1. Epigenetics Immunology/Inflammation Apoptosis NF-κB PI3K/Akt/mTOR Metabolic Enzyme/Protease
  2. Akt TNF Receptor Interleukin Related Reactive Oxygen Species (ROS) Apoptosis PI3K AMPK
  3. (±)-10-Gingerol

(±)-10-Gingerol is the racemic form of 10-Gingerol (HY-N0448). 10-Gingerol is an AMPK agonist, which is found in the ginger oleoresin from fresh rhizome with anti-inflammatory, antioxidant and anti-proliferative activities. 10-Gingerol suppresses neointimal hyperplasia and inhibits vascular smooth muscle cell proliferation. 10-Gingerol exhibits substantial scavenging activities with an IC50 value of 10.47 μM against DPPH radical, an IC50 value of 1.68 μM against superoxide radical and an IC50 value of 1.35 μM against hydroxyl radical. 10-Gingerol inhibits the proliferation of MDA-MB-231 tumor cell line with an IC50 of 12.1 μM. 10-Gingerol suppresses the proliferation, migration, invasion, and induced apoptosis through targeting the PI3K/Akt signaling pathway in MDA-MB-231/IR cells. 10-Gingerol can be used in research on various common cancers such as ovarian cancer and colon cancer, as well as colitis and neurodegenerative diseases.

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(±)-10-Gingerol

(±)-10-Gingerol Chemical Structure

CAS No. : 107257-18-1

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Description

(±)-10-Gingerol is the racemic form of 10-Gingerol (HY-N0448). 10-Gingerol is an AMPK agonist, which is found in the ginger oleoresin from fresh rhizome with anti-inflammatory, antioxidant and anti-proliferative activities. 10-Gingerol suppresses neointimal hyperplasia and inhibits vascular smooth muscle cell proliferation. 10-Gingerol exhibits substantial scavenging activities with an IC50 value of 10.47 μM against DPPH radical, an IC50 value of 1.68 μM against superoxide radical and an IC50 value of 1.35 μM against hydroxyl radical. 10-Gingerol inhibits the proliferation of MDA-MB-231 tumor cell line with an IC50 of 12.1 μM. 10-Gingerol suppresses the proliferation, migration, invasion, and induced apoptosis through targeting the PI3K/Akt signaling pathway in MDA-MB-231/IR cells. 10-Gingerol can be used in research on various common cancers such as ovarian cancer and colon cancer, as well as colitis and neurodegenerative diseases[1][2][3][4][5].

Cellular Effect
Cell Line Type Value Description References
HCT-116 IC50
33.36 μM
Compound: N3
Cytotoxicity against human HCT116 cells assessed as reduction in cell viability after 48 hrs by WST1 assay
Cytotoxicity against human HCT116 cells assessed as reduction in cell viability after 48 hrs by WST1 assay
[PMID: 28065501]
In Vitro

(±)-10-Gingerol (29.19-50.87 μM) potently inhibits cervical cancer HeLa cells with an IC50 of 29.19 μM and IC80 of 50.87 μM by inducing G0/G1 phase cell cycle arrest and apoptosis[1].
(±)-10-Gingerol (15.24-21.59 μM) potently inhibits LTA4H aminopeptidase (IC50 = 21.59 μM) and epoxide hydrolase (IC50 = 15.24 μM) in human colon cancer HCT-116 cells, showing greater activity than other tested gingerols[1].
(±)-10-Gingerol inhibits proliferation and invasion of human breast cancer MDA-MB-231 cells through inactivation of AKT and p38/MAPK signaling and suppression of epidermal growth factor receptor expression[1].
(±)-10-Gingerol (30 μM) inhibits proliferation of human colon cancer HCT-116 cells and induces mitochondrial-mediated apoptosis via activation of the MAPK pathway[1].
(±)-10-Gingerol (50 μM) inhibits growth of human prostate cancer PC-3 cells with an IC50 of 50 μM (17.53 μg mL-1)[1].
(±)-10-Gingerol selectively induces cytotoxicity and reverts the malignant phenotype of T4-2 breast cancer cells in in vitro 3D culture, while sparing non-malignant HMT3522 S1 mammary epithelial cells[1].
(±)-10-Gingerol shows greater cytotoxicity against human A549 lung adenocarcinoma, SK-OV-3 ovarian cancer, SK-MEL-2 skin melanoma, and HCT15 colon cancer cells than other tested gingerols[1].
(±)-10-Gingerol (12.1 μM) potently inhibits growth of human triple-negative breast cancer MDA-MB-231 cells by inducing S-phase cell cycle arrest and mitochondrial-mediated apoptosis[1].
(±)-10-Gingerol (10-100 μM) induces concentration-dependent cell death in human colorectal cancer SW480 cells by increasing intracellular calcium levels[1].
(±)-10-Gingerol (20 μM) potently inhibits LPS-induced neuroinflammation in murine BV2 microglial cells by suppressing NF-κB activation and proinflammatory cytokine production, and is the primary contributor to fresh Zingiber officinale's anti-neuroinflammatory capacity[1].
(±)-10-Gingerol (1.35-10.47 μM) is the most potent anti-oxidant among tested gingerols, with IC50 values of 10.47 μM for DPPH radical scavenging, 1.68 μM for superoxide radical scavenging, and 1.35 μM for hydroxyl radical scavenging[1].
(±)-10-Gingerol (4-50 μg mL-1) exhibits potent anti-bacterial activity against periodontal bacteria, Mycobacterium species, and CagA+ Helicobacter pylori, with MIC ranges from 6.25-50 μg mL-1 and MBC ranges from 4-20 μg mL-1 for periodontal pathogens[1].
(±)-10-Gingerol moderately inhibits the growth of human A549, SK-OV-3, SK-MEL-2, and HCT15 tumor cells in vitro with ED50 values of 5.09 μg/mL, 4.52 μg/mL, 5.92 μg/mL, and 6.57 μg/mL, respectively[2].
(±)-10-Gingerol (5-20 μM; 20 h) dose-dependently inhibits LPS-induced NO production in BV2 microglial cells, with 84.1% inhibition at 20 μM[4].
(±)-10-Gingerol (20 μM; 12 h (protein analysis); 6 h (mRNA analysis)) inhibits LPS-induced iNOS protein and mRNA expression in BV2 microglial cells, with 73.5% suppression of iNOS protein at 20 μM[4].
(±)-10-Gingerol (20 μM; 20 h) inhibits LPS-induced TNF-α, IL-1β, and IL-6 secretion in BV2 microglial cells, with 72.1% inhibition of TNF-α, 55.9% inhibition of IL-1β, and potent inhibition of IL-6 at 20 μM[4].
(±)-10-Gingerol (20 μM; 6 h) downregulates LPS-induced TNF-α, IL-1β, and IL-6 mRNA expression in BV2 microglial cells at 20 μM, with effects correlating closely with reduced cytokine secretion[4].
(±)-10-Gingerol (20 μM; 1 h) moderately inhibits LPS-induced NF-κB DNA binding activity in BV2 microglial cells at 20 μM[4].
(±)-10-Gingerol (12.5 μM; 20 h) inhibits LPS-induced NO production in BV2 microglial cells by 71.7%, and is the primary contributor to the NO-suppressing activity of fresh ginger ethanolic extract[4].
(±)-10-Gingerol (12.5 μM; 12 h (protein analysis); 6 h (mRNA analysis)) inhibits LPS-induced iNOS protein expression by 61.0% and iNOS mRNA expression by 36.7% in BV2 microglial cells, and is the primary contributor to the iNOS-suppressing activity of fresh ginger ethanolic extract[4].
(±)-10-Gingerol (12.5 μM; 20 h (cytokine secretion); 6 h (mRNA analysis)) inhibits LPS-induced TNF-α, IL-1β, and IL-6 secretion and mRNA expression in BV2 microglial cells, and is the primary contributor to the proinflammatory cytokine-suppressing activity of fresh ginger ethanolic extract[4].
(±)-10-Gingerol (Multiple concentrations; 30 min) potently scavenges DPPH radicals with an IC50 of 10.47 μM, and activity increases with higher concentrations[5].
(±)-10-Gingerol (Multiple concentrations; first 1 min) potently scavenges superoxide radicals with an IC50 of 1.68 μM, with activity increasing in a dose-dependent manner[5].
(±)-10-Gingerol (Multiple concentrations; first 1 min) potently scavenges hydroxyl radicals with an IC50 of 1.35 μM, with activity increasing in a dose-dependent manner[5].
(±)-10-Gingerol (6 μM; 15 min pre-incubation, 10 min monitoring) significantly inhibits f-MLP-induced ROS production in human polymorphonuclear neutrophils[5].
(±)-10-Gingerol (1-6 μM; 24 h) inhibits LPS-induced nitrite production in RAW 264.7 macrophages in a dose-dependent manner, achieving 75% inhibition at 6 μM without causing cytotoxicity[5].
(±)-10-Gingerol (1-6 μM; 24 h) inhibits LPS-induced PGE2 production in RAW 264.7 macrophages in a dose-dependent manner, achieving 73% inhibition at 6 μM[5].
10-Gingerol (25 μg/mL) inhibits growth of Mycobacterium avium in vitro with a minimum inhibitory concentration of 25 μg/mL[6].
10-Gingerol (50 μg/mL) inhibits growth of Mycobacterium tuberculosis in vitro with a minimum inhibitory concentration of 50 μg/mL[6].

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

Western Blot Analysis[4]

Cell Line: BV2 microglial cells
Concentration: 20 μM
Incubation Time: 12 h (protein analysis); 6 h (mRNA analysis)
Result: Suppressed LPS-induced iNOS protein expression by 73.5% at 20 μM.
Reduced corresponding iNOS mRNA levels in BV2 microglia.
Showed strong correlation between inhibition of iNOS gene expression and NO secretion (r = 0.976 for protein, r = 0.927 for mRNA).

ELISA Assay[4]

Cell Line: BV2 microglial cells
Concentration: 20 μM
Incubation Time: 20 h
Result: Moderately inhibited LPS-induced TNF-α secretion by 72.1% at 20 μM.
Moderately inhibited LPS-induced IL-1β secretion by 55.9% at 20 μM.
Strongly inhibited LPS-induced IL-6 secretion in BV2 microglia at 20 μM.

RT-PCR[4]

Cell Line: BV2 microglial cells
Concentration: 20 μM
Incubation Time: 6 h
Result: Reduced LPS-induced TNF-α, IL-1β, and IL-6 mRNA levels in BV2 microglia at 20 μM.
Showed strong correlations between cytokine secretion and mRNA levels (TNF-α r = 0.976, IL-1β r = 0.957, IL-6 r = 0.931).

Western Blot Analysis[4]

Cell Line: BV2 microglial cells
Concentration: 12.5 μM
Incubation Time: 12 h (protein analysis); 6 h (mRNA analysis)
Result: Attenuated LPS-induced iNOS protein expression by 61.0% at 12.5 μM.
Attenuated LPS-induced iNOS mRNA expression by 36.7% at 12.5 μM.
Showed nearly equivalent inhibitory effect to a mixture of 12.5 μM (±)-10-Gingerol and 60.0 μM 6-gingerol.

ELISA Assay[5]

Cell Line: RAW 264.7 mouse leukaemic monocyte macrophages
Concentration: 1-6 μM
Incubation Time: 24 h (at 37 °C in 5% CO2 with LPS)
Result: Evoked a dose-dependent inhibition of LPS-activated PGE2 release in RAW 264.7 cells, with 73% inhibition observed at 6 μM.
In Vivo

(±)-10-Gingerol exhibits potent wound healing activity in Mus musculus with induced wounds[1].
(±)-10-Gingerol promotes hematopoietic recovery in phenylhydrazone-induced anemic Danio rerio embryos[1].
(±)-10-Gingerol stimulates hematopoiesis in normal zebrafish embryos[1].
(±)-10-Gingerol (30 mg/kg; i.p.; daily; 7 days) exhibits strong efficacy in ameliorating dextran sulfate sodium-induced acute ulcerative colitis in rats via antioxidant and antiinflammatory activities, with potency comparable to related gingerol analogs[3].

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

Animal Model: Sprague-Dawley (male, 180-220 g, ulcerative colitis induced by 5% (w/v) dextran sulfate sodium drinking water for 7 days)[3]
Dosage: 30 mg/kg
Administration: i.p.; daily; 7 days
Result: Reversed body weight loss and significantly reduced disease activity index (DAI) scores compared to untreated colitis rats.
Significantly decreased colonic malondialdehyde (MDA) levels and myeloperoxidase (MPO) activity, and restored colonic superoxide dismutase (SOD) activity compared to untreated colitis rats.
Significantly reduced elevated serum tumor necrosis factor alpha (TNF-α) and Interleukin 1 beta (IL-1β) levels compared to untreated colitis rats.
Reduced colonic congestion and hemorrhagic spots, ameliorated mucosal inflammation and defect, and lowered histopathological scores compared to untreated colitis rats.
Molecular Weight

350.49

Formula

C21H34O4

CAS No.
SMILES

O=C(CC(CCCCCCCCC)O)CCC1=CC=C(C(OC)=C1)O

Structure Classification
Initial Source
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