Curcumin

Catalog No.S1848 Synonyms: Diferuloylmethane

Curcumin Chemical Structure

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.

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In DMSO USD 130 In stock
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Cited by 12 Publications

7 Customer Reviews

  • Oncol Res 2014 21(3), 137-44. Curcumin purchased from Selleck.

    Oncol Res 2014 21(3), 137-44. Curcumin purchased from Selleck.

  • EC9706 and TE13 cells were treated with different concentrations of curcumin for 24 h. Then, cells were prepared for immunoblotting against p-JAK2, JAK2 and GAPDH.

    J Exp Clin Cancer Res, 2018, 37(1):303. Curcumin purchased from Selleck.

    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.

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Biological Activity

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.
Targets
Nrf2 [1]
(Cell-free assay)
HDAC [7]
(Cell-free assay)
NF-κB [8]
(Cell-free assay)
p300 histone acetylatransferase [6]
(Cell-free assay)
~25 μM
In vitro

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[2]. 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[3].

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
U87 Mor6R4VtdCC4aXHibYxqfHliYYPzZZk> M2HkclAtKDFyLDCyNEwhOzBuIESwMEBidmRiNUCgxtVON0x? NE\H[GMzPCCqb4Xydy=> MoHVRZQh[2:wY3XueJJifGmxboOgbIlocGW{IIToZY4hOjBiwsXNM2wtKGOnbHygeoli[mmuaYTp[ZMhe3SnZYDsfUBl\WOuaX7l[C=> MVOzNVA3OjV{Nx?=
HEL cells MoHoR4VtdCC4aXHibYxqfHliYYPzZZk> NX7tS3VZOC1|MDFCuY1wdC:O NE[5OFEzPC92ONMgbI92enN? NIfGfIFVcGVidnnhZoltcXS7IH;mJJRp\SCKRVygZ4VtdHNiZYjwc5Nm\CC2bzDjeZJkfW2rbjD3ZZMhe2mpbnnmbYNidnSueTDsc5dmeiClb33wZZJm\CC2bzDjc451em:uIHPlcIx{KGW4ZX6gZZQhdG:5IHPvcoNmdnS{YYTpc45{Ng>? MlfFN|ExOzN{MEm=
Raw246.7 MUfD[YxtKH[rYXLpcIl1gSCjc4PhfS=> M4TWPVEtKDVuIEGwMEA2OCxiMUCwMEAzODBuIHHu[EA2ODBiZz;tUC=> M{jEeFMyODB5N{Cx
RT112 M334VWNmdGxidnnhZoltcXS7IHHzd4F6 NXL4PGR5OC5zIH;yJFAvPCEQvHevcYw> M4rF[|I1NCB2ODygZY5lKDd{IHi= MWjDeZJkfW2rbjDhcI9v\SxiYXTk[YQh[XRiYTDjc45k\W62cnH0bY9vKG[{b32gNE4yKHSxIECuOEDPxGdxbXysJIRq\CCwb4SgZYx1\XJiY3XscEBoem:5dHigc4YhWlRzMUKgZ4VtdHNuIIPsbYdpfGy7IILl[JVk\WRiVV3VR|Mh[2WubDDndo94fGhiYYSgNE41KM7:Zz;tcEwh[W6mIH;ucJkhdW:mZYLheIVtgSC|dYDwdoV{e2WmIHfyc5d1cCCxZjDUR2NUXVBiYYSgNE4zKGGwZDCwMlQh|rypL33sMEBm[WOqIHPvcZBiemWmIITvJJJme3CnY4TpeoUh[2:wdILvcJM> MV[zNFk5PDJ5OB?=
UMUC3 MX7D[YxtKH[rYXLpcIl1gSCjc4PhfS=> NVvB[Wd2OC5zIH;yJFAvPMLizsznM41t MnruNlQtKDR6LDDhcoQhPzNiaB?= MoPHR5Vz[3WvaX6gZYxwdmVuIHHk[IVlKGG2IHGgZ49v[2WwdILheIlwdiCocn;tJFAvOSC2bzCwMlQh|rypL33sMEBlcWRibn;0JIFtfGW{IHPlcIwh\3Kxd4ToJI9nKFKWMUGyJINmdGy|LDDzcIlocHSueTDy[YR2[2WmIGXNWWM{KGOnbHyg[5Jwf3SqIHH0JFAvPCEQvHevcYwtKGGwZDDvcox6KG2xZHXyZZRmdHlic4XwdJJme3OnZDDndo94fGhib3[gWGNEW1WSIHH0JFAvOiCjbnSgNE42KM7:Zz;tcEwh\WGlaDDjc41x[XKnZDD0c{Bz\XOyZXP0bZZmKGOxboTyc4x{ NETxdlA{ODl6NEK3PC=>
TCCSUP NUTUdHR7S2WubDD2bYFjcWyrdImgZZN{[Xl? NVHCO4V1OC5zIH;yJFAvPMLizsznM41t MXGyOEwhPDhuIHHu[EA4PCCq NFW2NmVEfXKldX3pckBidG:wZTygZYRl\WRiYYSgZUBkd26lZX70doF1cW:wIH\yc40hOC5zIITvJFAvPCEQvHevcYwtKGSrZDDuc5Qh[Wy2ZYKgZ4VtdCCpcn;3eIghd2ZiUmSxNVIh[2WubIOsJJNtcWeqdHz5JJJm\HWlZXSgWW1WSzNiY3XscEBoem:5dHigZZQhOC52IN88[{9udCxiYX7kJI9vdHlibX;k[ZJifGWueTDzeZBxemW|c3XkJIdzd3e2aDDv[kBVS0OVVWCgZZQhOC5{IHHu[EAxNjZizsznM41tNCCnYXPoJINwdXCjcnXkJJRwKHKnc4DlZ5RqfmViY3;ueJJwdHN? NFLEOXc{ODl6NEK3PC=>

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
p-IRE1α / IREα ; 

PubMed: 29901626     


Curcumin increases the phosphorylation of IRE1α in BCPAP cells. The protein levels of phosphorylated IRE1α and total IRE1α were detected by western blot analysis. β-actin was used as a loading control. 

HDAC1/ HDAC2 ; 

PubMed: 31196210     


Curcumin-induced suppression of HDCA1 and HDCA2 proteins in H157 and H1299 cells.

p-STAT3 / STAT3 ; 

PubMed: 23874455     


Dose-dependent inhibition of STAT3 phosphorylation by curcumin. SiHa cells treated with indicated concentration of curcumin for 24 h were tested for expression of phospho-STAT3 by immunoblotting. Subsequently the blots were stripped and reprobed with STAT3 and β-actin. 

29901626 31196210 23874455
Immunofluorescence
β-catenin ; 

PubMed: 22523587     


C4-2 cells were cultured on glass coverslips overnight in 12 well plates. The cells were treated with DMSO (upper panel) or curcumin (20 µM) (lower panel) for 1 h, washed, fixed and immunostained for β-catenin (red) and counter-stained with DAPI (blue). Higher β-catenin staining was observed on the cell surface at 1 h of curcumin treatment, compared to DMSO control treated cells. Original Magnifications 600×.

PKD1; 

PubMed: 22523587     


Effect of curcumin treatment on the cellular localization of β-catenin and PKD1. C4-2 cells treated with curcumin (20 µM) or DMSO for 24 h were immunostained for β-catenin (green) or PKD1 (red) and counter-stained with DAPI (blue). Curcumin treated cells showed lower cytoplasmic and higher membrane β-catenin staining compared to control cells. In addition, while PKD1 was predominantly localized in the cytoplasm in control cells, curcumin treated cells exhibited staining primarily on the cell membrane and in the nucleus (white arrows), with faint cytoplasmic staining. Original Magnifications 600× with 2× zoom. 

EGFR / LC3 ; 

PubMed: 31196210     


H157 and H1299 cells were treated with gefitinib, or curcumin alone, or gefitinib plus curcumin at indicated concentration for 48 h and then were fixed with methanol, immunostained with anti-EGFR (green), anti-LC3 (red), and DAPI (blue), and analyzed by confocal microscopy to determine the intracellular locations of EGFR and LC3.

22523587 31196210
Growth inhibition assay
Cell proliferation ; 

PubMed: 22523587     


Effect of curcumin on proliferation of various prostate cancer cell lines. LNCaP, C4-2, DU145 and PC3 cell were treated with curcumin or vehicle control DMSO for 48 h and cell proliferation was determined using MTS assay. The percent cell proliferation was calculated by normalizing the proliferation of curcumin treated cells with proliferation of control treated cells. Concentration dependent inhibition in cell proliferation was observed with curcumin treatment. Mean ± SE; n = 3; *p<0.05.

Cell viability; 

PubMed: 19809577     


Triple negative MDA468, HCC1806, and HCC1937, and ER+/HER2-over-expressing BT474, HER2-over-expressing SKBR3, ER+ MCF7, and non-transformed MCF12A cells were treated with 5, 10, or 20 μM curcumin for 72 h. Control cells were treated with ethanol corresponding to the highest dose of curcumin, since curcumin is dissolved in ethanol. Surviving cells were counted by trypan blue exclusion. For each treatment group, cell viability is shown as a percentage of the ethanol control group per line. Experiments were done in duplicate or triplicate at least twice. Error bars represent standard deviation between replicates. In comparison to MCF12A non-transformed mammary epithelial cells, curcumin inhibited viability of all cancer lines (**p < 0.005 at 10 μM and 20 μM).

22523587 19809577
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[4].

Protocol

Cell Research:

[5]

+ Expand
  • Cell lines: murine melanoma cell subline(B16-R)
  • Concentrations: 0-100 μM
  • Incubation Time: 24-48 h
  • Method:

    1×104 B16-R cells are cultivated as monolayer culture for 12 hr. They were then incubated in 200 μL of RPMI, 10% FBS containing curcumin at final concentrations from 1–100 μM in 96-multiwell plates for 24-48 hr. After these incubations, cells are washed twice in PBS and 500 μl of fresh culture medium containing MTT (0.3 mg/mL) are added for colorimetric assay.


    (Only for Reference)
Animal Research:

[5]

+ Expand
  • Animal Models: Female B6D2F1 mice (6-8 weeks old)
  • Formulation: Dissolved in DMSO and diluted with 0.85% NaCl
  • Dosages: 25 mg/kg
  • Administration: i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 73 mg/mL (198.16 mM)
Water Insoluble
Ethanol Insoluble
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.
40mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 368.38
Formula

C21H20O6

CAS No. 458-37-7
Storage powder
in solvent
Synonyms Diferuloylmethane

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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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Histone Acetyltransferase Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID