Eca109 cells and induces apoptosis through regulation of MMP-2, MMP-9, E-cadherin, Bcl-2, and Bax. [1]

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It has been reported that α-solanine is found in potatoes (Solanum tuberosum), plants of the genus Solanum, and other organisms with relevant data. α-Soanine and mixtures of α-solanine have been found in plants of the Solanaceae family.

C45H73NO15

868.0588

867.498

20562-02-1

6537493

White to off-white solid

1.4±0.1 g/cm3

780.78°C (rough estimate)

285℃ (dec.)

1.631

5.67

9

16

8

61

1590

25

O([C@@]1([H])[C@@]([H])([C@]([H])([C@]([H])([C@@]([H])(C([H])([H])O[H])O1)O[H])O[C@@]1([H])[C@@]([H])([C@]([H])([C@@]([H])([C@@]([H])(C([H])([H])O[H])O1)O[H])O[H])O[H])O[C@@]1([H])[C@@]([H])([C@@]([H])([C@]([H])([C@]([H])(C([H])([H])[H])O1)O[H])O[H])O[H])[C@@]1([H])C([H])([H])C([H])([H])[C@@]2(C([H])([H])[H])C(C1([H])[H])=C([H])C([H])([H])[C@]1([H])C2([H])C([H])([H])C([H])([H])[C@@]2(C([H])([H])[H])[C@@]1([H])C([H])([H])C1([H])[C@]2([H])[C@]([H])(C([H])([H])[H])[C@@]2([H])C([H])([H])C([H])([H])[C@]([H])(C([H])([H])[H])C([H])([H])N12

ZGVSETXHNHBTRK-UDJLNJFBSA-N

InChI=1S/C45H73NO15/c1-19-6-9-27-20(2)31-28(46(27)16-19)15-26-24-8-7-22-14-23(10-12-44(22,4)25(24)11-13-45(26,31)5)57-43-40(61-41-37(54)35(52)32(49)21(3)56-41)39(34(51)30(18-48)59-43)60-42-38(55)36(53)33(50)29(17-47)58-42/h7,19-21,23-43,47-55H,6,8-18H2,1-5H3/t19-,20+,21-,23-,24+,25-,26-,27+,28-,29+,30+,31-,32-,33+,34-,35+,36-,37+,38+,39-,40+,41-,42-,43+,44-,45-/m0/s1

(2S,3R,4R,5R,6S)-2-[(2R,3R,4S,5S,6R)-5-hydroxy-6-(hydroxymethyl)-2-[[(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-yl]oxy]-4-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyoxan-3-yl]oxy-6-methyloxane-3,4,5-triol

alpha-Solanine; 20562-02-1; DTXSID9030707; RefChem:111392; DTXCID601527922;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~50 mg/mL (~57.60 mM)

Solubility in Formulation 1: ≥ 1.25 mg/mL (1.44 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 12.5 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.

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Solubility in Formulation 2: ≥ 1.25 mg/mL (1.44 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 12.5 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.

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Solubility in Formulation 3: ≥ 1.25 mg/mL (1.44 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (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 12.5 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)