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Description: Curcumol is a selective, potent, naturally occuring and pure monomer isolated from Rhizoma Curcumaeis with potential antitumor activities. It shows potent in vitro antiproliferative activity and high in vivo antitumor efficacy.vAs an inducer of apoptosis, curcumol induced cell death in human lung adenocarcinoma (ASTC-a-1) cells by inducing G(2)/M phase arrest, nuclear fragmentation, phosphatidylserine externalization and a rapid translocation of Bax from cytosol into mitochondria. Curcumol also benefits rheumatoid arthritis treatment through suppressing the fibroblast-like synoviocytes (FLS) proliferation and DNA synthesis.
References: Med Oncol. 2011 Mar;28(1):307-14; Evid Based Complement Alternat Med. 2012;2012:746426.
Chemical Name: (3S,3aS,5S,6R,8aS)-Octahydro-3-methyl-8-methylene-5-(1-methylethyl)-6H-3a,6-epoxyazulen-6-ol
InChi Key: QRMPRVXWPCLVNI-YYFQZIEXSA-N
InChi Code: InChI=1S/C15H24O2/c1-9(2)13-8-14-11(4)5-6-12(14)10(3)7-15(13,16)17-14/h9,11-13,16H,3,5-8H2,1-2,4H3/t11-,12-,13-,14-,15+/m0/s1
SMILES Code: O[[email protected]@]1(C2)[[email protected]](C(C)C)C[[email protected]]3(O1)[[email protected]@H](C)CC[[email protected]@]3([H])C2=C
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2
In vitro activity: Curcumol induced cell death in human lung adenocarcinoma (ASTC-a-1) cells by inducing G(2)/M phase arrest, nuclear fragmentation, phosphatidylserine externalization and a rapid translocation of Bax from cytosol into mitochondria. While, caspases are not involved in Curcumol-induced apoptosis. Curcumol also benefits rheumatoid arthritis treatment through suppressing the fibroblast-like synoviocytes (FLS) proliferation and DNA synthesis. It attenuates PDGF-BB-induced Jak2 phosphorylation and downregulates STAT1 and STAT3 DNA-binding activities.
Cell Assay: Curcumol exhibited time- and concentration-dependent anti-proliferative effects in SPC-A-1 human lung adenocarcinoma cells with cell cycle arrest in the G0/G1 phase while apoptosis-induction was also confirmed with flow cytometry and morphological analyses. Curcumol-induced growth inhibition correlated with apoptosis induction as evidenced by Annexin V staining, and cleavage of caspase-3 and poly (ADP-ribose) polymerase (PARP) in HSC-T6. Suppression of the NF-κB translocation via inhibition of IκB-α phosphorylation by the curcumol led to the inhibition of expression of NF-κB-regulated gene, e.g. Bcl-xL and Bcl-2, in a PI3K-dependent manner, which is upstream of NF-κB activation. Curcumol exhibits an inhibitory effect on receptor activator of nuclear factor kappaB ligand (RANKL)-induced osteoclast differentiation with both bone marrow-derived macrophages and RAW264.7 cells in a dose-dependent manner.
Med Oncol. 2011 Mar;28(1):307-14; Evid Based Complement Alternat Med. 2012;2012:746426; Asian Pac J Cancer Prev. 2015;16(6):2307-12.
Purity ≥98%
COA
MSDS
NMR
Curcumol inhibited p-Jak2 protein expression of FLS, and the STAT1 and STAT3 protein expression in FLS from patients with RA was not inhibited by curcumol. Evid Based Complement Alternat Med.2012;2012:746426.
Inhibitory effect of different concentration curcumol on FLS proliferation in patients with RA. Evid Based Complement Alternat Med. 2012;2012:746426.
Curcumol inhibited STAT1 DNA-binding activity in FLS from patients with RA. Evid Based Complement Alternat Med.2012;2012:746426.
Inhibitory effect of different concentration curcumol on FLS DNA synthesis in patients with RA.
Curcumol inhibited STAT3 DNA-binding activity in FLS from patients with RA.