| Size | Price | Stock | Qty |
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| 50mg |
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| Other Sizes |
| Targets |
NF-kappaB (nuclear factor kappa-light-chain-enhancer of activated B cells), Nrf2 (nuclear factor erythroid 2-related factor 2), COX-2 (cyclooxygenase-2), 5-LOX (5-lipoxygenase), and various pro-inflammatory cytokines (TNF-alpha, IL-6, IL-1beta). Ginger extract inhibits NF-kappaB activation, activates Nrf2, and downregulates the expression of COX-2 and iNOS, thereby exerting its anti-inflammatory and antioxidant effects. The bioactive component 6-gingerol also targets TRPV1 (transient receptor potential vanilloid 1) contributing to its analgesic effects.
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| ln Vitro |
In vitro, ginger extract (50-400 ug/mL; 24-72 hours) exhibits anti-cancer, anti-inflammatory, and chemotherapeutic effects. It inhibits the proliferation of various cancer cell lines including hepatic (HepG2, IC50 ~ 60-150 ug/mL), breast (MCF-7, MDA-MB-231), prostate (PC3, DU-145), colon (HT-29, HCT116), and gastric (AGS) cancer cells. The extract induces cell cycle arrest (G0/G1 or G2/M phase) and triggers apoptosis via the mitochondrial pathway (caspase-3, -9, PARP cleavage, and Bax/Bcl-2 ratio modulation). For anti-inflammatory activity, ginger extract (10-200 ug/mL, 1-2 h pre-treatment) significantly suppresses LPS-induced NF-kappaB activation in RAW 264.7 macrophages, reducing the production of TNF-alpha, IL-6, IL-1beta, NO, and PGE2. It also inhibits the expression of COX-2 and iNOS at the mRNA and protein levels. Ginger extract also exhibits antioxidant activity by scavenging free radicals (DPPH, ABTS), increasing the activity of antioxidant enzymes (SOD, CAT, GPx), and upregulating Nrf2-mediated antioxidant response element (ARE) activation, leading to the induction of phase II detoxifying enzymes (HO-1, NQO1, GST). Ginger extract (50-400 ug/mL) also inhibits the growth of Gram-positive and Gram-negative bacteria and has antifungal activity against Candida species.
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| ln Vivo |
Ginger extract (oral gavage; 100 mg/kg; 8 weeks) can inhibit the increased expression of NF-κB in rats with liver cancer and lowers the risk of hepatic neoplasms in rats[1].
In vivo, ginger extract (oral gavage; 50-500 mg/kg body weight) exhibits significant anti-inflammatory, anti-cancer, and chemotherapeutic effects in various animal models. In a rat model of liver cancer induced by a choline-deficient diet (CDE) or diethylnitrosamine (DEN), oral administration of ginger extract (100 mg/kg; 8 weeks) reduces the incidence and multiplicity of hepatic neoplasms by blocking the elevated expression of NF-kappaB in liver tissue and decreasing serum levels of TNF-alpha, IL-6, and oxidative stress markers (MDA, 8-OHdG). In carrageenan-induced paw edema in rats (200-400 mg/kg, PO), ginger extract significantly reduces paw swelling within 2-4 hours (edema inhibition up to 40-60%). In collagen-induced arthritis (CIA) models, ginger extract (200 mg/kg, PO, daily for 21 days) reduces joint inflammation, pannus formation, and cartilage erosion, and lowers serum IL-1beta, IL-6, and TNF-alpha levels. In chemotherapy-induced nausea and vomiting (CINV) models, ginger extract (50-200 mg/kg, PO) reduces the frequency of emetic episodes in ferrets and decreases the expression of substance P and NK1 receptors in the gut and brainstem. Ginger extract also exhibits anti-ulcer activity in ethanol- or indomethacin-induced gastric ulcer models (100-300 mg/kg, PO), reducing ulcer index, gastric acid secretion, and increasing gastric mucus production. In all models, ginger extract shows a favorable safety profile with no significant weight loss or organ toxicity at therapeutic doses. |
| Enzyme Assay |
No specific enzyme binding protocol; ginger extract is a complex mixture of bioactive compounds. For in vitro assay: (1) Evaluate NF-kappaB inhibition via a luciferase reporter assay: transfect RAW 264.7 or HEK293T cells with pNF-kappaB-Luc and pRL-TK plasmids. (2) Pre-treat cells with ginger extract (10-200 ug/mL) for 1-2 h, then stimulate with LPS (1 ug/mL) for 6 h. (3) Perform dual-luciferase assay; measure firefly and Renilla luminescence. (4) For COX-2/5-LOX inhibition: incubate purified ovine COX-2 enzyme (0.1 U) or human recombinant 5-LOX (0.05 U) with ginger extract (1-1000 ug/mL) and arachidonic acid (10-100 uM) as substrate. (5) Measure COX-2 activity by quantifying PGE2 production via ELISA. (6) For 5-LOX activity: measure leukotriene B4 (LTB4) or 5-HETE production by LC-MS. (7) For Nrf2 activation: perform an ARE-luciferase reporter assay: transfect cells with pGL4-ARE-Luc plasmid, treat with ginger extract (10-200 ug/mL) for 24 h, measure luciferase activity. (8) For protein binding: Use surface plasmon resonance (SPR) or biolayer interferometry (BLI) to test binding of purified compounds (e.g., 6-gingerol) to target proteins (e.g., TRPV1, NF-kappaB p50/p65).
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| Cell Assay |
(1) Seed RAW 264.7 macrophages (5,000-10,000 cells/well) in 96-well plates overnight. (2) Pre-treat cells with ginger extract (10-200 ug/mL, 1-2 h). (3) Stimulate with LPS (1 ug/mL) for 6-24 h. (4) For cytokine measurement: collect supernatant, measure TNF-alpha, IL-6, and IL-1beta by ELISA. (5) For NO measurement: add Griess reagent to supernatant, measure OD540. (6) For PGE2 and COX-2 activity: measure PGE2 in supernatant by ELISA. (7) For cancer cell growth inhibition: seed HepG2, MCF-7, or PC3 cells (5,000-10,000 cells/well). (8) Treat with ginger extract (10-400 ug/mL) for 24-72 h. (9) Add MTT or CCK-8 reagent, measure OD570 or OD450. (10) Calculate IC50 using dose-response curve. (11) For apoptosis: treat cancer cells with ginger extract (50-200 ug/mL) for 48 h, stain with Annexin V-FITC/PI, analyze by flow cytometry. (12) For cell cycle analysis: fix cells in 70% ethanol, stain with PI (50 ug/mL) plus RNase A, analyze by FACS. (13) For Western blot: treat cells with ginger extract (50-200 ug/mL) for 24-48 h, lyse in RIPA buffer, run SDS-PAGE, blot for NF-kappaB p65, phospho-p65, IkappaBalpha, COX-2, iNOS, Nrf2, HO-1, NQO1, and apoptosis markers (caspase-3, PARP, Bcl-2, Bax). (14) For ROS measurement: treat cells with ginger extract (10-100 ug/mL) for 24 h, add DCFH-DA (10 uM) for 30 min, measure fluorescence at 485/535 nm.
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| Animal Protocol |
Animal/Disease Models: Male Wistar rat[1]
Doses: 100 mg/kg Route of Administration: po (oral gavage); 8 weeks Experimental Results: Exhibits anti-cancer effects in the liver cancer-induced group (CDE). (1) For anti-cancer activity: use 6-8 week old male BALB/c nude mice (20-25 g) bearing subcutaneous HepG2 or MCF-7 xenografts (tumor volume 100-150 mm3). (2) Randomize into treatment groups (n=8-10). (3) Administer ginger extract by oral gavage (100, 200, 300 mg/kg/day) for 14-21 days. (4) Formulation: suspend ginger extract in 0.5% sodium carboxymethyl cellulose (CMC-Na) with 0.1% Tween-80; sonicate to obtain a uniform suspension. (5) Vehicle control: 0.5% CMC-Na + 0.1% Tween-80. (6) Positive control: cisplatin (3 mg/kg, IP, weekly) or 5-FU (20 mg/kg, IP, q3d). (7) Monitor tumor volume by caliper twice weekly; calculate TGI%. (8) For liver cancer model (in situ): use Sprague-Dawley rats (150-200 g) fed a choline-deficient diet (CDE) for 8-12 weeks to induce liver neoplasms, treat with ginger extract (100 mg/kg/day, PO) starting at week 4. (9) For anti-inflammatory model: carrageenan-induced paw edema in male Wistar rats (200-250 g). Inject 0.1 mL of 1% carrageenan into right hind paw. Administer ginger extract (200-400 mg/kg) PO 1 h before carrageenan injection. Measure paw volume using a plethysmometer at 1, 2, 3, 4, and 24 h post-injection. (10) For chemotherapy-induced nausea (CINV): use male ferrets (1.2-1.5 kg). Administer cisplatin (10 mg/kg, IP) to induce emesis; treat with ginger extract (50-200 mg/kg, PO) 1 h before cisplatin. Count number of emetic episodes (vomiting and retching) over 4-6 h. (11) For all models: at endpoint, collect blood for serum chemistry (ALT, AST, BUN, creatinine, TNF-alpha, IL-6), collect target tissues (tumor, liver, stomach, jejunum) for histopathology (H&E, IHC for Ki-67, NF-kappaB, COX-2), TUNEL assay, and Western blot analysis. |
| ADME/Pharmacokinetics |
For in vitro use: dissolve ginger extract in DMSO (100-200 mg/mL stock). For cell culture, dilute DMSO stock in culture medium (final DMSO <0.1-0.5%). For in vivo oral administration: suspend extract in 0.5% CMC-Na + 0.1% Tween-80 (stable suspension). For IP injection: dissolve in 10% DMSO, 40% PEG300, 5% Tween-80, 45% saline (clear solution). Density: 0.878-0.878 g/cm3 at 20degC. Bioactive component levels in standardized extracts: 6-gingerol typically 5-10% w/w, 6-shogaol 1-3% w/w. PK of 6-gingerol in rodents: oral bioavailability ~10-30%, t1/2 ~ 1-2 h, Cmax ~ 0.5-2 uM (at 100 mg/kg PO). 6-Shogaol is more stable and has higher oral bioavailability (~40%) than 6-gingerol. Metabolism: gingerols are rapidly metabolized by phase II conjugation (glucuronidation, sulfation) in the liver and intestine. Storage: ginger extract should be stored in airtight containers at 2-8degC (refrigerator) or -20degC for long-term storage, protected from light and moisture to prevent degradation of active gingerols.
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| Toxicity/Toxicokinetics |
Ginger extract has an excellent safety profile. In vitro: CCK-8 assay on normal human hepatocytes (LO2) or HEK293 cells (10-500 ug/mL) shows IC50 > 500 ug/mL for 48 h (selectivity index: cancer cell IC50 ~ 60-150 ug/mL vs. normal cell IC50 > 500 ug/mL). In vivo acute toxicity: oral LD50 in rats > 5000 mg/kg. Sub-chronic toxicity: NOAEL (No Observed Adverse Effect Level) in rats for up to 90 days is 1000 mg/kg/day (oral). At high doses (2000-5000 mg/kg), mild gastrointestinal irritation and transient diarrhea may occur. No teratogenic or reproductive toxicity has been observed at doses up to 1000 mg/kg/day. Ginger extract does not cause significant organ damage (liver, kidney, heart) as evidenced by serum chemistry (ALT, AST, BUN, creatinine) and histopathology. The extract is generally recognized as safe (GRAS) by the FDA for food use, but for pharmacological research doses, caution should be taken as high doses may cause gastric irritation and thinning of blood (mild antiplatelet activity). The compound is for research use only, not for human therapeutic use without appropriate regulatory approval.
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| References | |
| Additional Infomation |
Ginger extract (Zingiber officinale extract) is a complex botanical mixture with a long history of medicinal use for treating nausea, inflammation, arthritis, and digestive disorders. In modern pharmacology, it is studied for its anti-cancer, anti-inflammatory, antioxidant, antiemetic, and chemopreventive properties. The primary bioactive compounds, gingerols (especially 6-gingerol) and shogaols (especially 6-shogaol), are responsible for most of the biological activities. Ginger extract is not a single-molecule drug and has not been approved by the FDA for specific therapeutic indications (although ginger supplements are available as dietary supplements). In clinical trials, ginger extract (250-1000 mg/day, PO) has shown efficacy in reducing chemotherapy-induced nausea and vomiting (CINV), postoperative nausea and vomiting (PONV), and osteoarthritis pain. However, for research purposes, ginger extract is a valuable tool for studying the mechanisms of inflammation, oxidative stress, and cancer chemoprevention. This product is strictly for laboratory research use only and is not intended for human consumption as a drug. Standardization of ginger extracts is critical, with 5-10% 6-gingerol content common in research-grade materials.
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| Exact Mass |
350.246
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| CAS # |
84696-15-1
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| PubChem CID |
6850776
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| Appearance |
Light yellow to yellow solid powder
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| Flash Point |
76℃
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| Index of Refraction |
n20/D1.527
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| LogP |
4.794
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
19
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| Heavy Atom Count |
41
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| Complexity |
589
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| Defined Atom Stereocenter Count |
0
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| SMILES |
CCCCC/C=C/C(=O)CCC1=CC(=C(C=C1)O)OC.CCCCCC(C)CC(=O)CCC1=CC(=C(C=C1)O)OC
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| InChi Key |
QCVRFSPGUWEKFC-ILHSMLOTSA-N
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| InChi Code |
InChI=1S/C18H28O3.C17H24O3/c1-4-5-6-7-14(2)12-16(19)10-8-15-9-11-17(20)18(13-15)21-3;1-3-4-5-6-7-8-15(18)11-9-14-10-12-16(19)17(13-14)20-2/h9,11,13-14,20H,4-8,10,12H2,1-3H3;7-8,10,12-13,19H,3-6,9,11H2,1-2H3/b;8-7+
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| Chemical Name |
(E)-1-(4-hydroxy-3-methoxyphenyl)dec-4-en-3-one;1-(4-hydroxy-3-methoxyphenyl)-5-methyldecan-3-one
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO :~100 mg/mL
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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