Catalog No.S1848 Synonyms: Diferuloylmethane
Molecular Weight(MW): 368.38
Curcumin is the principal curcuminoid of the popular Indian spice turmeric, which is a member of the ginger family (Zingiberaceae). It is an inhibitor of p300 histone acetylatransferase（IC50~25 μM） and Histone deacetylase; activates Nrf2 pathway and supresses the activation of transcription factor NF-κB.
Cited by 14 Publications
7 Customer Reviews
Curcumin increased the expression of FOXA2 in NCI-H292 cells. Cultured NCI-H292 cells were treated with curcumin (40 μM) or vehicle (DMSO, control) at different time intervals. The mRNA and protein expression level of FOXA2 were determined via qRT-PCR (A) and western blotting (B), respectively. Data are presented as mean ± SEM from three independent, ∗p < 0.05, ∗∗p < 0.01.
Front Pharmacol, 2018, 9:60. Curcumin purchased from Selleck.
Effect of NC1, NC1-CUR, NC2 and NC2-CUR on SH-SY5Y cell viability. The cells were treated for 24 h with different dilutions(1:1, 1:2 and 1:4) of empty nanocapsules (NC1 and NC2) and nanocapsules containing curcumin (NC1-CUR and NC2-CUR) followed by measurement of cell viability by MTT reduction assay (panel A) and cell toxicity by LDH release assay (panel B). Data after normalization to vehicle-treated cells (100%, MTT assay) or to total LDH release (TritonX100-treated cells, 100%) are presented as a mean±SEM from 3-8 independent experiments with five replicates. *p < 0.05, **p < 0.01 and ***p<0.001 versus vehicle-treated cells; &&&p<0.001 NC1 versus NC1-CUR.
Nanotechnology, 2016, 27(35):355101. Curcumin purchased from Selleck.
Translocation of AIF from the cytosol to the nucleus after RN5 cells were treated with curcumin for 24 h. Following incubation with an AIF primary antibody, cells were stained with an Alexa Fluor-555-conjugated goat anti-rabbit immunoglobulin G secondary antibody. Nuclei were stained with DAPI. Scale bar, 25 µm. AIF, apoptosis-inducing factor; DMSO, dimethyl sulfoxide.
Int J Oncol, 2018, 53(6):2531-2541. Curcumin purchased from Selleck.
Inhibition of [3H]uridine uptake in MIA PaCa-2 (A & B) and PANC-1 (C) cells by curcumin (CUR) and A13. Results are normalised to the disintegrations/min (dpm) of DMSO-only control and are means ±S.D. of n =3 independent experiments done in triplicates. ***P<0.001 significantly different from DMSO-control, calculated using one-way ANOVA and Dunnett's post-hoc test. NBMPR-Nitrobenzylthioinosine. Conc-concentration.
Eur J Pharmacol, 2017, 803:167-173. Curcumin purchased from Selleck.
Purity & Quality Control
Choose Selective Histone Acetyltransferase Inhibitors
|Description||Curcumin is the principal curcuminoid of the popular Indian spice turmeric, which is a member of the ginger family (Zingiberaceae). It is an inhibitor of p300 histone acetylatransferase（IC50~25 μM） and Histone deacetylase; activates Nrf2 pathway and supresses the activation of transcription factor NF-κB.|
Curcumin induces the expression of forkhead box protein O1 (FOXO1) through activation of extracellular signal-regulated kinase 1/2 signaling. Curcumin inhibits cell proliferation, which was associated with upregulation of the cyclin-dependent kinase inhibitors, p27 and p21, and downregulation of cyclin D1. Curcumin induces endoplasmic reticulum (ER) stress and mitochondrial dysfunction as evidenced by up-regulation of CCAAT/enhancer binding protein homologous protein (CHOP), phosphorylation of JNK and down-regulation of SERCA2ATPase, release of cytochrome c, decrease of Bcl-2 and reduction of mitochondrial membrane potential in both AGS and HT-29 cells.
|In vivo||Chronic treatment with curcumin significantly reverses the CMS-induced behavioral abnormalities in stressed rats. Additionally, curcumin effectively inhibits cytokine gene expression at both the mRNA and the protein level and reduces the activation of NF-κB.|
-  Gao S, et al. Food Chem Toxicol. 2013, 59:739-47.
-  Nasiri M, et al. Asian Pac J Cancer Prev. 2013, 14(6):3449-3453.
-  Cao A, et al. Apoptosis. 2013, 18(11):1391-1402.
-  Jiang H, et al. Prog Neuropsychopharmacol Biol Psychiatry. 2013, 47:33-39.
-  Odot J, et al. Int J Cancer. 2004, 111(3):381-387.
-  Balasubramanyam K, et al. J Biol Chem. 2004, 279(49):51163-71.
-  Chen Y, et al. Basic Clin Pharmacol Toxicol. 2007, 101(6):427-33.
-  Singh S, et al. J Biol Chem. 1995, 270(42):24995-5000.
|In vitro||DMSO||73 mg/mL (198.16 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
10% DMSO+50% PEG 300+ddH2O
For best results, use promptly after mixing.
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Clinical Trial Information
|NCT Number||Recruitment||interventions||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03746158||Not yet recruiting||Dietary Supplement: curcumin||Metabolites|Gut Microbiota||University of Massachusetts Amherst||December 1 2018||Not Applicable|
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