2. Stem Cell/Wnt JAK/STAT Signaling Protein Tyrosine Kinase/RTK Apoptosis NF-κB
  3. STAT VEGFR Bcl-2 Family Survivin IAP NF-κB Apoptosis Caspase
  4. Isolinderalactone

Isolinderalactone is a sesquiterpene that exhibits anti-cancer, anti-inflammatory, and neuroprotective effects. Isolinderalactone inhibits VEGF expression and tyrosine phosphorylation of VEGFR2. Isolinderalactone decreases viability and induces apoptosis in U-87 glioblastoma (GBM) cells and colorectal cancer (CRC) cells. Isolinderalactone induces G2/M phase cell cycle arrest, ROS generation, pJNK/p38 MAPK activation, in colorectal cancer (CRC) cells. Isolinderalactone blocks LPS (HY-D1056)-induced NF-κB activation while activating Nrf2-HMOX1 signaling in RAW264.7 macrophages. Isolinderalactone improves cognitive dysfunction in APP/PS1 mice. Isolinderalactone can be used for the study of Glioblastoma multiforme (GBM), colorectal cancer, Alzheimer’s disease and acute lung injury.

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Isolinderalactone

Isolinderalactone Chemical Structure

CAS No. : 957-66-4

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Based on 1 publication(s) in Google Scholar

Isolinderalactone Related Antibodies

Top Publications Citing Use of Products

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STAT3 STAT5 STAT6 STAT1

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Description

Isolinderalactone is a sesquiterpene that exhibits anti-cancer, anti-inflammatory, and neuroprotective effects. Isolinderalactone inhibits VEGF expression and tyrosine phosphorylation of VEGFR2. Isolinderalactone decreases viability and induces apoptosis in U-87 glioblastoma (GBM) cells and colorectal cancer (CRC) cells. Isolinderalactone induces G2/M phase cell cycle arrest, ROS generation, pJNK/p38 MAPK activation, in colorectal cancer (CRC) cells. Isolinderalactone blocks LPS (HY-D1056)-induced NF-κB activation while activating Nrf2-HMOX1 signaling in RAW264.7 macrophages. Isolinderalactone improves cognitive dysfunction in APP/PS1 mice. Isolinderalactone can be used for the study of Glioblastoma multiforme (GBM), colorectal cancer, Alzheimer’s disease and acute lung injury[1][2][3][4][5].

IC50 & Target[1]

VEGFR2

 

Bcl-2

 

Cellular Effect
Cell Line Type Value Description References
RAW264.7 IC50
0.3 μM
Compound: 7
Inhibition of iNOS-mediated NO production in LPS-stimulated mouse RAW264.7 cells after 24 hrs by Griess reagent method
Inhibition of iNOS-mediated NO production in LPS-stimulated mouse RAW264.7 cells after 24 hrs by Griess reagent method
[PMID: 22148193]
RAW264.7 CC50
66.41 μM
Compound: 7
Cytotoxicity against mouse RAW264.7 cells assessed as reduction in cell viability after 3 hrs by alamar blue assay
Cytotoxicity against mouse RAW264.7 cells assessed as reduction in cell viability after 3 hrs by alamar blue assay
[PMID: 22148193]
In Vitro

Isolinderalactone (0.5-2.5 μg/mL, 24-72 h) inhibits U-87 glioblastoma cell growth[1].
Isolinderalactone (0.5-2.5 μg/mL, 48 h) activates the apoptotic pathway in U-87 GBM cells by decreasing BCL-2, survivin, and XIAP expression, increasing cleaved caspase-3, and inducing DNA breakage, thereby promoting cell apoptosis[1].
Isolinderalactone (0.5-2 μg/mL, 48 h) suppresses VEGF expression in U-87 GBM cells and inhibits VEGF-induced angiogenesis of human brain microvascular endothelial cells (HBMECs)[2].
Isolinderalactone (2 μg/mL, 8 days) inhibits angiogenic sprouting in a 3D microfluidic chip[2].
Isolinderalactone (2.5-5 μg/mL, 48 h) decreases HIF expression and activity in U-87 cells and VEGFR2 activation in HBMECs[2].
Isolinderalactone (0-9 μM, 24-48 h) suppresses proliferation and colony formation of colorectal cancer cells (HCT116, HCT116-OxR, HT29, and HT29-OxR cells)[3].
Isolinderalactone (0-9 μM, 48 h) induces apoptosis, G2/M cell cycle arrest, ROS generation, and ER stress in colorectal cancer cells[3].
Isolinderalactone (0-9 μM, 48 h) induces apoptosis in CRC cells via mitochondrial and caspase-dependent pathways, potentially by modulating JNK/p38 MAPK activation, with ROS playing a critical role in this process[3].
Isolinderalactone (10 μM, 2-27 h) attenuates Aβ1-42-induced cell damage and reduces neurotoxicity in PC12 cells[4].
Isolinderalactone (10 μM, 27 h) reduces neuronal cell damage by inhibiting JNK in PC12 cells[4].
Isolinderalactone (0.5-10 μM, 19 h) inhibits LPS or TNF-α-induced inflammatory response in RAW264.7 cells, MH-S cells and BMDMs[5].
Isolinderalactone (1-10 μM, 13 h) suppresses the mRNA expression of proinflammatory enzymes and cytokines in LPS-exposed RAW264.7 macrophages[5].
Isolinderalactone (1-10 μM, 2-9 h) blocks LPS-induced NF-κB activation while activating Nrf2-HMOX1 signaling in RAW264.7 macrophages[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Isolinderalactone Related Antibodies

Cell Viability Assay[1][2]

Cell Line: U-87 GBM cells and HBMECs
Concentration: 0.5, 1, 2, 2.5 μg/mL
Incubation Time: 24, 48, 72 h
Result: Inhibited cell viability in a dose-dependent manner.
Decreased VEGF-induced HBMEC proliferation in a dose-dependent manner.

Western Blot Analysis[1][2]

Cell Line: U-87 GBM cells and HBMECs
Concentration: 0.5, 1, 2.5,5 μg/mL
Incubation Time: 48 h
Result: Decreased BCL-2, survivin, and XIAP expression.
Increased the level of cleaved caspase-3 and cleaved PARP.
Decreased the expression of the potent angiogenic factor, VEGF.
Decreased HIF expression and activity in U-87 cells.
Reduced phosphorylation of VEGFR2 in HBMECs.

Immunofluorescence[1]

Cell Line: U-87 GBM cells
Concentration: 2.5 μg/mL
Incubation Time: 48 h
Result: Showed predominantly bright γ-H2AX nuclear staining.

Cell Viability Assay[3]

Cell Line: HCT116, HCT116-OxR, HT29, and HT29-OxR cells
Concentration: 3, 6, 9 μM
Incubation Time: 24, 48 h
Result: Suppressed colorectal cancer cells proliferation with IC50 values of 8.05 μM (HCT116), 5.13 μM (HCT116-OxR), 10.38 μM (HT29) and 9.46 μM (HT29-OxR).

Cell Cycle Analysis[3]

Cell Line: HCT116, HCT116-OxR, HT29, and HT29-OxR cells
Concentration: 3, 6, 9 μM
Incubation Time: 48 h
Result: Contributed to G2/M phase cell cycle arrest.

Western Blot Analysis[3]

Cell Line: HCT116, HCT116-OxR, HT29, and HT29-OxR cells
Concentration: 3, 6, 9 μM
Incubation Time: 48 h
Result: Increased the expression levels of ER stress related proteins (GRP78, CHOP, DR4, and DR5).
Activated JNK/p38 MAPK.
Increased the levels of pro-apoptotic proteins (Bim and Bax), apaf-1, and cleaved (c)-PARP.
Decreased expression levels of anti-apoptotic proteins (Mcl-1, Bid, Bcl-xL and Bcl-2), mitochondrial cyto c and caspase 3 in a dose-dependent manner.

Western Blot Analysis[4]

Cell Line: Aβ1-42-induced PC12 cells
Concentration: 10 μM
Incubation Time: 27 h
Result: Decreased Bax expression and intracellular levels of caspase-3 activation and increased Bcl2 levels.
Decreased the level of p-JNK, but had no significant effect on ERK and P38MAPK.

Real Time qPCR[5]

Cell Line: LPS-exposed RAW264.7 macrophages
Concentration: 1, 10 μM
Incubation Time: 13 h
Result: Decreased the mRNA levels of iNOS, COX2, IL-1β, IL-6, and TNF-α.

Western Blot Analysis[5]

Cell Line: LPS-exposed RAW264.7 macrophages
Concentration: 1, 5, 10 μM
Incubation Time: 2, 9 h
Result: Down-regulated LPS-induced phosphorylation of IKKα/β and the level of NF-κB p65.
Increased the protein level of Nrf2 protein in the cytoplasmic fraction and nuclear fraction.
In Vivo

Isolinderalactone (1-5 mg/kg, i.p., every other day, 12 days) inhibits tumor growth in a human GBM xenograft mouse model[1].
Isolinderalactone (2.5-5 mg/kg, i.p., every other day, 16 days) reduces tumor growth and vasculature in a human GBM xenograft model [2].
Isolinderalactone (5 mg/kg, i.p., daily, 6 days) inhibits VEGF-mediated angiogenesis in an in vivo Matrigel plug assay in mice[2].
Isolinderalactone (1-10 mg/kg, i.p., daily, 30 days) ameliorates learning and memory deficits in APP/PS1 mice[4].
Isolinderalactone (2.5-10 mg/kg, i.p., daily, 5 days) alleviates LPS-induced lung inflammatory injury in mice[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: U-87 GBM cells (3 × 106 cells/100 μL of serum-free DMEM) were subcutaneously implanted into the right flank of the BALB/C nude mice[1]
Dosage: 1, 2.5, 5 mg/kg
Administration: i.p., every other day for 12 days
Result: Reduced tumor volume and weight Showed no differences on body weight.
Increased cleaved caspase-3 fluorescence.
Showed a significantly higher number of TUNEL-positive cells.
Animal Model: U-87 GBM cells (3 × 106 cells/100 μL of serum-free DMEM) were subcutaneously implanted into the right flank of the BALB/C nude mice[2]
Dosage: 2.5, 5 mg/kg
Administration: i.p., every other day for 16 days
Result: Decreased tumor volume and suppressed tumor progression.
Inhibited tumor angiogenesis.
Reduced VEGF immunoreactivity.
Animal Model: C57BL/6 mice (6-week-old, male)[2]
Dosage: 5 mg/kg
Administration: i.p. daily for 6 days
Result: Decreased hemoglobin concentration and CD31 staining.
Inhibited VEGF-induced new vessel formation in vivo.
Animal Model: 10-month-old APP/PS1 transgenic mice[4]
Dosage: 1, 10 mg/kg
Administration: i.p. daily for 30 days
Result: Enhanced the exploration of the novel object by the mice.
Ameliorated learning and memory deficits in APP/PS1mice.
Reduced the level of APP/β-amyloid.
Increased the levels of synapse-associated proteins, including PSD95 and Map2.
Reduced neuronal apoptosis in the cortex and hippocampus.
Increased the SOD content and decreased MDA levels in the hippocampus.
Increased Bcl2 levels, decreased Bax, p-JNK expression, and decreased caspase-3 activation.
Animal Model: Male Institute of Cancer Research (ICR) mice (SPF grade, 20-22 g, 6 weeks old) injected with LPS (15 mg/kg)[5]
Dosage: 2.5-10 mg/kg
Administration: i.p., daily for 5 days
Result: Improved the lung injury scores.
Reduced the MPO activity in LPS-exposed lung tissue.
Reduced the levels of PGE2, IL-1β, IL-6, and TNF-α.
Molecular Weight

244.29

Formula

C15H16O3
CAS No.
Appearance

Solid

Color

White to off-white

SMILES

C=C[C@@]1([C@]2([H])[C@](OC(C2=C)=O)([H])C3=C(OC=C3C)C1)C
Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

4°C, sealed storage, away from moisture and light

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

Solvent & Solubility
In Vitro: 

DMSO : 50 mg/mL (204.67 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 4.0935 mL 20.4675 mL 40.9350 mL
5 mM 0.8187 mL 4.0935 mL 8.1870 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 (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

  • Molarity Calculator

  • Dilution Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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Molecular Weight *

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start)

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

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.

  • Protocol 1

    Add each solvent one by one:  10% DMSO    90% Corn Oil

    Solubility: ≥ 5 mg/mL (20.47 mM); Clear solution

    This protocol yields a clear solution of ≥ 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 μL DMSO stock solution (50.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:

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g

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(per animal)

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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
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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).

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

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.
 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.
Purity & Documentation
References

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 (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 4.0935 mL 20.4675 mL 40.9350 mL 102.3374 mL
5 mM 0.8187 mL 4.0935 mL 8.1870 mL 20.4675 mL
10 mM 0.4093 mL 2.0467 mL 4.0935 mL 10.2337 mL
15 mM 0.2729 mL 1.3645 mL 2.7290 mL 6.8225 mL
20 mM 0.2047 mL 1.0234 mL 2.0467 mL 5.1169 mL
25 mM 0.1637 mL 0.8187 mL 1.6374 mL 4.0935 mL
30 mM 0.1364 mL 0.6822 mL 1.3645 mL 3.4112 mL
40 mM 0.1023 mL 0.5117 mL 1.0234 mL 2.5584 mL
50 mM 0.0819 mL 0.4093 mL 0.8187 mL 2.0467 mL
60 mM 0.0682 mL 0.3411 mL 0.6822 mL 1.7056 mL
80 mM 0.0512 mL 0.2558 mL 0.5117 mL 1.2792 mL
100 mM 0.0409 mL 0.2047 mL 0.4093 mL 1.0234 mL
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    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.

Keywords:

Isolinderalactone957-66-4STATVEGFRBcl-2 FamilySurvivinIAPNF-κBApoptosisCaspaseVascular endothelial growth factor receptorNuclear factor-κBNuclear factor-kappaBBrain tumor3D microfluidic chiphypoxia-inducible factorvascular endothelialgrowth factorangiogenesis,Reactive oxygen speciesJNK/p38 MAPKColorectal cancerAlzheimer’s diseaseInhibitorinhibitorinhibit

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