Cat. No.: HY-116474

Viridicatol

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Based on 1 Customer Validation

Viridicatol is a quinolone alkaloid with anti-inflammatory, antibacterial, antifungal, osteogenic and chondrogenic activities. Viridicatol reduces the phosphorylation levels of ERK, JNK, p38 and STAT6; inhibits MMP-2, MMP-9, NF-κB signaling pathway and PTP1B; downregulates genes related to mast cell activation; and binds to SHN3 to activate the Wnt/SHN3 signaling pathway. Viridicatol inhibits the expression of pro-inflammatory mediators and cytokines, and promotes osteogenic/chondrogenic differentiation. Viridicatol can be used in studies related to fibrosarcoma, allergy, bacterial infection, fungal infection and osteoporosis.

For research use only. We do not sell to patients.

Purity: 99.93%
CAS No.: 14484-44-7
Formula: C₁₅H₁₁NO₃
Molecular Weight:253.25

Storage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month

Viridicatol Chemical Structure

CAS No.: 14484-44-7

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Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target^[1]^[4]

ERK

p38 MAPK

JNK

MMP-9

MMP-2

NF-κB

All ERK Isoforms :

All JNK Isoforms :

All MMP Isoforms :

All p38 MAPK Isoforms :

All STAT Isoforms :

All NO Synthase Isoforms :

All NF-κB Isoforms :

All Wnt Isoforms :

In Vitro

Viridicatol (10-100 μM; 24 h) exhibits no cytotoxicity toward HT1080 human fibrosarcoma cells at 10, 20, and 50 μM, but induces cytotoxicity at 100 μM^[1].
Viridicatol (10-50 μM; 1 h pre-incubation, followed by 24 h PMA stimulation) inhibits PMA-induced MMP-2 and MMP-9 enzymatic activity in HT1080 human fibrosarcoma cells^[1].
Viridicatol (10-50 μM; 1 h pre-incubation, followed by 24 h PMA stimulation) reduces PMA-induced MMP-2 protein expression in HT1080 human fibrosarcoma cells, but does not affect MMP-9 protein expression^[1].
Viridicatol (10-50 μM; 1 h pre-incubation, followed by 24 h PMA stimulation) inhibits PMA-induced phosphorylation of ERK, JNK, and p38 in HT1080 human fibrosarcoma cells^[1].
Viridicatol (10 μg/mL; 1 h pre-incubation prior to 1 h DNP-BSA stimulation) regulates 128 differentially expressed genes in IgE-mediated activated RBL-2H3 cells, primarily down-regulating mast cell activation-related inflammatory factor and chemokine genes^[2].
Viridicatol (10 μg/mL; 1 h pre-incubation prior to 1 h DNP-BSA stimulation) significantly down-regulates the expression of mast cell activation-related genes (Tnfα, Ccl2, Jun, Fos, Il4, Ccl7, Il13, and Socs1) in IgE-mediated activated RBL-2H3 cells^[2].
Viridicatol (2.5-10 μg/mL; 1 h pre-incubation prior to 15 min DNP-BSA stimulation) dose-dependently inhibits the phosphorylation of JNK, ERK, P38, and STAT6 proteins in IgE-mediated activated RBL-2H3 cells, suppressing MAPK and JAK-STAT pathway activation^[2].
Viridicatol (compound 2) (0.98-500 μg/mL; 1 day) exhibits potent antibacterial activity against Staphylococcus aureus (MIC = 15.6 μg/mL) and moderate activity against Escherichia coli, Pseudomonas aeruginosa, Streptococcus lactis, Colletotrichum gloeosporioides, and Fusarium graminearum.^[3].
Viridicatol (0.98-500 μg/mL; 2 days) exhibits potent antifungal activity against Alternaria brassicae, Botrytis cinerea, and Valsa mali (MIC = 31.2 μg/mL) and moderate activity against Alternaria alternata, Setosphearia turcica, Sclerotinia sclerotiorum, Phytophthora capsici, and Peony anthracnose^[3].
Viridicatol (compound 1) (5-160 μM; 24 h) is non-cytotoxic to RAW264.7 and BV2 cells^[4].
Viridicatol (10-80 μM; 3 h pre-treatment, followed by 24 h LPS stimulation) dose-dependently inhibits pro-inflammatory mediator production and related protein expression in LPS-stimulated RAW264.7 cells, with IC₅₀ values of 46.03 μM for NO and 30.37 μM for PGE₂^[4].
Viridicatol (10-80 μM; 3 h pre-treatment, followed by 24 h LPS stimulation) dose-dependently inhibits pro-inflammatory mediator production and related protein expression in LPS-stimulated BV2 cells, with IC₅₀ values of 43.03 μM for NO and 34.20 μM for PGE₂^[4].
Viridicatol (10-80 μM; 3 h pre-treatment, followed by 6 h LPS stimulation) differentially inhibits inflammatory gene expression in LPS‑activated RAW264.7 and BV2 cells^[4].
Viridicatol (10-80 μM; 3 h pre-treatment, followed by 1 h LPS stimulation) inhibits the NF-κB signaling pathway in LPS-stimulated RAW264.7 cells and BV2 cells by blocking IκB-α phosphorylation/degradation, NF-κB p65/p50 nuclear translocation, and NF-κB DNA-binding activity^[4].
Viridicatol (1-10 μM; 5 days) promotes early osteogenic differentiation of MC3T3-E1 pre-osteoblasts, as evidenced by concentration-dependent increases in alkaline phosphatase activity after 5 days of treatment^[5].
Viridicatol (1-20 μM; 21 days) promotes late osteogenic mineralization of MC3T3-E1 pre-osteoblasts with an EC₅₀ of 5.204 μM after 21 days of treatment^[5].
Viridicatol (1-20 μM; 14 days) promotes osteogenic mineralization of mouse bone-derived mesenchymal stem cells with an EC₅₀ of 4.132 μM after 14 days of treatment^[5].
Viridicatol (1-10 μM; ~21 days) promotes chondrogenic differentiation of mouse bone-derived mesenchymal stem cells in a concentration-dependent manner after ~21 days of treatment^[5].
Viridicatol (5 μM; 0-48 h, 3 days, 5 days, 8 days) time-dependently inhibits Hivep3 mRNA expression and upregulates osteogenic marker genes Alpl and Bglap in MC3T3-E1 pre-osteoblasts^[5].
Viridicatol (5 μM; 8 days) promotes osteogenic mineralization of WT mouse bone-derived mesenchymal stem cells, but this effect is dependent on the presence of SHN3^[5].
Viridicatol (1-10 μM; 5 days) activates the Wnt/SHN3 signaling pathway in MC3T3-E1 pre-osteoblasts by upregulating β-catenin, p-GSK-3β, and p-ERK1/2 and inhibiting SHN3 protein expression^[5].
Viridicatol (1-10 μM; 5 days, 5 μM; 3, 5, 8 days) upregulates osteocalcin and β-catenin protein levels in mouse bone-derived mesenchymal stem cells^[5].

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

Cell Viability Assay^[1]

Cell Line:

HT1080 human fibrosarcoma cells
Concentration:

10 μM, 20 μM, 50 μM, 100 μM
Incubation Time:

24 h
Result:

Showed no obvious cytotoxic effect at 10, 20, and 50 μM.
Caused clear cytotoxicity at 100 μM.

Western Blot Analysis^[1]

Cell Line:

HT1080 human fibrosarcoma cells
Concentration:

10 μM, 20 μM, 50 μM
Incubation Time:

1 h pre-incubation, followed by 24 h PMA stimulation
Result:

Significantly inhibited MMP-2 protein expression in a dose-dependent manner.
Had no inhibitory effect on MMP-9 protein expression in PMA-stimulated cells.\n
Dose-dependently reduced the phosphorylation of ERK, JNK, and p38 in PMA-stimulated cells.
Showed significant inhibition at all tested concentrations for each MAPK subtype.

Real Time qPCR^[2]

Cell Line:

IgE-mediated activated RBL-2H3 cells
Concentration:

10 μg/mL
Incubation Time:

1 h (pre-incubation prior to 1 h DNP-BSA stimulation)
Result:

Significantly down-regulated the mRNA expression levels of Tnfα, Ccl2, Jun, Fos, Il4, Ccl7, Il13, and Socs1.

Western Blot Analysis^[2]

Cell Line:

IgE-mediated activated RBL-2H3 cells
Concentration:

2.5, 5, 10 μg/mL
Incubation Time:

1 h (pre-incubation prior to 15 min DNP-BSA stimulation)
Result:

Dose-dependently reduced the levels of phosphorylated JNK, ERK, P38, and STAT6, while total protein levels of these proteins remained unchanged.
Caused the most significant reduction in JNK and ERK phosphorylation at 10 μg/mL.
Significantly reduced P38 and STAT6 phosphorylation at all tested doses.

Cell Viability Assay^[4]

Cell Line:

murine macrophage-like RAW264.7 cells, murine immortalized microglial BV2 cells
Concentration:

5, 10, 20, 40, 80, 160 μM
Incubation Time:

24 h
Result:

Did not reduce cell viability of RAW264.7 or BV2 cells.
Decreased cell viability of RAW264.7 or BV2 cells relative to untreated controls at 160 μM.

RT-PCR^[4]

Cell Line:

LPS-stimulated murine macrophage-like RAW264.7 cells
Concentration:

10, 20, 40, 80 μM
Incubation Time:

3 h pre-treatment, followed by 6 h LPS stimulation
Result:

Reduced LPS-induced IL-1β, IL-6 and TNF-α mRNA expression dose-dependently.
Significantly inhibited IL-1β, IL-6 and TNF-α mRNA expression at 40 and 80 μM.

Cell Differentiation Assay^[5]

Cell Line:

mouse bone-derived mesenchymal stem cells (BMSCs)
Concentration:

1, 5, 10 μM
Incubation Time:

~21 days
Result:

Induced chondrogenic differentiation of BMSCs in a concentration-dependent manner.
Showed the highest relative Alcian blue staining fold change at 10 μM compared to control groups.

Real Time qPCR^[5]

Cell Line:

MC3T3-E1 pre-osteoblast cells
Concentration:

5 μM
Incubation Time:

0 h, 6 h, 12 h, 24 h, 48 h, 3 days, 5 days, 8 days
Result:

Inhibited Hivep3 (SHN3) mRNA expression in a time-dependent manner over 8 days.
Promoted time-dependent increases in Alpl (early osteogenic marker) and Bglap (late osteogenic marker) mRNA expression.

Western Blot Analysis^[5]

Cell Line:

MC3T3-E1 pre-osteoblast cells
Concentration:

1, 5, 10 μM
Incubation Time:

5 days
Result:

Upregulated β-catenin, p-GSK-3β, and p-ERK1/2 protein levels in a concentration-dependent manner.
Left NF-κB, total ERK1/2, and GSK-3β levels unchanged.
Significantly inhibited SHN3 protein expression.

Immunofluorescence^[5]

Cell Line:

mouse bone-derived mesenchymal stem cells (BMSCs)
Concentration:

1, 5, 10 μM (5 days); 5 μM (3, 5, 8 days)
Incubation Time:

3 days, 5 days, 8 days
Result:

Significantly upregulated OCN and β-catenin protein levels in BMSCs, with 5 μM and 10 μM showing significant increases over control after 5 days.
Showed time-dependent increases in OCN and β-catenin protein levels at 5 μM over 3, 5, and 8 days.

In Vivo

Viridicatol (5 mg/kg; i.v.; daily; 6 weeks) stimulates bone formation by enhancing osteoblast activity, increasing BV/TV and trabecular bone number to prevent bone loss in ovariectomized mice^[5].
Viridicatol (5 mg/kg; i.v.; every 2 days; 14 days) promotes fracture healing by increasing callus volume, bone mass, and cartilage and bone areas at the fracture site^[5].
Free viridicatol (5 mg/kg; i.v.; every 2 days; 4 weeks) provides limited mitigation of bone loss in the Col1a2^oim/oim osteogenesis imperfecta mouse model^[5].
Viridicatol delivered via bone-targeting nanovesicles (5 mg/kg; i.v.; every 2 days; 4 weeks) significantly reduces spontaneous fractures and increases bone volume fraction in the Col1a2^oim/oim osteogenesis imperfecta mouse model^[5].

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

Animal Model:

C57BL/6J (female, 10-week-old, bilateral ovariectomy-induced osteoporosis model)^[5]
Dosage:

5 mg/kg
Administration:

i.v.; daily; 6 weeks
Result:

Increased femur BV/TV and Tb.N versus untreated OVX group.
Increased 5th lumbar spine bone mass via Von Kossa staining.
Elevated MS/BS, MAR and BFR/BS.
Increased Ob.S/BS in 5th lumbar vertebrae and femur without altering N.Oc.S/BS.
Caused no significant weight changes, deaths or organ abnormalities.

Animal Model:

C57BL/6J (female, 8-week-old, closed transverse diaphyseal femur fracture model stabilized with an intramedullary needle)^[5]
Dosage:

5 mg/kg
Administration:

i.v.; every 2 days; 14 days
Result:

Significantly increased callus volume and BV/TV at the fracture site by micro-CT.
Increased cartilage and bone areas at the fracture site by Safranin O/Fast Green staining.
Increased Ob.S/BS without affecting osteoclast parameters.

Animal Model:

Col1a2oim/oim (male, 4-week-old, osteogenesis imperfecta genetic model)^[5]
Dosage:

5 mg/kg
Administration:

i.v.; every 2 days; 4 weeks
Result:

Showed limited therapeutic effects on severe osteopenic phenotype and spontaneous fracture incidence versus bone-targeted nanovesicle viridicatol, but trended toward improved bone parameters versus PBS control.
Significantly mitigated osteopenic phenotype, reduced spontaneous fractures, and increased femur BV/TV and Ob.S/BS versus PBS, free viridicatol and non-targeted nanovesicle controls.

Chemical Information

CAS No. 14484-44-7
Appearance Solid
Molecular Weight 253.25
Formula C₁₅H₁₁NO₃
Color White to off-white
SMILES

O=C1NC2=C(C=CC=C2)C(C3=CC=CC(O)=C3)=C1O
Structure Classification
- Alkaloids
- Quinoline Alkaloids
- Phenols
- Monophenols
Initial Source
- Microorganisms
Penicillium griseofulvum
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

Solvent & Solubility

In Vitro:

DMSO : 125 mg/mL (493.58 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

3.9487 mL

19.7433 mL

39.4867 mL

5 mM

0.7897 mL

3.9487 mL

7.8973 mL

10 mM

0.3949 mL

1.9743 mL

3.9487 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. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molarity Calculator

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

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

Dilution Calculator

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

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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: ≥ 2.08 mg/mL (8.21 mM); Clear solution

This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 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: ≥ 2.08 mg/mL (8.21 mM); Clear solution

This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

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.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

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

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (300 KB)
SDS (480 KB)
- English - EN (480 KB)
- Français - FR (480 KB)
- Deutsch - DE (480 KB)
- Norwegian - NO (480 KB)
- Español - ES (480 KB)
- Swedish - SV (480 KB)
- Italian - IT (480 KB)
- Korean - KR (480 KB)
- Portuguese - PT (480 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Liang P, et al. Viridicatol and viridicatin isolated from a shark-gill-derived fungus Penicillium polonicum AP2T1 as MMP-2 and MMP-9 inhibitors in HT1080 cells by MAPKs signaling pathway and docking studies. Medicinal Chemistry Research. 2019;28:1039-1048.

[2]. Liu Y, et al. Deep-sea-derived viridicatol relieves allergic response by suppressing MAPK and JAK-STAT signalling pathways of RBL-2H3 cells. Food and Agricultural Immunology. 2023;34(1).

[3]. Ma YM, et al. A new isoquinolone alkaloid from an endophytic fungus R22 of Nerium indicum. Nat Prod Res. 2017;31(8):951-958. [Content Brief]

[4]. Ko W. Viridicatol from Marine-derived Fungal Strain Penicillium sp. SF-5295 Exerts Anti-inflammatory Effects through Inhibiting NF-κB Signaling Pathway on Lipopolysaccharide-induced RAW264.7 and BV2 Cells. Natural Product Sciences. 2015;21(4):240.

[5]. Xie CL, et al. Viridicatol from the Deep-Sea-Derived Fungus Alleviates Bone Loss by Targeting the Wnt/SHN3 Pathway. Adv Sci (Weinh). 2025;12(21):e2416140. [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

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. 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	3.9487 mL	19.7433 mL	39.4867 mL	98.7167 mL
	5 mM	0.7897 mL	3.9487 mL	7.8973 mL	19.7433 mL
	10 mM	0.3949 mL	1.9743 mL	3.9487 mL	9.8717 mL
	15 mM	0.2632 mL	1.3162 mL	2.6324 mL	6.5811 mL
	20 mM	0.1974 mL	0.9872 mL	1.9743 mL	4.9358 mL
	25 mM	0.1579 mL	0.7897 mL	1.5795 mL	3.9487 mL
	30 mM	0.1316 mL	0.6581 mL	1.3162 mL	3.2906 mL
	40 mM	0.0987 mL	0.4936 mL	0.9872 mL	2.4679 mL
	50 mM	0.0790 mL	0.3949 mL	0.7897 mL	1.9743 mL
	60 mM	0.0658 mL	0.3291 mL	0.6581 mL	1.6453 mL
	80 mM	0.0494 mL	0.2468 mL	0.4936 mL	1.2340 mL
	100 mM	0.0395 mL	0.1974 mL	0.3949 mL	0.9872 mL

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Viridicatol

Anti-Infection Compound Library

Immunology/Inflammation Compound Library

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All ERK Isoforms

All JNK Isoforms

All MMP Isoforms

All p38 MAPK Isoforms

All STAT Isoforms

All NO Synthase Isoforms

All NF-κB Isoforms

All Wnt Isoforms

Biological Activity