Anti-infection Immunology/Inflammation MAPK/ERK Pathway Stem Cell/Wnt JAK/STAT Signaling Apoptosis Metabolic Enzyme/Protease NF-κB PI3K/Akt/mTOR
Beta-lactamase COX Interleukin Related Bacterial JNK ERK p38 MAPK STAT Apoptosis NO Synthase Nuclear Factor of activated T Cells (NFAT) Lactate Dehydrogenase Reactive Oxygen Species (ROS) SOD Akt Caspase Bcl-2 Family
3′,4′,7-Trihydroxyflavone

Cat. No.: HY-N2736

3′,4′,7-Trihydroxyflavone

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Based on 1 publication(s) in Google Scholar

3′,4′,7-Trihydroxyflavone is an orally active inhibitor of OXA-48 (IC₅₀ = 1.89 μM) and COX-1 (IC₅₀ = 36.37 μM). 3′,4′,7-Trihydroxyflavone exhibits antioxidant and anti-inflammatory properties, inhibiting the release of inflammatory cytokines such as IL-6, IL-8, and TNF-α. 3′,4′,7-Trihydroxyflavone inhibits H₂O₂-induced neuronal apoptosis and ROS accumulation, and exerts anti-neuroinflammatory effects by suppressing the JNK-STAT1 pathway. 3′,4′,7-Trihydroxyflavone exhibits antimicrobial and antibiotic-modifying activities against multidrug-resistant Gram-negative enteric bacteria. 3′,4′,7-Trihydroxyflavone inhibits RANKL-induced osteoclast formation via NFATc1. 3′,4′,7-Trihydroxyflavone activates the CREB-BDNF axis and restores scopolamine (HY-N0296)-induced memory deficits in mice.

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Pureté: 99.04%
CAS No.: 2150-11-0
Formule: C₁₅H₁₀O₅
Masse moléculaire:270.24

Stockage:

RT, protect from light.

In solvent -80°C, 1 year , -20°C, 6 months

3′,4′,7-Trihydroxyflavone Chemical Structure

CAS No.: 2150-11-0

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

Activité biologique

Description

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Cellular Effect

Cell Line	Type	Value	Description	References
CHO	IC₅₀	49.3 μM Compound: 12	Cytotoxicity against CHO cells by MTT assay Cytotoxicity against CHO cells by MTT assay	[PMID: 19572738]
HEK293	IC₅₀	>40 μM Compound: 1d	Inhibition of human telomerase from HEK293 cell extracts by Flash-Plate assay Inhibition of human telomerase from HEK293 cell extracts by Flash-Plate assay	[PMID: 15588081]
HEK293	IC₅₀	>40 μM Compound: Fig 20, R2C1	Inhibition of telomerase extracted from HEK293 cells using 5'-bAATCCGTCGAGCAGAGTT as primer assessed as polymerization of telomeric repeats to the end of the primers after 2 hrs by Flash-Plate assay Inhibition of telomerase extracted from HEK293 cells using 5'-bAATCCGTCGAGCAGAGTT as primer assessed as polymerization of telomeric repeats to the end of the primers after 2 hrs by Flash-Plate assay	10.1039/C0MD00241K
Neutrophil	IC₅₀	13.5 μM Compound: 3d	Inhibition of oxidative burst in PMA-stimulated human neutrophils assessed as inhibition of ROS-induced luminol oxidation incubated for 5 mins prior to PMA challenge by chemiluminescence assay Inhibition of oxidative burst in PMA-stimulated human neutrophils assessed as inhibition of ROS-induced luminol oxidation incubated for 5 mins prior to PMA challenge by chemiluminescence assay	[PMID: 23871908]
Neutrophil	IC₅₀	14.7 μM Compound: 3d	Inhibition of oxidative burst in PMA-stimulated human neutrophils assessed as inhibition of superoxide anion radical-induced lucigenin oxidation incubated for 5 mins prior to PMA challenge by chemiluminescence assay Inhibition of oxidative burst in PMA-stimulated human neutrophils assessed as inhibition of superoxide anion radical-induced lucigenin oxidation incubated for 5 mins prior to PMA challenge by chemiluminescence assay	[PMID: 23871908]
Neutrophil	IC₅₀	3.7 μM Compound: 3d	Inhibition of oxidative burst in PMA-stimulated human neutrophils assessed as inhibition of H2O2-induced oxidation of amplex red incubated for 5 mins prior to PMA challenge by fluorescence assay Inhibition of oxidative burst in PMA-stimulated human neutrophils assessed as inhibition of H2O2-induced oxidation of amplex red incubated for 5 mins prior to PMA challenge by fluorescence assay	[PMID: 23871908]
Neutrophil	IC₅₀	5.2 μM Compound: 3d	Inhibition of oxidative burst in PMA-stimulated human neutrophils assessed as inhibition of HOCl-induced oxidation of APF after 6 mins by fluorescence assay Inhibition of oxidative burst in PMA-stimulated human neutrophils assessed as inhibition of HOCl-induced oxidation of APF after 6 mins by fluorescence assay	[PMID: 23871908]
Peritoneal macrophage	IC₅₀	26 μM Compound: kp15	Inhibition of LPS-stimulated nitric oxide production in ddy mouse peritoneal macrophages measured after 20 hrs by Greiss method Inhibition of LPS-stimulated nitric oxide production in ddy mouse peritoneal macrophages measured after 20 hrs by Greiss method	[PMID: 27955927]

In Vitro

3′,4′,7-Trihydroxyflavone (0.1-20 μM, 24 h) enhances the cell viability and survival against Scopolamine (HY-N0296)-induced damage in SH-SY5Y cells^[1].
3′,4′,7-Trihydroxyflavone (0.1-100 µM) reduces the secretion of IL-6 and IL-8 in TNFα-stimulated HaCaT cells, with IC₅₀s of 17.8, 126.2 µg/mL, with maximum inhibition rates of 74.4, 40.2 %, reduces HaCaT cell viability to 74%^[2].
3′,4′,7-Trihydroxyflavone (50 µM, 64 μg/mL) inhibits OXA-48 activity by 80% and exhibits antimicrobial activity against BW25113 ∆acrA∆bamB (OXA-48) in combination with β-lactam antibiotics^[3].
3′,4′,7-Trihydroxyflavone (1-20 μM, 30 min) prevents H₂O₂-induced cell death and lactate dehydrogenase (LDH) release in SH-SY5Y and hippocampal neuronal cells^[4].
3′,4′,7-Trihydroxyflavone (1-20 µM, 30 min) inhibits H₂O₂-induced apoptotic features of SH-SY5Y cells, reverses induced nuclear necrosis, and condenses cell shrinkage^[4].
3′,4′,7-Trihydroxyflavone (0.5-20 µM, 30 min) inhibits H₂O₂-induced ROS accumulation, SOD, CAT, and GSH reduction, and activation of F-κB p65 translocation from the cytosol to the nucleus in SH-SY5Y cells^[4].
3′,4′,7-Trihydroxyflavone (1-20 µM, 30 min) inhibits H₂O₂-induced phosphorylation of JNK, p38, ERK 1/2 MAPKs and PI3K/Akt levels, upregulation of Bax, caspase-3, caspase-9 and PARP levels, downregulation of Bcl-2 and Bcl-xL levels, release of cytochrome c and loss of MMP in SH-SY5Y cells^[4].
3′,4′,7-Trihydroxyflavone shows antibacterial activity against 12 Gram-negative bacteria E. coli, E. aerogenes, K. pneumonia, with MIC values ranging from 4 to 256 μg/mL^[5].
3′,4′,7-Trihydroxyflavone improves the activity of Tetracycline (HY-A0107) and Erythromycin (HY-B0220) on 80% of the tested bacteria, with FIC values ranging from 0.5 to < 0.062^[5].
3′,4′,7-Trihydroxyflavone (0.1-100 μM) has no effect at 0.1–30 µM, but decreases cell viability at 100 µM for MG6 cells^[6].
3′,4′,7-Trihydroxyflavone (0.1-10 μM, 6-48 h) reduces NO, TNF-α, and iNOS levels, inhibits STAT1 phosphorylation and total STAT1 expression in LPS (HY-D1056)-induced MG6 cells^[6].
3′,4′,7-Trihydroxyflavone (0.1-10 μM, 0.5 h) inhibits JNK phosphorylation but not p38 or ERK phosphorylation in LPS-induced MG6 cells^[6].
3′,4′,7-Trihydroxyflavone (0.1-10 μM, 24-48 h) inhibits NO release, iNOS expression, STAT1 phosphorylation in IFN-γ-induced MG6 cells^[6].
3′,4′,7-Trihydroxyflavone (0-5 μg/mL, 1-7 days) inhibits RANKL-induced osteoclast formation and bone resorption in BMMs^[7].
3′,4′,7-Trihydroxyflavone (5 μg/mL, 7 days) suppresses RANKL-induced NFATc1 expression via Blimp-1 and p38 MAPK pathway in BMMs^[7].

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

Cell Viability Assay^[1]

Cell Line:

SH-SY5Y cells
Concentration:

0.1, 1, 5, 10, and 20 μM
Incubation Time:

24 h
Result:

Enhanced the cell viability and survival against Scopolamine (HY-N0296)-induced damage.

Apoptosis Analysis^[4]

Cell Line:

SH-SY5Y cells
Concentration:

0.1, 1, 5, 10, and 20 μM
Incubation Time:

30 min
Result:

Inhibited apoptosis, reversed H₂O₂-induced nuclear necrosis and condensation, and cell shrinkage.

Immunofluorescence^[4]

Cell Line:

SH-SY5Y cells
Concentration:

0.5, 1, 5, 10, and 20 μM
Incubation Time:

30 min
Result:

Reduced ROS, SOD, CAT and GSH fluorescence intensity.
Increased the fluorescence intensity of MMP and rhodamine 123, eliminated cytochrome c diffusion caused by H₂O₂.

Western Blot Analysis^[4]

Cell Line:

SH-SY5Y cells
Concentration:

1, 5, 10, and 20 μM
Incubation Time:

30 min
Result:

Reduced the phosphorylation of Akt, JNK, p38 MAPK, and Akt to 40.64%, 111%, 105%, and 95% of the control value, respectively.
Inhibited the upregulation or downregulation of Bax and Bcl-xL to 118% and 62% of control values, respectively at 1 µM, inhibited the upregulation or downregulation of Bax, Bcl-2, and Bcl-xL to 111%, 87%, and 82% of control values, respectively, at 5 µM, inhibited the upregulation or downregulation of Bax, Bcl-2, and Bcl-xL to 102%, 98%, and 93% of control values, respectively at 20 µM.
Reduced the release of cytochrome c from mitochondria to the cytosol.
Significantly inhibited the increase in cleaved PARP, cleaved caspase-3 and cleaved caspase-9.

Western Blot Analysis^[6]

Cell Line:

LPS-induced MG6 cells
Concentration:

0.1, 1, and 10 μM
Incubation Time:

0.5, 6, 24 h
Result:

Reduced iNOS levels.
Inhibited STAT1 phosphorylation and total STAT1 expression.
Inhibited JNK phosphorylation but not p38 or ERK phosphorylation.

Western Blot Analysis^[6]

Cell Line:

IFN-γ-induced MG6 cells
Concentration:

0.1, 1, and 10 μM
Incubation Time:

24 h
Result:

Inhibited NO release and increased iNOS expression.
Inhibited STAT1 phosphorylation but did not inhibit the increase in total STAT1 levels.

RT-PCR^[7]

Cell Line:

BMMs
Concentration:

5 μg/mL with RANKL (100 ng/mL) and M-CSF (30 ng/mL)
Incubation Time:

7 days
Result:

Suppressed the mRNA expression levels of CTR and cathepsin K.
Suppressed the expression of DC-STAMP and ATP6v0d2 induced by RANKL. Decreased the mRNA level of Blimp1.

Western Blot Analysis^[7]

Cell Line:

BMMs
Concentration:

5 μg/mL with RANKL (200 ng/mL)
Incubation Time:

30 min
Result:

Abolished RANKL-induced NFATc1 expression, but not c-Fos protein expression.
Suppressed phosphorylation of p38.

In Vivo

3′,4′,7-Trihydroxyflavone (10/50 mg/kg, p.o., once a day, 3 days/three times per week, 28 days; 10 ng, ICV, twice a week, 28 days) plays a neuroprotective role by inducing CREB-BDNF activation, improving long-term potentiation (LTP) in Scopolamine-induced cognitive deficits mice model^[1].

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

Animal Model:

Scopolamine-induced cognitive deficits mice (male C57BL/6J, 8 weeks old) model^[1]
Dosage:

10/50 mg/kg
Administration:

p.o., once a day, 3 days/three times per week, 28 days
Result:

Improved cognitive abilities at 50 mg/kg.
Had no acute cognitive improvement after three days.
Restored ACh and ChAT levels and reduced AChE activity, increased BDNF mRNA and protein levels, and restored pCREB levels at 50 mg/kg.
Increased the number of neurons and restored astrocyte levels (GFAP marker).

Animal Model:

Scopolamine-induced cognitive deficits mice (male C57BL/6J, 8 weeks old) model^[1]
Dosage:

10 ng
Administration:

ICV, twice a week, 28 days
Result:

Improved spontaneous change, novel object recognition index and passive avoidance, acetylcholine activity, and restored acetylcholinesterase and choline acetyltransferase activities.
Induced the enhancement of the CREB-BDNF signaling pathway and increased LTP.

Chemical Information

CAS No. 2150-11-0
Appearance Solid
Masse moléculaire 270.24
Formule C₁₅H₁₀O₅
Color Off-white to light yellow
SMILES

O=C1C2=CC=C(O)C=C2OC(C3=CC(O)=C(O)C=C3)=C1
Structure Classification
- Flavonoids
- Flavones
- Phenols
- Polyphenols
Initial Source
Livraison

Room temperature in continental US; may vary elsewhere.

Stockage

RT, protect from light

In solvent	-80°C	1 year
	-20°C	6 months

Publications (1)

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Spectrochim Acta A Mol Biomol Spectrosc

Communication of bifunctional G-quadruplex chaperone with aptamer for highly selective adenosine signaling by an ESIPT fluorogen. [Abstract]

2026 Jun 5:354:127637. PMID: 41762796

Solvant et solubilité

In Vitro:

DMSO : 2.5 mg/mL (9.25 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

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10 mg

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Solvent

Mass

1 mM

3.7004 mL

18.5021 mL

37.0041 mL

5 mM

0.7401 mL

3.7004 mL

7.4008 mL

10 mM

---

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Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

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Pureté et documentation

Select Batch:

Pureté: 99.98%

Assay: 99.98%

ee.: 99.98%

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Références

[1]. Kim SS, et al. 3',4',7-trihydroxyflavone activates the CREB-BDNF axis and restores scopolamine-induced memory deficit in mice. Eur J Pharmacol. 2025 Jul 15;999:177645 [Content Brief]

[2]. Codo Toafode NM, et al. Anti-Inflammatory Potential of Phenolic Compounds Isolated From Entada africana Guill. & Perr. Used in the Republic of Benin. Front Pharmacol. 2022 Jun 30;13:931240. [Content Brief]

[3]. Zhang Y, et al. Discovery of Quercetin and Its Analogs as Potent OXA-48 Beta-Lactamase Inhibitors. Front Pharmacol. 2022 Jun 22;13:926104. [Content Brief]

[4]. Kwon SH, et al. 3',4',7-Trihydroxyflavone prevents apoptotic cell death in neuronal cells from hydrogen peroxide-induced oxidative stress. Food Chem Toxicol. 2015 Jun;80:41-51. [Content Brief]

[5]. Dzotam JK, et al. In vitro antibacterial and antibiotic modifying activity of crude extract, fractions and 3',4',7-trihydroxyflavone from Myristica fragrans Houtt against MDR Gram-negative enteric bacteria. BMC Complement Altern Med. 2018 Jan 15;18(1):15. [Content Brief]

[6]. Akaishi T, et al. 3',4',7-Trihydroxyflavone Downregulates NO Production in LPS- or IFN-γ-Activated MG6 Microglial Cells by Attenuating the JNK-STAT1 Pathway. Biol Pharm Bull. 2022;45(3):301-308. [Content Brief]

[7]. Kang JH, et al. 3'4'7-Trihydroxyflavone inhibits RANKL-induced osteoclast formation via NFATc1. Pharmazie. 2015 Oct;70(10):661-7. [Content Brief]

[8]. Selvam C, et al. Cyclooxygenase inhibitory flavonoids from the stem bark of Semecarpus anacardium Linn. Phytother Res. 2004 Jul;18(7):582-4. [Content Brief]

[9]. Jung MJ, et al. Antioxidant activity from the stem bark of Albizzia julibrissin. Arch Pharm Res. 2003 Jun;26(6):458-62. [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, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	3.7004 mL	18.5021 mL	37.0041 mL	92.5104 mL
DMSO	5 mM	0.7401 mL	3.7004 mL	7.4008 mL	18.5021 mL

3′,4′,7-Trihydroxyflavone

1 Cited Publications

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3′,4′,7-Trihydroxyflavone

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