Cat. No.: HY-N0608

Myrislignan

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Myrislignan is a PI3K/AKT/NF-κB inhibitor that can cross the blood-brain barrier. Myrislignan exerts anticancer activity by inducing apoptosis and ferroptosis. Myrislignan inhibits the replication and invasion of Toxoplasma gondii; it induces reactive oxygen species (ROS) imbalance, autophagy, and the death of Toxoplasma gondii tachyzoites. Myrislignan inhibits mitochondrial function and ERK1/2 phosphorylation to improve ovariectomy-induced osteoporosis. Myrislignan can be used in studies related to gastric cancer, glioblastoma, osteoporosis, and toxoplasmosis.

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Pureté: 99.53%
CAS No.: 171485-39-5
Formule: C₂₁H₂₆O₆
Masse moléculaire:374.43

Stockage:

4°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Myrislignan Chemical Structure

CAS No.: 171485-39-5

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Activité biologique
- Description
- In Vitro
- In Vivo
Chemical Information
Publications (1)
Solvant et solubilité
- In Vitro
- In Vivo
Pureté et documentation
Références
Help & FAQs
Classifications
Bioz

Activité biologique

Description

Voir tous les produits spécifiques à Isoform NF-κB :

Voir tous les produits spécifiques à Isoform PI3K :

Voir tous les produits spécifiques à Isoform Akt :

Voir tous les produits spécifiques à Isoform ERK :

In Vitro

Myrislignan (50-200 μM; 48-72 h) inhibits the viability of human gastric cancer SGC-7901 cells in a dose-dependent manner^[1].
Myrislignan (50-200 μM; 48 h) promotes apoptosis of human gastric cancer SGC-7901 cells in a dose-dependent manner^[1].
Myrislignan (50-200 μM; 48 h) downregulates the protein expression of PI3K and AKT in a dose-dependent manner in human gastric cancer SGC-7901 cells in vitro, and upregulates the protein expression of BAX, Caspase-3 and Caspase-9^[1].
Myrislignan (5-60 μg/mL; 24-48 h) inhibits the growth of human glioblastoma cell lines U87 and U251, as well as human low-grade glioma cell lines SHG44, HS683, and SW1088 in a dose- and time-dependent manner, while a low dose (30 μg/mL) shows no toxicity to the human normal astrocyte cell line NHA^[2].
Myrislignan (5-30 μg/mL; 24 h) inhibits the migration and invasion abilities of human glioblastoma cell lines U87 and U251 in a dose-dependent manner^[2].
Myrislignan (5-30 μg/mL; 48 h) dose-dependently impairs the wound healing capacity of human glioblastoma cell lines U87 and U251^[2].
Myrislignan (5-30 μg/mL) dose-dependently regulates the expression of EMT-related proteins in human glioblastoma cell lines U87 and U251, and inhibits the activation of the NF-κB pathway by reducing the levels of p-p65 and p-IκB-α^[2].
Myrislignan (5-30 μg/mL; 48 h) dose-dependently inhibits the activity of the NF-κB signaling pathway in human glioblastoma cell lines U87 and U251^[2].
Myrislignan (15 μg/mL) reduces the levels of nuclear and total phosphorylated p65 in the human glioblastoma cell line U87 without altering the total p65 level^[2].
Myrislignan (10 μg/mL) induces growth inhibition of the human glioma cell line U87 via ferroptosis. This effect is reversed by the ferroptosis inhibitor Fer-1 (HY-100579) and enhanced by the GPX4 inhibitor RSL3 (HY-100218A)^[2].
Myrislignan (5-15 μg/mL) dose-dependently induces lipid peroxidation and reduces the levels of antioxidant molecules without affecting the labile iron pool in the human glioblastoma cell line U87^[2].
Myrislignan (5-15 μg/mL) induces dose-dependent ultrastructural changes of mitochondria associated with ferroptosis in the human glioblastoma cell line U87^[2].
Myrislignan (5-15 μg/mL) downregulates the protein level of SLC7A11 in the human glioblastoma cell line U87 in a dose-dependent manner, without altering the expression levels of Nrf2, TFR1 or GPX4^[2].
Myrislignan (0-80 μM; 48-96 h) exerts no effect on the viability of primary mouse bone marrow macrophages and does not induce their apoptosis even at concentrations up to 80 μM and treatment durations as long as 96 h^[3].
Myrislignan (0-30 μM; 7 days) inhibits RANKL-induced osteoclast differentiation of primary mouse bone marrow macrophages in a dose-dependent manner, and its inhibitory effect peaks at the middle stage of differentiation (days 3-4) at a concentration of 30 μM^[3].
Myrislignan (15-30 μM; 7 days) inhibits the formation of podosome belts-a key cytoskeletal feature of mature osteoclasts-in primary mouse bone marrow macrophages treated with RANKL for 7 days^[3].
Myrislignan (15-30 μM; 2 days) impairs the bone resorption function of mature osteoclasts derived from primary mouse bone marrow macrophages^[3].
Myrislignan (15-30 μM; 7 days) dose-dependently inhibits the expression of osteoclast-specific genes in RANKL-treated primary mouse bone marrow macrophages^[3].
Myrislignan (15-30 μM; 3-7 days) inhibits mitochondrial function in primary mouse bone marrow macrophages treated with RANKL, reduces mtROS production on day 3, and decreases mitochondrial membrane potential on day 7^[3].
Myrislignan (30 μM; 60 min) specifically inhibits RANKL-induced phosphorylation of ERK in primary mouse bone marrow macrophages without affecting other MAPK or NF-κB pathway proteins; meanwhile, it blocks H₂O₂-induced ERK activation at a concentration of 30 μM^[3].
Myrislignan (30 μM; 60 min-7 days) inhibits osteoclastogenesis in primary mouse bone marrow macrophages by suppressing ERK phosphorylation and downstream protein expression; this effect is partially reversed by the ERK agonist LM22B-10 (HY-104047) at a concentration of 30 μM^[3].
Myrislignan (32-70 mg/mL; 24 h) alters the gene expression of tachyzoites of the RH strain of Toxoplasma gondii; differentially expressed genes (DEGs) are enriched in redox processes and the oxidative phosphorylation pathway^[4].
Myrislignan (32-70 mg/mL; 8-24 h) induces a statistically significant time-dependent increase in ROS activity in tachyzoites of the RH strain of Toxoplasma gondii^[4].
Myrislignan (32-70 mg/mL) induces a statistically significant increase in SOD activity in tachyzoites of the RH strain of Toxoplasma gondii, but SOD levels do not increase over time^[4].
Myrislignan (32-70 mg/mL; 16-24 h) induces the formation of autophagosome-like structures in tachyzoites of Toxoplasma gondii RH strain within infected Vero cells, followed by subsequent degeneration after treatment at 32 or 70 mg/mL for 16 or 24 h^[4].
Myrislignan (32-70 mg/mL; 16 h) induces autophagosome formation in tachyzoites of the RH strain of Toxoplasma gondii^[4].
Myrislignan (16-70 mg/mL; 16 h) upregulates the autophagy marker TgATG8-PE in a dose-dependent manner in tachyzoites of the RH strain of Toxoplasma gondii^[4].
Myrislignan (32-70 mg/mL; 24 h) induces concentration-dependent cell death in tachyzoites of the RH strain of Toxoplasma gondii^[4].

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

Cell Viability Assay^[1]

Cell Line:

human gastric cancer SGC-7901 cells
Concentration:

25; 50; 100; 200 μM
Incubation Time:

48 h; 72 h
Result:

Significantly inhibited SGC-7901 cell viability in a dose-dependent manner at 50, 100, and 200 μM after 48 h and 72 h.
Showed no significant difference in cell viability at 25 μM compared with control groups.

Apoptosis Analysis^[1]

Cell Line:

human gastric cancer SGC-7901 cells
Concentration:

25; 50; 100; 200 μM
Incubation Time:

48 h
Result:

Increased the apoptosis rate of SGC-7901 cells, with a significant difference between the 200 μM group and the 100 μM group.

Western Blot Analysis^[1]

Cell Line:

human gastric cancer SGC-7901 cells
Concentration:

25; 50; 100; 200 μM
Incubation Time:

48 h
Result:

Downregulated the expression levels of PI3K and AKT proteins, and upregulated the expression levels of BAX, Caspase-3, and Caspase-9 proteins in a dose-dependent manner.
Showed relative PI3K expression of approximately 0.6, relative AKT expression of approximately 0.6, relative Caspase-9 expression of approximately 1.0, relative Caspase-3 expression of approximately 1.1, and relative BAX expression of approximately 1.1 at 200 μM.

Cell Viability Assay^[2]

Cell Line:

human glioblastoma cell lines U87, U251; human low-grade glioma cell lines SHG44, HS683, SW1088; human normal astrocyte cell line NHA
Concentration:

5, 10 and 15 μg/mL (U87); 10, 20 and 30 μg/mL (U251); 30, 40, 50 and 60 μg/mL (NHA)
Incubation Time:

24 h, 48 h (U87, U251); null (NHA)
Result:

Significantly inhibited the growth of U87 and U251 cells in a time- and dose-dependent manner.
Suppressed the growth of SHG44, HS683, and SW1088 cells.
Did not affect apoptosis or ferroptosis-associated protein levels in NHA cells at 30 μg/mL.
Inhibited NHA growth and caused lipid peroxidation at 40, 50, and 60 μg/mL.

Cell Migration Assay ^[2]

Cell Line:

human glioblastoma cell lines U87, U251
Concentration:

5, 10 and 15 μg/mL (U87); 10, 20 and 30 μg/mL (U251)
Incubation Time:

24 h
Result:

Significantly reduced the number of migrated U87 and U251 cells in a dose-dependent manner.
Caused statistically significant decreases at all tested concentrations compared to untreated controls.

Cell Invasion Assay^[2]

Cell Line:

human glioblastoma cell lines U87, U251
Concentration:

5, 10 and 15 μg/mL (U87); 10, 20 and 30 μg/mL (U251)
Incubation Time:

48 h
Result:

Significantly reduced the wound healing percentage of U87 and U251 cells in a dose-dependent manner.
Caused statistically significant decreases at all tested concentrations compared to untreated controls.

In Vivo

Myrislignan (5 mg/kg; i.p.; every 3 days; 21 days) suppresses glioblastoma progression in an intracranial xenograft model, improving mouse survival, reducing tumor weight, and modulating EMT and ferroptosis-related protein expression^[2].
Myrislignan (15-30 mg/kg; i.p.; daily; 6 weeks) dose-dependently reduces ovariectomy-induced bone loss in female C57BL/6J mice^[3].

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

Animal Model:

Nude mice (male, 5 weeks old, intracranial xenograft model via stereotactic implantation of U87 cells)^[2]
Dosage:

5 mg/kg
Administration:

i.p.; every 3 days; 21 days
Result:

Improved mouse survival compared to the control group.
Reduced tumor weight.
Decreased tumor tissue levels of phosphorylated p65 (p-p65), Slug, and SLC7A11.
Increased tumor tissue levels of E-cadherin.

Animal Model:

C57BL/6J (11-weeks-old female; osteoporosis induced via bilateral ovariectomy)^[3]
Dosage:

15 mg/kg; 30 mg/kg
Administration:

i.p.; daily; 6 weeks
Result:

Increased bone volume/total volume (BV/TV) and trabecular number (Tb.N), and decreased trabecular separation (Tb.Sp) in the 30 mg/kg group compared to the ovariectomy-only group.
Showed intermediate improvements in BV/TV, Tb.N, and Tb.Sp in the 15 mg/kg group compared to the ovariectomy-only group.
Reduced bone surface/trabecular surface (BS/TS) and the number of TRAP-positive osteoclasts per trabecular surface (N.Oc/BS) in both dose groups compared to the ovariectomy-only group, with greater effects at 30 mg/kg.
Reduced the ratio of phosphorylated ERK (p-ERK) to total ERK in both dose groups compared to the ovariectomy-only group, with a more significant reduction at 30 mg/kg.

Chemical Information

CAS No. 171485-39-5
Appearance Solid
Masse moléculaire 374.43
Formule C₂₁H₂₆O₆
Color White to off-white
SMILES

C[C@@H]([C@@H](C1=CC(OC)=C(O)C=C1)O)OC(C(OC)=CC(CC=C)=C2)=C2OC
Structure Classification
- Phenylpropanoids
- Simple Phenylpropanols
- Phenols
- Monophenols
Initial Source
Livraison

Room temperature in continental US; may vary elsewhere.
Stockage

4°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Publications (1)

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University of Edinburgh

2025 May 29.

Solvant et solubilité

In Vitro:

DMSO : 100 mg/mL (267.07 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

2.6707 mL

13.3536 mL

26.7073 mL

5 mM

0.5341 mL

2.6707 mL

5.3415 mL

10 mM

0.2671 mL

1.3354 mL

2.6707 mL

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.

Calculateur de molarité

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

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Volume Volume

Molecular Weight Molecular Weight

Calculateur de dilution

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

Concentration _(start) Concentration _(start)

Volume _(start) Volume _(start)

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In Vivo:

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

Stock Solution Working Solution

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 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 2.5 mg/mL (6.68 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 μL DMSO 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.

Protocol 2

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: ≥ 2.5 mg/mL (6.68 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 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 3

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

Solubility: ≥ 2.5 mg/mL (6.68 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 μL DMSO stock solution (25.0 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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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

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Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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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).

Working solution concentration: 0.22 mg/mL

Pureté et documentation

Select Batch:

Pureté: 99.98%

Assay: 99.98%

ee.: 99.98%

Fiche technique (290 KB)
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Instruction de manipulation (2659 KB)

Références

[1]. Zhou YJ, et al. Myrislignan Induces Apoptosis in Gastric Cancer Cell Line Through PI3K/AKT Signaling Pathway. Sichuan Da Xue Xue Bao Yi Xue Ban. 2023 Jan;54(1):136-141. Chinese.
[Content Brief]

[2]. Zhou Y, et al. NF-B Inhibitor Myrislignan Induces Ferroptosis of Glioblastoma Cells via Regulating Epithelial-Mesenchymal Transformation in a Slug-Dependent Manner. Oxidative medicine and cellular longevity. 2023;2023:7098313. [Content Brief]

[3]. Yang T, et al. Myrislignan targets extracellular signal-regulated kinase (ERK) and modulates mitochondrial function to dampen osteoclastogenesis and ovariectomy-induced osteoporosis. Journal of translational medicine. 2023 Nov 22;21(1):839. [Content Brief]

[4]. Zhang J, et al. Myrislignan Induces Redox Imbalance and Activates Autophagy in Toxoplasma gondii. Front Cell Infect Microbiol. 2021 Sep 3;11:730222.
[Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.6707 mL	13.3536 mL	26.7073 mL	66.7682 mL
	5 mM	0.5341 mL	2.6707 mL	5.3415 mL	13.3536 mL
	10 mM	0.2671 mL	1.3354 mL	2.6707 mL	6.6768 mL
	15 mM	0.1780 mL	0.8902 mL	1.7805 mL	4.4512 mL
	20 mM	0.1335 mL	0.6677 mL	1.3354 mL	3.3384 mL
	25 mM	0.1068 mL	0.5341 mL	1.0683 mL	2.6707 mL
	30 mM	0.0890 mL	0.4451 mL	0.8902 mL	2.2256 mL
	40 mM	0.0668 mL	0.3338 mL	0.6677 mL	1.6692 mL
	50 mM	0.0534 mL	0.2671 mL	0.5341 mL	1.3354 mL
	60 mM	0.0445 mL	0.2226 mL	0.4451 mL	1.1128 mL
	80 mM	0.0334 mL	0.1669 mL	0.3338 mL	0.8346 mL
	100 mM	0.0267 mL	0.1335 mL	0.2671 mL	0.6677 mL

Myrislignan

1 Cited Publications

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Myrislignan

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Activité biologique

Chemical Information

Publications (1)

Solvant et solubilité

Pureté et documentation

Références

Help & FAQs

Complete Stock Solution Preparation Table

Myrislignan Related Classifications

HY-N0608 Related Classifications