Nordihydroguaiaretic acidAnti-tumor agent;lipoxygenase inhibitor CAS# 500-38-9 |
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Quality Control & MSDS
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| 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. |
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| 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. |
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| 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. | ||
| Description | Nordihydroguaiaretic 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: | |||||
Nordihydroguaiaretic acid Dilution Calculator
Nordihydroguaiaretic acid Molarity Calculator
| 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. | |||||
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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
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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.
