TetrahydrocurcuminCAS# 36062-04-1 |
2D Structure
Quality Control & MSDS
3D structure
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Number of papers citing our products
Cas No. | 36062-04-1 | SDF | Download SDF |
PubChem ID | 124072 | Appearance | Powder |
Formula | C21H24O6 | M.Wt | 372.41 |
Type of Compound | Phenols | Storage | Desiccate at -20°C |
Synonyms | HZIV 81-2 | ||
Solubility | DMSO : ≥ 3.8 mg/mL (10.20 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | 1,7-bis(4-hydroxy-3-methoxyphenyl)heptane-3,5-dione | ||
SMILES | COC1=C(C=CC(=C1)CCC(=O)CC(=O)CCC2=CC(=C(C=C2)O)OC)O | ||
Standard InChIKey | LBTVHXHERHESKG-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C21H24O6/c1-26-20-11-14(5-9-18(20)24)3-7-16(22)13-17(23)8-4-15-6-10-19(25)21(12-15)27-2/h5-6,9-12,24-25H,3-4,7-8,13H2,1-2H3 | ||
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 | Tetrahydrocurcumin can inhibit tumor angiogenesis, treat human breast cancer,and be a promising candidate for the prevention of CIPN by chemotherapeutic agents.Tetrahydrocurcumin exhibits protective effects against cisplatin-induced oxidative renal damage in rats by inhibiting cyclooxygenase-2 and caspase-3 activation; it has a protective effect over arsenic induced toxicity in rat. |
Targets | COX | Caspase | p38MAPK | Bcl-2/Bax | p21 | VEGFR | HIF |
In vivo | Ameliorative efficacy of tetrahydrocurcumin against arsenic induced oxidative damage, dyslipidemia and hepatic mitochondrial toxicity in rats.[Pubmed: 25869292]Chem Biol Interact. 2015 Jun 25;235:95-105.Arsenic (As) is a well-known human carcinogen and a potent hepatotoxin. Environmental exposure to arsenic imposes a serious health hazard to humans and other animals worldwide. Tetrahydrocurcumin (THC), one of the major metabolites of curcumin, exhibits many of the same physiological and pharmacological activities as curcumin and in some systems may exert greater antioxidant activity than the curcumin. It has been reported that THC has antioxidant efficacy attributable to the presence of identical β-diketone of 3rd and 5th substitution in heptane moiety. Tetrahydrocurcumin exerts protective effect on vincristine induced neuropathy: Behavioral, biochemical, neurophysiological and histological evidence.[Pubmed: 26102012]Chem Biol Interact. 2015 Jun 20;238:118-128.Hyperalgesia, allodynia, delayed motor nerve conduction velocity, oxidative stress and axonal damage are signs and symptoms of chemotherapy induced peripheral neuropathy (CIPN). Present treatment/preventive strategies of CIPN are futile and the neuropathy may even lead to discontinuation of chemotherapy. Effects of tetrahydrocurcumin on hypoxia-inducible factor-1α and vascular endothelial growth factor expression in cervical cancer cell-induced angiogenesis in nude mice.[Pubmed: 25789317]Biomed Res Int. 2015;2015:391748.Tetrahydrocurcumin (THC), one of the important in vivo metabolites of curcumin, inhibits tumor angiogenesis. Its effects on angiogenesis in cervical cancer- (CaSki-) implanted nude mice and its mechanisms on hypoxia-inducible factor-1α and vascular endothelial growth factor expression were investigated. |
Kinase Assay | Tetrahydrocurcumin induces G2/M cell cycle arrest and apoptosis involving p38 MAPK activation in human breast cancer cells.[Pubmed: 24593988]Food Chem Toxicol. 2014 May;67:193-200.Curcumin (CUR) is a major naturally-occurring polyphenol of Curcuma species, which is commonly used as a yellow coloring and flavoring agent in foods. In recent years, it has been reported that CUR exhibits significant anti-tumor activity in vivo. However, the pharmacokinetic features of CUR have indicated poor oral bioavailability, which may be related to its extensive metabolism. The CUR metabolites might be responsible for the antitumor pharmacological effects in vivo. Tetrahydrocurcumin (THC) is one of the major metabolites of CUR. |
Animal Research | Protective effect of tetrahydrocurcumin against cisplatin-induced renal damage: in vitro and in vivo studies.[Pubmed: 25719941]Planta Med. 2015 Mar;81(4):286-91.We investigated the protective effect and mechanism of Tetrahydrocurcumin on cisplatin-induced kidney damage, oxidative stress, and inflammation to evaluate its possible use in renal damage. Cisplatin-induced LLC-PK1 renal cell damage was significantly reduced by Tetrahydrocurcumin treatment. Additionally, the protective effect of Tetrahydrocurcumin on cisplatin-induced oxidative renal damage was investigated in rats. Tetrahydrocurcumin was orally administered every day at a dose of 80 mg/kg body weight for ten days, and a single dose of cisplatin was administered intraperitoneally (7.5 mg/kg body weight) in 0.9 % saline on day four. The creatinine clearance levels, which were markers of renal dysfunction, in cisplatin-treated rats were recovered nearly back to normal levels after administration of Tetrahydrocurcumin. Moreover, Tetrahydrocurcumin exhibited protective effects against cisplatin-induced oxidative renal damage in rats by inhibiting cyclooxygenase-2 and caspase-3 activation. These results collectively provide therapeutic evidence that Tetrahydrocurcumin ameliorates renal damage by regulating inflammation and apoptosis. |
Tetrahydrocurcumin Dilution Calculator
Tetrahydrocurcumin Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.6852 mL | 13.4261 mL | 26.8521 mL | 53.7043 mL | 67.1303 mL |
5 mM | 0.537 mL | 2.6852 mL | 5.3704 mL | 10.7409 mL | 13.4261 mL |
10 mM | 0.2685 mL | 1.3426 mL | 2.6852 mL | 5.3704 mL | 6.713 mL |
50 mM | 0.0537 mL | 0.2685 mL | 0.537 mL | 1.0741 mL | 1.3426 mL |
100 mM | 0.0269 mL | 0.1343 mL | 0.2685 mL | 0.537 mL | 0.6713 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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Tetrahydrocurcumin is a Curcuminoid found in turmeric (Curcuma longa) that is produced by the reduction of Curcumin. Tetrahydrocurcumin inhibit CYP2C9 and CYP3A4.
In Vitro:Tetrahydrocurcumin (THC) has a number of attractive properties not shared with Curcumin that may make it superior. Tetrahydrocurcumin inhibited lipoxygenase as low as 1 μM. Tetrahydrocurcumin is tested for its ability to inhibit CYP2C9, CYP3A4, CYP1A2 and CYP2D6. Tetrahydrocurcumin yields dose-dependent inhibition of CYP2C9, and to a lesser extent, CYP3A4. Tetrahydrocurcumin exhibits maximum inhibition of CYP2C9 and CYP3A4 at 50 to 100 μM. Tetrahydrocurcumin does not show a consistent dose-response inhibition of CYP1A2 or CYP2D6 over the range of concentrations tested. In some cases, the percent inhibition exceeds 100%. The effect of Tetrahydrocurcumin on cancer cell viability is measured. Sup-T1 cells, T-cell lymphoblastic lymphoma cells, are treated with Tetrahydrocurcumin to determine its ability to induce growth inhibition using an MTS assay, and the corresponding IC50 values are in the mid-to-high micromolar range[1].
In Vivo:The serum Tetrahydrocurcumin (THC) concentration versus time curve shows that more than one absorption and distribution phase is present. Initially, a rapid absorption phase with an average Tmax of 6.8 μg/mL at 1 h is observed, followed by a short elimination phase. This is followed by two redistributions with two smaller Tetrahydrocurcumin maxima at 6 and 24 h. Both redistribution phases has similar maxima of about 1 μg/mL. The total amount of Tetrahydrocurcumin excrets unchanged in urine was up to 8 μg at 24 h[1].
References:
[1]. Novaes JT, et al. Disposition, Metabolism and Histone Deacetylase and Acetyltransferase Inhibition Activity of Tetrahydrocurcumin and Other Curcuminoids. Pharmaceutics. 2017 Oct 12;9(4). pii: E45.
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Tetrahydrocurcumin exerts protective effect on vincristine induced neuropathy: Behavioral, biochemical, neurophysiological and histological evidence.[Pubmed:26102012]
Chem Biol Interact. 2015 Aug 5;238:118-28.
Hyperalgesia, allodynia, delayed motor nerve conduction velocity, oxidative stress and axonal damage are signs and symptoms of chemotherapy induced peripheral neuropathy (CIPN). Present treatment/preventive strategies of CIPN are futile and the neuropathy may even lead to discontinuation of chemotherapy. In this study, we evaluated the protective effect of Tetrahydrocurcumin (THC) 40 and 80mg/kg in experimental vincristine induced neuropathy in rats. Hyperalgesia was assessed by hot plate (thermal), Randall-Selitto (mechanical) test, allodynia was assessed by cold plate (thermal) test, functional loss was measured by sciatic function index, nociception was evaluated by formalin test. Neurophysiological recordings were carried out to assess motor nerve conduction velocity. Total calcium levels, oxidative stress and TNF-alpha was measured in sciatic nerve tissue homogenate to assess neuropathy. Histopathological changes was observed on sciatic nerve to assess the protective effect of THC against the vincristine. Pregabalin was used as a standard in this study. Rats administered with THC at 80mg/kg significantly attenuated the vincristine induced neuropathic pain manifestations which may be due to its multiple actions including anti-nociceptive, anti-inflammatory, neuroprotective, calcium inhibitory and antioxidant effect. This study delineates that THC can be a promising candidate for the prevention of CIPN by chemotherapeutic agents.
Effects of tetrahydrocurcumin on hypoxia-inducible factor-1alpha and vascular endothelial growth factor expression in cervical cancer cell-induced angiogenesis in nude mice.[Pubmed:25789317]
Biomed Res Int. 2015;2015:391748.
Tetrahydrocurcumin (THC), one of the important in vivo metabolites of curcumin, inhibits tumor angiogenesis. Its effects on angiogenesis in cervical cancer- (CaSki-) implanted nude mice and its mechanisms on hypoxia-inducible factor-1alpha and vascular endothelial growth factor expression were investigated. Female BALB/c nude mice were divided into control (CON) and CaSki-implanted groups (CaSki group). One month after the injection with cervical cancer cells, mice were orally administered vehicle or 100, 300, and 500 mg/kg of THC daily for 30 consecutive days. The microvascular density (MVD) was evaluated using the CD31 expression. VEGF, VEGFR-2, and HIF-1alpha expression were also detected by immunohistochemistry. The MVD in CaSki + vehicle group was significantly increased compared to the CON + vehicle group. Interestingly, when treated with THC at all doses, the CaSki group showed a significant smaller number of the MVD. The CaSki + vehicle group also showed significantly increased VEGF, VEGFR-2, and HIF-1alpha expressions, but they were downregulated when mice were treated with THC at all doses. THC demonstrated an inhibitory effect against tumor angiogenesis in CaSki-implanted nude mice model. This effect is likely to be mediated by the downregulation of HIF-1-alpha, VEGF expression, and its receptor. THC could be developed into a promising agent for cancer therapy in the future.
Tetrahydrocurcumin induces G2/M cell cycle arrest and apoptosis involving p38 MAPK activation in human breast cancer cells.[Pubmed:24593988]
Food Chem Toxicol. 2014 May;67:193-200.
Curcumin (CUR) is a major naturally-occurring polyphenol of Curcuma species, which is commonly used as a yellow coloring and flavoring agent in foods. In recent years, it has been reported that CUR exhibits significant anti-tumor activity in vivo. However, the pharmacokinetic features of CUR have indicated poor oral bioavailability, which may be related to its extensive metabolism. The CUR metabolites might be responsible for the antitumor pharmacological effects in vivo. Tetrahydrocurcumin (THC) is one of the major metabolites of CUR. In the present study, we examined the efficacy and associated mechanism of action of THC in human breast cancer MCF-7 cells for the first time. Here, THC exhibited significant cell growth inhibition by inducing MCF-7 cells to undergo mitochondrial apoptosis and G2/M arrest. Moreover, co-treatment of MCF-7 cells with THC and p38 MAPK inhibitor, SB203580, effectively reversed the dissipation in mitochondrial membrane potential (Deltapsim), and blocked THC-mediated Bax up-regulation, Bcl-2 down-regulation, caspase-3 activation as well as p21 up-regulation, suggesting p38 MAPK might mediate THC-induced apoptosis and G2/M arrest. Taken together, these results indicate THC might be an active antitumor form of CUR in vivo, and it might be selected as a potentially effective agent for treatment of human breast cancer.
Protective effect of tetrahydrocurcumin against cisplatin-induced renal damage: in vitro and in vivo studies.[Pubmed:25719941]
Planta Med. 2015 Mar;81(4):286-91.
The adverse effects of anticancer drugs can prompt patients to end their treatment despite the efficacy. Cisplatin is a platinum-based molecule widely used to treat various forms of cancer, but frequent and long-term use of cisplatin is limited due to severe nephrotoxicity. In the present study, we investigated the protective effect and mechanism of Tetrahydrocurcumin on cisplatin-induced kidney damage, oxidative stress, and inflammation to evaluate its possible use in renal damage. Cisplatin-induced LLC-PK1 renal cell damage was significantly reduced by Tetrahydrocurcumin treatment. Additionally, the protective effect of Tetrahydrocurcumin on cisplatin-induced oxidative renal damage was investigated in rats. Tetrahydrocurcumin was orally administered every day at a dose of 80 mg/kg body weight for ten days, and a single dose of cisplatin was administered intraperitoneally (7.5 mg/kg body weight) in 0.9 % saline on day four. The creatinine clearance levels, which were markers of renal dysfunction, in cisplatin-treated rats were recovered nearly back to normal levels after administration of Tetrahydrocurcumin. Moreover, Tetrahydrocurcumin exhibited protective effects against cisplatin-induced oxidative renal damage in rats by inhibiting cyclooxygenase-2 and caspase-3 activation. These results collectively provide therapeutic evidence that Tetrahydrocurcumin ameliorates renal damage by regulating inflammation and apoptosis.
Ameliorative efficacy of tetrahydrocurcumin against arsenic induced oxidative damage, dyslipidemia and hepatic mitochondrial toxicity in rats.[Pubmed:25869292]
Chem Biol Interact. 2015 Jun 25;235:95-105.
Arsenic (As) is a well-known human carcinogen and a potent hepatotoxin. Environmental exposure to arsenic imposes a serious health hazard to humans and other animals worldwide. Tetrahydrocurcumin (THC), one of the major metabolites of curcumin, exhibits many of the same physiological and pharmacological activities as curcumin and in some systems may exert greater antioxidant activity than the curcumin. It has been reported that THC has antioxidant efficacy attributable to the presence of identical beta-diketone of 3rd and 5th substitution in heptane moiety. In the present study, rats were orally treated with arsenic alone (5 mg kg(-1) bw/day) with THC (80 mg kg(-1) bw/day) for 28 days. Hepatotoxicity was measured by the increased activities of serum hepatospecific enzymes, namely aspartate transaminase, alanine transaminase, alkaline phosphatase and bilirubin along with increased elevation of lipid peroxidative markers, thiobarbituric acid reactive substances. And also elevated levels of serum cholesterol, triglycerides, free fatty acids and phospholipids were observed in arsenic intoxicated rats. These effects of arsenic were coupled with enhanced mitochondrial swelling, inhibition of cytochrome c oxidase, Ca(2+)ATPase and a decrease in mitochondrial calcium content. The toxic effect of arsenic was also indicated by significantly decreased activities of enzymatic antioxidants such as superoxide dismutase, catalase, and glutathione peroxidase along with non-enzymatic antioxidant such as reduced glutathione. Administration of THC exhibited significant reversal of arsenic induced toxicity in hepatic tissue. All these changes were supported by the reduction of arsenic concentration and histopathological observations of the liver. These results suggest that THC has a protective effect over arsenic induced toxicity in rat.