Home >> Research Area >>PI3K/Akt/mTOR Signaling>>mTOR>>Phenylpropanes>> Nordihydroguaiaretic acid

Nordihydroguaiaretic acid

Anti-tumor agent;lipoxygenase inhibitor CAS# 500-38-9

Nordihydroguaiaretic acid

Catalog No. BCC1805----Order now to get a substantial discount!

Product Name & Size Price Stock
Nordihydroguaiaretic acid: 5mg $2 In Stock
Nordihydroguaiaretic acid: 10mg Please Inquire In Stock
Nordihydroguaiaretic acid: 20mg Please Inquire Please Inquire
Nordihydroguaiaretic acid: 50mg Please Inquire Please Inquire
Nordihydroguaiaretic acid: 100mg Please Inquire Please Inquire
Nordihydroguaiaretic acid: 200mg Please Inquire Please Inquire
Nordihydroguaiaretic acid: 500mg Please Inquire Please Inquire
Nordihydroguaiaretic acid: 1000mg Please Inquire Please Inquire
Related Products
  • WYE-354

    Catalog No.:BCC1059
    CAS No.:1062169-56-5
  • GDC-mTOR inhibitor

    Catalog No.:BCC1781
    CAS No.:1207358-59-5
  • GDC-0349

    Catalog No.:BCC1094
    CAS No.:1207360-89-1
  • QL-IX-55

    Catalog No.:BCC1876
    CAS No.:1223002-54-7
  • LY 303511

    Catalog No.:BCC1715
    CAS No.:154447-38-8

Quality Control of Nordihydroguaiaretic acid

Number of papers citing our products

Chemical structure

Nordihydroguaiaretic acid

3D structure

Chemical Properties of Nordihydroguaiaretic acid

Cas No. 500-38-9 SDF Download SDF
PubChem ID 71398 Appearance White powder
Formula C18H22O4 M.Wt 302.36
Type of Compound Phenylpropanes Storage Desiccate at -20°C
Synonyms NDGA
Solubility DMSO : 75 mg/mL (248.05 mM; Need ultrasonic)
Chemical Name 4-[(2S,3R)-4-(3,4-dihydroxyphenyl)-2,3-dimethylbutyl]benzene-1,2-diol
SMILES CC(CC1=CC(=C(C=C1)O)O)C(C)CC2=CC(=C(C=C2)O)O
Standard InChIKey HCZKYJDFEPMADG-TXEJJXNPSA-N
Standard InChI InChI=1S/C18H22O4/c1-11(7-13-3-5-15(19)17(21)9-13)12(2)8-14-4-6-16(20)18(22)10-14/h3-6,9-12,19-22H,7-8H2,1-2H3/t11-,12+
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Nordihydroguaiaretic acid

DescriptionNordihydroguaiaretic acid is a 5-lipoxygenase (5LOX) (IC50=8±3 μM) and tyrosine kinase inhibitor.In Vitro:The natural dicatechol Nordihydroguaiaretic acid (NDGA) is a selective 5LOX inhibitor from the creosote plant (Larrea tridentata: Zygophyllaceae). The 5LOX-inhibiting natural dicatechol Nordihydroguaiaretic acid is a very effective, non-toxic antagonist of TNFα-stimulated microglial activation. Nordihydroguaiaretic acid is approximately six times more potent than Minocycline in vitro, with an IC50 value of 8±3 μM and no toxicity at 100 μM. Significant NO2- suppression is observed at 800 nM Nordihydroguaiaretic acid. Similar efficacy is observed for natural and synthetic Nordihydroguaiaretic acid, as well as for the acetyl ester of Nordihydroguaiaretic acid. Nordihydroguaiaretic acid also suppresses TNFα-stimulated PGE2 production by EOC-20 cells with an IC50 of 841 nM[1].To test the proliferation effect of prostaglandin E1 and Nordihydroguaiaretic acid (NDGA) on cancer cell lines, HepG2 cell lines are treated with various doses of the two compounds and the positive compounds 8-anilino-1-naphtalene sulfonate (ANS), respectively, for 24 h and cell viability is examined by the MTT assay. ANS displays a dose-dependent inhibition (0, 10, 30, 50, 80, 100, 120, and 150 μM) with the estimated IC50 being 25.888 μM. The tested IC50 of prostaglandin E1 is 41.223 μM and Nordihydroguaiaretic acid is 45.646 μM, respectively, at different concentrations of 0, 30, 60, 80, 100, 120, and 140 μM[2].In Vivo:Compared with the control ob/ob chow diet group, there is a significant reduction of body weight starting from 9 wk treatment in the high-dose Nordihydroguaiaretic acid (NDGA) diet group, and from 12 wk in the low-dose group. Nordihydroguaiaretic acid treatment results in higher body (rectal) temperatures of ob/ob mice, especially with the high dose of Nordihydroguaiaretic acid[3].

References:
[1]. West M, et al. The arachidonic acid 5-lipoxygenase inhibitor Nordihydroguaiaretic acid inhibits tumor necrosis factor alpha activation of microglia and extends survival of G93A-SOD1 transgenic mice. J Neurochem. 2004 Oct;91(1):133-43. [2]. Lu F, et al. Virtual Screening for Potential Allosteric Inhibitors of Cyclin-Dependent Kinase 2 from Traditional Chinese Medicine. Molecules. 2016 Sep 21;21(9). pii: E1259. [3]. Zhang H, et al. Nordihydroguaiaretic acid improves metabolic dysregulation and aberrant hepatic lipid metabolism in mice by both PPARα-dependent and -independent pathways. Am J Physiol Gastrointest Liver Physiol. 2013 Jan 1;304(1):G72-86.

Protocol

Cell Assay [2]
MTT assay is used to measure cell growth-inhibitory activity of the selected most promising compounds in HepG2 cell lines. Cells are cultured in 96-well culture plate at 1×104 cells/well. After 24 h cultured at 37 °C in the atmosphere of 5% CO2, cells are adhered and treated with different concentrations of the targeted compounds (e.g., Nordihydroguaiaretic acid, 0, 30, 60, 80, 100, 120, and 140 μM) and incubated for 24 h. Then, the supernatants are discarded and MTT (0.5 mg/mL) is added to each well and incubated at 37°C in 5% CO2 for an additional 4 h. Following, the MTT is removed and 150 μL of formazan in DMSO is added to terminate response and then plates are set to the table shaker for 5 min at low speed. Cell proliferation is evaluated by measuring the absorbance at 570 nm using ELISA Plate Reader. The IC50 values are calculated by SPSS statistics 17.0[2].

Animal Administration [3]
Mice[3] Seven-week-old male control C57BL/6J mice, male leptin-deficient (ob/ob) mice, and male Pparα-deficient mutant mice (B6.129S4-Pparatm1Gonz/J) are used. These mice are fed a standard chow diet for 1 wk to allow them to acclimatize to a controlled new environment (25±2°C, 55±5% relative humidity with a 12-h light-dark cycle). Subsequently, one group of ob/ob mice is switched to a chow diet supplemented with either low- (0.83 g/kg chow diet) or high-dose (2.5 g/kg chow diet) Nordihydroguaiaretic acid and maintained on this diet for 16 wk. The other groups of ob/ob mice and control mice continue to be fed a normal chow diet for 16 wk. In another set of studies, C57BL/6J mice and Pparα-deficient mutant mice are fed either a high-fat diet (~60% of total calories come from fat), or the same high-fat diet supplemented with a high dose of Nordihydroguaiaretic acid (2.5 g/kg diet). Food intake and body weights are measured once a week throughout the experiment.

References:
[1]. West M, et al. The arachidonic acid 5-lipoxygenase inhibitor Nordihydroguaiaretic acid inhibits tumor necrosis factor alpha activation of microglia and extends survival of G93A-SOD1 transgenic mice. J Neurochem. 2004 Oct;91(1):133-43. [2]. Lu F, et al. Virtual Screening for Potential Allosteric Inhibitors of Cyclin-Dependent Kinase 2 from Traditional Chinese Medicine. Molecules. 2016 Sep 21;21(9). pii: E1259. [3]. Zhang H, et al. Nordihydroguaiaretic acid improves metabolic dysregulation and aberrant hepatic lipid metabolism in mice by both PPARα-dependent and -independent pathways. Am J Physiol Gastrointest Liver Physiol. 2013 Jan 1;304(1):G72-86.

Nordihydroguaiaretic acid Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

Nordihydroguaiaretic acid Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of Nordihydroguaiaretic acid

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.3073 mL 16.5366 mL 33.0732 mL 66.1463 mL 82.6829 mL
5 mM 0.6615 mL 3.3073 mL 6.6146 mL 13.2293 mL 16.5366 mL
10 mM 0.3307 mL 1.6537 mL 3.3073 mL 6.6146 mL 8.2683 mL
50 mM 0.0661 mL 0.3307 mL 0.6615 mL 1.3229 mL 1.6537 mL
100 mM 0.0331 mL 0.1654 mL 0.3307 mL 0.6615 mL 0.8268 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University

Background on Nordihydroguaiaretic acid

Description: IC50 Value: N/A Nordihydroguaiaretic acid (NDGA) is a natural phenolic compound isolated from the creosote bush Larrea divaricata, which has anti-tumor activities both in vitro and in vivo. Its analogs are in clinical development for use in refractory solid tumors. in vitro: NDGA may also direct target mTORC1 complex because NDGA suppressed amino acids- and insulin-stimulated mTORC1 and acted like rapamycin to disrupt mTOR-Raptor interaction [1]. NDGA increased PPARα promoter activity in AML12 hepatocytes and also prevented the fatty acid suppression of PPARα expression. In contrast, PPARα siRNA abrogated the stimulatory effect of NDGA on fatty acidcatabolism [2]. in vivo: NDGA was able to induce Nrf2 translocation in vivo in kidneys of rats submitted to both U-NX and I/R injury and to protect against renal histological damage and apoptosis [3]. Comparison of the proportion of live mice at the age of 90% mortality was used as a surrogate for measurement of maximum lifespan;neither NDGA (p=0.12) nor aspirin (p=0.16) had a significant effect in this test. Measures of blood levels of NDGA or aspirin and its salicylicacid metabolite suggest that the observed lack of effects of NDGA or aspirin on life span in females could be related to gender differences in drug disposition or metabolism [4]. Clinical trial: Nordihydroguaiaretic Acid in Treating Patients With Nonmetastatic Relapsed Prostate Cancer . Phase 1

Featured Products
New Products
 

References on Nordihydroguaiaretic acid

Nordihydroguaiaretic acid impairs prostate cancer cell migration and tumor metastasis by suppressing neuropilin 1.[Pubmed:27863391]

Oncotarget. 2016 Dec 27;7(52):86225-86238.

Tumor metastasis is a major cause leading to the deaths of cancer patients. Nordihydroguaiaretic acid (NDGA) is a natural product that has been demonstrated to show therapeutic values in multiple diseases. In this study, we report that NDGA can inhibit cell migration and tumor metastasis via a novel mechanism. NDGA suppresses NRP1 function by downregulating its expression, which leads to attenuated cell motility, cell adhesion to ECM and FAK signaling in cancer cells. Moreover, due to its cross-cell type activity on NRP1 suppression, NDGA also impairs angiogenesis function of endothelial cells and fibronectin assembly by fibroblasts, both of which are critical to promote metastasis. Based on these comprehensive effects, NDGA effectively suppresses tumor metastasis in nude mice model. Our findings reveal a novel mechanism underlying the anti-metastasis function of NDGA and indicate the potential value of NDGA in NRP1 targeting therapy for selected subtypes of cancer.

Anti-anaphylactic action of nordihydroguaiaretic acid in antigen sensitized guinea pigs.[Pubmed:27595978]

Respir Physiol Neurobiol. 2016 Dec;234:26-31.

Therapeutic natural products and medicinal herbs has gained popularity. The anti-antigenic action of the plant alkaloid Nordihydroguaiaretic acid (NDGA) was studied in ovalbumin (OA)-sensitized guinea pigs. In one series of experiments conscious, non-sedated guinea pigs were challenged with OA aerosol. Specific airway resistance (SRAW) was monitored using a two-chambered whole-body plethysmograph. OA aerosol increased SRAW above that produced by vehicle administration. Prior NDGA administration by a 1min 0.9% aerosol (w/vol) attenuated the increase in SRAW resulting from OA challenge. In the anesthetized guinea pig pretreated with indomethacin, pyrilamine and propranolol, intravenous OA injection increased intra-tracheal pressure above vehicle injection. Intravenous NDGA administration (5mg/kg) reduced the intra-tracheal pressure increases. In a third series of experiments plasma leukotriene C4 was measured by radio-immunoassay in 3 groups challenged with OA aerosol: vehicle-treated OA-sensitized, OA-sensitized receiving NDGA and vehicle treated guinea pigs. NDGA pretreatment reduced plasma LTC4 in response to OA challenge in OA sensitized guinea pigs. This study demonstrates that NDGA is an effective antigenic agent when given by aerosol or intravenous injection in either conscious or anesthetized guinea pigs, respectively. The mechanism of action of NDGA is presumed primarily be due to the blockage of 5-lipoxygenase and therefore the synthesis of leukotrienes.

Repositioning nordihydroguaiaretic acid as a potent inhibitor of systemic amyloidosis and associated cellular toxicity.[Pubmed:27789205]

Arch Biochem Biophys. 2016 Dec 15;612:78-90.

Although the cure of amyloid related neurodegenerative diseases, non-neuropathic amyloidogenic diseases and non-neuropathic systemic amyloidosis are appealing energetic research attempts, beneficial medication is still to be discovered. There is a need to explore intensely stable therapeutic compounds, potent enough to restrict, disrupt or wipe out such toxic aggregates. We had performed a comprehensive biophysical, computational and cell based assay, that shows Nordihydroguaiaretic acid (NA) not only significantly inhibits heat induced hen egg white lysozyme (HEWL) fibrillation but also disaggregates preformed HEWL fibrils and reduces the cytoxicity of amyloid fibrils as well as disaggregated fibrillar species. The inhibitory potency of NA was determined by an IC50 of 26.3 muM. NA was also found to effectively inhibit human lysozyme (HL) fibrillation. NA interferes in the amyloid fibrillogenesis process by interacting hydrophobically with the amino acid residues found in highly prone amyloid fibril forming region of HEWL as explicated by molecular docking results. The results recommend NA as a probable neuroprotective and promising inhibitor for the therapeutic advancement prospective against amyloid related diseases.

Long chain polyunsaturated fatty acids (LCPUFAs) and nordihydroguaiaretic acid (NDGA) modulate metabolic and inflammatory markers in a spontaneous type 2 diabetes mellitus model (Stillman Salgado rats).[Pubmed:27884155]

Lipids Health Dis. 2016 Nov 25;15(1):205.

BACKGROUND: Diabetes mellitus (DM) is a complex disease with alterations in metabolic and inflammatory markers. Stillman Salgado rats (eSS) spontaneously develop type 2 DM by middle age showing progressive impairment of glucose tolerance with hyperglycemia, hypertriglyceridemia and hyperinsulinemia. We analyzed the effects of supplementation of omega-3 and omega-6 polyunsaturated fatty acids (PUFAs) with or without Nordihydroguaiaretic acid (NDGA) added, an antioxidant and lipoxygenase inhibitor, on metabolic and inflammatory parameters in eSS rats to evaluate whether they can delay development and/or prevent progression of DM. METHODS: After weaning, eSS rats received, intraperitoneally, once a month omega-3 (EPA 35% and DHA 40%-6.25 mg/Kg) or omega-6 (90% arachidonic acid- 6. 25 mg/Kg) for twelve months. Two additional groups of rats received 1.9 mg/kg NDGA added to omega-3 and omega-6 fatty acids. Blood samples were collected at day 40, and at the end of the 6th month and 12th month of age to determine plasma triglycerides (TGs), total plasma fatty acids (FA), A1C hemoglobin (HbA1C), C-reactive protein (CRP), gamma glutamyl transpeptidase (GGT), lipo and hydro peroxides, nitrites and IL-6 (in plasma and liver, kidney, and pancreas) and underwent oral glucose tolerance test (OGTT) as well. Wistar and eSS rats that received saline solution were used as controls. RESULTS: Plasma lipids profile, TG, fasting and post-prandial blood glucose levels, and glycosylated HbA1C showed significant improvements in omega-3 and omega-3 + NDGA treated animals compared to eSS control group. omega-3 and omega-3 + NDGA groups showed an inverse correlation with fasting blood glucose and showed lower plasma levels of GGT, TG, and CRP. eSS rats treated with omega-3 LCPUFAs showed reduced level of inflammatory and oxidative indices in plasma and liver, kidney and pancreas tissues in comparison with eSS control (non-treated) and omega-6 treated groups. CONCLUSIONS: eSS rats are a useful model to study type 2 DM pathophysiology and related inflammatory indices. omega-3 + NDGA supplementation, at the doses tested, ameliorated inflammatory, metabolic and oxidative stress markers studied.

Description

Nordihydroguaiaretic acid is a 5-lipoxygenase (5LOX) (IC50=8 μM) and tyrosine kinase inhibitor.

Keywords:

Nordihydroguaiaretic acid,500-38-9,NDGA,Natural Products,mTOR, buy Nordihydroguaiaretic acid , Nordihydroguaiaretic acid supplier , purchase Nordihydroguaiaretic acid , Nordihydroguaiaretic acid cost , Nordihydroguaiaretic acid manufacturer , order Nordihydroguaiaretic acid , high purity Nordihydroguaiaretic acid

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: