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Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosisapoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway. Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes.
For research use only. We do not sell to patients.
Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosisapoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway. Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes[1][2][3][4][5][6][7][8][9][10].
Cellular Effect
Cell Line
Type
Value
Description
References
AGS
IC50
107 μM
Compound: 1
Cytotoxicity against human AGS cells after 24 hrs by MTT assay
Cytotoxicity against human AGS cells after 24 hrs by MTT assay
Jujuboside B (40-200 μM; 24-72 h) reduces the viability of acute leukemia cell lines U937, HL-60, Jurkat and Kasumi-1 in a dose- and time-dependent manner, and decreases the survival rate of primary human acute myeloid leukemia (AML) cells[1]. Jujuboside B (0-120 μM; 2 weeks) significantly reduces the clonogenic capacity of U937 acute leukemia cells[1]. Jujuboside B (40-120 μM; 24 h) mediates necroptosis of U937 acute leukemia cells via the RIPK1/RIPK3/MLKL pathway, and upregulates the total and phosphorylated protein levels of RIPK1, RIPK3 and MLKL in U937 acute leukemia cells[1]. Jujuboside B (20-100 μM; 72 h) potently inhibits the proliferation of human breast cancer cells MDA-MB-231 (IC50 = 54.38 μM) and MCF-7 (IC50 = 74.94 μM) after a 72 h treatment[2]. Jujuboside B (25-75 μM; 10-14 days) reduces the clonogenic survival rate of MDA-MB-231 and MCF-7 human breast cancer cells[2]. Jujuboside B (25-75 μM; 16-48 h) dose-dependently inhibits the migration of human breast cancer MDA-MB-231 cells, induces dose-dependent apoptosis in human breast cancer MDA-MB-231 and MCF-7 cells, upregulates the expressions of apoptosis markers cleaved PARP and cleaved caspase-3 in human MDA-MB-231 and MCF-7 cells, upregulates NOXA expression in MDA-MB-231 and MCF-7 cells, and activates AMPK[2]. Jujuboside B (25-75 μM; 12-48 h) induces dose-dependent and time-dependent autophagy in human breast cancer cell lines MDA-MB-231 and MCF-7, enhances the conversion of LC3-I to LC3-II, and reduces the expression level of p62. It induces autophagy in an AMPK-dependent manner in human breast cancer MCF-7 cells[2]. Jujuboside B (1-100 μM; 8-48 h) dose-dependently inhibits cell viability, migration, and Matrigel-based tube formation of HUVECs, while exerting minimal effects on the viability of HCT-15 cells[6]. Jujuboside B (1-100 μM; 24 h) dose-dependently arrests HUVECs at the G0/G1 phase of the cell cycle[6]. Jujuboside B (1-100 μM; 30 min pre-incubation) dose-dependently blocks VEGF165-induced phosphorylation of VEGFR2 and its downstream mediators (Akt, FAK, Src, PLCγ1) in HUVEC[6]. Jujuboside B (100 μM; 24 h) exerts better regulatory effects on the protein levels of DR4 and DR5 at 100 ng/mL in A549 and H460 cells than the single treatment[7]. Jujuboside B (30-300 μM; 5 min) dose-dependently inhibits collagen-, thrombin-, Arachidonic acid (AA) (HY-109590)- and adenosine diphosphate (ADP)-induced platelet aggregation in rat platelet-rich plasma, with IC50 values of 92.1 μM, 201.5 μM and 95.2 μM for collagen-, thrombin- and AA-induced aggregation, respectively, and exhibits no platelet cytotoxicity at the concentration of 300 μM[8]. Jujuboside B (30-300 μM; 5 min pre-treatment followed by 6 min incubation with collagen) dose-dependently inhibits collagen-induced TXA2 production in rat platelet-rich plasma[8]. Jujuboside B (30-100 μM) inhibits the currents of recombinant GluA1/GluA2 AMPA receptors in HEK293 cells in a dose-dependent manner in vitro[9]. Jujuboside B (pre-incubated for 1 min prior to AMPA stimulation at a concentration of 10 μM) significantly inhibits AMPA-induced intracellular calcium elevation in primary cultured rat cortical neurons, and reduces the peak and cumulative values of calcium responses[9]. Jujuboside B (20-100 μM; 60 μM for viability, colony formation, pathway analysis) inhibits the viability and colony formation of A549 cells, and blocks the PI3K/Akt and MAPK/ERK signaling pathways by reducing the phosphorylation levels of key pathway components, with an IC50 of 60 μM[10].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Inhibited the growth of all four leukemia cell lines in a dose- and time-dependent manner. Showed significant inhibitory effects after 24-h treatment, with potency increasing at longer incubation times.
Significantly inhibited colony formation of U937 cells at 80 μM and 120 μM, reflected by decreased colony number and size. Did not significantly affect colony counts at 40 μM.
Significantly increased protein levels of RIPK1, p-RIPK1, RIPK3, p-RIPK3, MLKL, and p-MLKL in U937 cells in a dose-dependent manner. Induced statistically significant upregulation of all target proteins and their phosphorylated forms at 80 μM and 120 μM.
Significantly inhibited the proliferation of MDA-MB-231 and MCF-7 in a dose-dependent manner. Achieved an IC50 of 54.38 μM for MDA-MB-231 and 74.94 μM for MCF-7.
Inhibited the migration of MDA-MB-231 cells in a dose-dependent manner, with significant reductions in migrated cell numbers at all tested concentrations.
Resulted in a remarkable dose-dependent increase in the apoptotic cell population (early apoptotic Annexin V(+)/PI(−) and late apoptotic Annexin V(+)/PI(+) cells) in both cell lines.
Significantly increased the expression of cleaved PARP and cleaved caspase-3 in a dose-dependent manner in both cell lines.\nRemarkably elevated NOXA expression in a dose-dependent pattern in both cell lines.\nIncreased phosphorylated AMPK levels in a dose-dependent manner in both cell lines.
25-75 μM (48 h treatment); 50 μM (12-48 h treatment)
Incubation Time:
48 h (dose-dependent autophagy); 12-48 h (time-dependent autophagy)
Result:
Increased the conversion of LC3-I to LC3-II in a dose-dependent manner after 48 h of treatment. Accumulated LC3-II in a time-dependent manner from 12 to 48 h of treatment at 50 μM. Decreased p62 expression in a dose-dependent manner after 48 h of treatment in both cell lines.
human umbilical vein endothelial cells (HUVECs), HCT-15 human colorectal adenocarcinoma cells
Concentration:
1, 3, 10, 30, and 100 μM
Incubation Time:
48 h
Result:
Significantly suppressed HUVEC viability in a dose-dependent manner, with minimal effect at 1-10 μM and strong suppression at ≥30 μM. Maintained over 65% of HCT-15 cell viability across all tested concentrations.
30 min (pre-incubation prior to VEGF165 stimulation)
Result:
Inhibited phosphorylation of VEGFR2 in a dose-dependent manner. Inhibited phosphorylation of downstream signaling proteins (Akt, FAK, Src, PLCγ1) in a dose-dependent manner.
Upregulated DR4 and DR5 protein levels more significantly than jujuboside B or TRAIL alone in A549 and H460 cells.
In Vivo
Jujuboside B (i.p.; once daily; for 17 consecutive days; 20 mg/kg) significantly inhibits the growth of MCF-7 and MDA-MB-231 breast cancer xenografts in nude mice, while inducing tumor cell apoptosis and autophagy, with no observed effect on animal body weight[2]. Jujuboside B (0.1-0.8 mg/kg; i.v.; 3 times within 2 days) significantly alleviates PM2.5-induced lung injury in BALB/c mice by regulating the TLR2/4-MyD88 and mTOR-autophagy pathways to reduce inflammation, apoptosis and autophagy dysfunction[3]. Jujuboside B (i.p./i.v.; once daily; consecutive 7 days/single administration, 20-40 mg/kg/0.4-1.5 mg/kg) dose-dependently ameliorates Acetaminophen (HY-66005)-induced acute liver injury in male C57BL/6 J mice, while inhibiting oxidative stress, inflammatory response, cell apoptosis and STING pathway activation, and activating the Nrf2 pathway. It also dose-dependently protects male C57BL/6 mice from cecal ligation and puncture (CLP)-induced liver injury by alleviating inflammation, enhancing antioxidant capacity, upregulating GR expression and downregulating 11β-HSD2 expression[4]. Jujuboside B (i.p., once every 2 days, 7 administrations, dose of 20 mg/kg) reduces the subcutaneous HCT-15 colorectal cancer tumor volume by 55.5% and tumor weight by 56.3% in female BALB/c nude mice through anti-angiogenic and anti-proliferative mechanisms, with no treatment-related body weight loss observed[6]. When applied topically to the chick chorioallantoic membrane, Jujuboside B (1-100 μM) inhibits angiogenesis in a dose-dependent manner, with an inhibition rate of up to 80% at the concentration of 100 μM[6]. When incorporated into subcutaneous Matrigel plugs at concentrations of 10-100 μM, Jujuboside B dose-dependently inhibits VEGF-induced angiogenesis in female BALB/c mice[6]. Jujuboside B (i.p., once every other day, 20-40 mg/kg) dose-dependently reduces the tumor volume of A549 non-small cell lung cancer in nude mice without inducing significant hepatotoxicity or nephrotoxicity[7]. Jujuboside B (10-100 mg/kg; p.o.; single administration) provides a statistically significant 63% protective effect against acute pulmonary thromboembolism induced by collagen and epinephrine in male ICR mice[8]. Jujuboside B (10-50 mg/kg; i.p.; single administration 1 hour prior to hyperthermia induction) dose-dependently inhibits the severity of febrile seizures in male P14 C57BL/6 mice[9]. Jujuboside B (40 mg/kg/day; i.p.; daily; for 2 consecutive weeks) significantly inhibits lung cancer progression in non-stressed and CUMS-stressed tumor-bearing female C57BL/6 mice by regulating apoptosis-related proteins, blocking the PI3K/Akt and MAPK/ERK signaling pathways, and reducing the levels of inflammatory cytokines[10]. Jujuboside B (40 mg/kg; i.p.; daily for 2 consecutive weeks) significantly ameliorates depression-like behaviors in female C57BL/6 mice subjected to CUMS modeling by increasing serum 5-HT and tryptophan levels, improving behavioral scores, and reducing inflammatory cytokine levels[10].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Significantly inhibited MCF-7 tumor growth, with tumor volumes and final tumor weights markedly lower than the control group. Showed no significant difference in animal body weight compared with the control group. Elevated expression of cleaved PARP, cleaved caspase-3, and LC3-II in tumor tissue, indicating induction of apoptosis and autophagy. Significantly inhibited MDA-MB-231 tumor growth, with tumor volumes and final tumor weights markedly lower than the control group. Showed no significant difference in animal body weight compared with the control group. Elevated expression of cleaved PARP, cleaved caspase-3, and LC3-II in tumor tissue, indicating induction of apoptosis and autophagy.
Animal Model:
BALB/c (7-week-old; acclimated for 12 days; PM2.5-induced lung injury model)[3]
Dosage:
0.1 mg/kg; 0.4 mg/kg; 0.8 mg/kg
Administration:
i.v.; three times over 2 days
Result:
Significantly reduced the PM2.5-induced increase in lung wet/dry weight ratio, total cell count in BALF, total neutrophil count in BALF, and lung injury score. Significantly reversed PM2.5-induced changes in apoptotic protein levels: restored anti-apoptotic Bcl-2 levels, reduced pro-apoptotic Bax, cleaved caspase-3, and cleaved PARP levels, and decreased the TUNEL-positive apoptotic cell percentage. Significantly reduced PM2.5-induced increases in pro-inflammatory cytokines IFN-γ, IL-1β, IL-6, IL-18, and TNF-α, and restored PM2.5-induced decreases in anti-inflammatory cytokines IL-2, IL-4, and IL-10. Significantly inhibited PM2.5-induced upregulation of autophagy-related proteins LC3 II and Beclin 1, reversed PM2.5-induced increases in TLR2, TLR4, and MyD88 levels, and restored PM2.5-induced reductions in phosphorylated mTOR, Akt, and PI3K levels.
Reversed acetaminophen-induced CYP2E1 upregulation in liver tissue in a dose-dependent manner. Reduced acetaminophen-induced mortality from 80% to 30% over 48 hours (40 mg/kg dose). Dose-dependently reduced serum ALT, AST, and LDH levels, improved liver histopathological scores, and attenuated liver tissue necrosis compared to acetaminophen-only controls. Dose-dependently suppressed acetaminophen-induced increases in serum and liver TNF-α, IL-6, and IFN-β levels, reduced liver macrophage infiltration (F4/80-positive cells), and lowered liver TNF-α and IL-6 protein expression. Dose-dependently reversed acetaminophen-induced increases in liver 4-HNE and MDA levels, restored liver GSH, SOD, and CAT activities, upregulated liver SOD1 and SOD2 mRNA levels, downregulated liver NOX2 and COX2 mRNA levels, reduced hepatocyte apoptosis (increased Bcl-2/Bax ratio, decreased cleaved caspase-3), inhibited acetaminophen-induced STING pathway activation (reduced STING, p-IRF3, and p-p65 protein levels in liver tissue), and activated the Nrf2 pathway (increased total, nuclear, and cytosolic Nrf2 protein levels, upregulated liver HO-1 and NQO-1 protein and mRNA levels).
Significantly reduced CLP-induced hepatic histopathological damage, including hemorrhagic necrosis, portal inflammation, parenchymal necrosis, and inflammatory cell infiltration at 0.75 mg/kg and 1.5 mg/kg. Significantly reduced elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels at 0.75 mg/kg and 1.5 mg/kg. Significantly reduced elevated liver tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and nitric oxide (NO) levels at 0.75 mg/kg and 1.5 mg/kg; significantly reduced elevated liver TNF-α and NO levels at 0.4 mg/kg. Reduced elevated liver malondialdehyde (MDA) levels at 0.75 mg/kg and 1.5 mg/kg. Restored reduced liver glutathione (GSH), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activity at 0.75 mg/kg and 1.5 mg/kg. Increased reduced liver glucocorticoid receptor (GR) protein expression at 0.4 mg/kg, 0.75 mg/kg, and 1.5 mg/kg. Reduced elevated liver 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) protein expression, with no effect on 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) expression at 0.75 mg/kg and 1.5 mg/kg. Did not significantly reduce serum ALT/AST levels or liver IL-1β levels at 0.4 mg/kg.
Reduced mean tumor volume by 55.5% compared to control group. Reduced mean tumor weight by 56.3% compared to control group. Significantly reduced tumor microvessel density. Significantly decreased Ki67-positive proliferative tumor cells. Significantly increased tumor necrosis area relative to controls. Caused no significant mouse body weight loss during treatment.
Reduced tumor volumes in a dose-dependent manner relative to controls, with statistically significant reductions observed over the study period. Showed no significant difference in body weights between treated and control groups. Exhibited no significant difference in serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), and creatinine (CRE) from controls.
Provided 17% protection against thromboembolism. Provided 43% protection against thromboembolism. Provided 63% protection against thromboembolism, which was statistically significant compared to vehicle.
Animal Model:
C57BL/6 (male, postnatal day 14, 6-7 g, LPS-primed hyperthermic induction)[9]
Dosage:
10 mg/kg; 30 mg/kg; 50 mg/kg
Administration:
i.p.; single dose 1 hour before hyperthermic induction
Result:
Increased seizure latency to 228.7, reduced the percentage of grade 5 seizures to 50%, and decreased seizure severity (Racine score) to 4.5. Significantly prolonged seizure latency to 563.3s, eliminated grade 5 seizures (90% of mice exhibited maximum grade 3 seizures), decreased seizure severity (Racine score) to 2.9, prolonged latency to EEG seizure onset to 680.0s, shortened total seizure duration to 551.9s, decreased seizure spike number to 39.88, and reduced hippocampal c-Fos-positive cells to 15.50 cells/mm2. Significantly prolonged seizure latency to 737.2 s, eliminated grade 5 seizures (80% of mice exhibited maximum grade 3 seizures), and decreased seizure severity (Racine score) to 2.8.
Animal Model:
C57BL/6 (female, 8 weeks old, subcutaneous inoculation of LLC lung cancer cells; chronic unpredictable mild stress exposure)[10]
Dosage:
40 mg/kg/day
Administration:
i.p.; daily; 2 weeks
Result:
Significantly reduced tumor volume and weight compared to vehicle controls in non-CUMS tumor-bearing mice. Significantly reduced tumor volume and weight compared to vehicle-treated CUMS-exposed tumor-bearing mice, reversing CUMS-promoted tumor progression. Significantly increased proapoptotic Bax protein and mRNA expression, and decreased antiapoptotic Bcl-2 protein and mRNA expression in tumor tissues compared to corresponding vehicle controls. Significantly reduced phosphorylation levels of PI3K, Akt, MAPK, ERK, and CREB in tumor tissues compared to corresponding vehicle controls. Significantly decreased serum levels of inflammatory cytokines TNF-α, IL-4, IL-6, and IL-10 compared to vehicle controls.
DMSO : 100 mg/mL (95.67 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
0.9567 mL
4.7837 mL
9.5675 mL
5 mM
0.1913 mL
0.9567 mL
1.9135 mL
10 mM
0.0957 mL
0.4784 mL
0.9567 mL
View the Complete Stock Solution Preparation Table
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Protocol 2
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (2.39 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
Protocol 3
Add each solvent one by one: 10% DMSO 90% Corn Oil
Solubility: ≥ 2.5 mg/mL (2.39 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μLCorn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO,
. All of co-solvents are available by MedChemExpress (MCE).
, Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration:
mg/mL
Method for preparing stock solution:
mg
drug dissolved in
μL
DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take
μL DMSO stock solution, add
μL .
μL , mix evenly, next add
μL Tween 80, mix evenly, then add
μL Saline.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
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