|Description:||1. Bisdemethoxycurcumin can regulate anti-inflammatory and anti-proliferative responses through a ROS-independent mechanism, also suppresses MCF-7 cells proliferation by inducing ROS accumulation and modulating senescence-related pathways. |
2. Bisdemethoxycurcumin directly accelerates gastric ulcer healing with potency equal to curcumin, its antiulcer effect might be due to its properties of decreasing gastric acid secretion and enhancing the mucosal defensive mechanism through suppression of iNOS-mediated inflammation.
3. Bisdemethoxycurcumin differentially inhibit cancer cell invasion through the down-regulation of MMPs and uPA.
4. Bisdemethoxycurcumin induces apoptosis in activated HSCs, but not in hepatocytes, by impairing cellular energetics and causing a downregulation of cytoprotective proteins, likely through a mechanism that involves CBR2.
5. Bisdemethoxycurcumin has effects on 12-Ο-tetradecanoylphorbol-13-acetate-induced tumor promotion.
6. Bisdemethoxycurcumin has antioxidant activities, inhibits ovarian cancer via reducing oxidative stress mediated MMPs expressions.
|Targets:||NOS | COX | NF-kB | ROS | MMP(e.g.TIMP) | VEGFR | TNF-α | Akt | ERK | Bcl-2/Bax | p53 | p21|
|Source:||The rhizome of Curcuma longa L.|
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: email@example.com
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||3.2433 mL||16.2164 mL||32.4328 mL||64.8656 mL||81.082 mL|
|5 mM||0.6487 mL||3.2433 mL||6.4866 mL||12.9731 mL||16.2164 mL|
|10 mM||0.3243 mL||1.6216 mL||3.2433 mL||6.4866 mL||8.1082 mL|
|50 mM||0.0649 mL||0.3243 mL||0.6487 mL||1.2973 mL||1.6216 mL|
|100 mM||0.0324 mL||0.1622 mL||0.3243 mL||0.6487 mL||0.8108 mL|
Molecules. 2015 Jan 14;20(1):1277-92.
|Bisdemethoxycurcumin Induces apoptosis in activated hepatic stellate cells via cannabinoid receptor 2.[Pubmed: 25594342]|
|the results demonstrate that Bisdemethoxycurcumin induces apoptosis in activated HSCs, but not in hepatocytes, by impairing cellular energetics and causing a downregulation of cytoprotective proteins, likely through a mechanism that involves CBR2.|
Oncol Lett. 2015 Jan;9(1):270-274. Epub 2014 Nov 7.
|Bisdemethoxycurcumin attenuates gastric adenocarcinoma growth by inducing mitochondrial dysfunction.[Pubmed: 25435973]|
|Bisdemethoxycurcumin (BDMC) is a demethoxy derivative of curcumin. In this study, a human gastric adenocarcinoma xenograft model was generated in vivo using nude mice and BDMC was observed to suppress the growth and activity of tumors, in addition to improving the physical and mental capacity of the mice. An increased number of apoptotic cells, decreased ratio of B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein and increased caspase-3 expression was also observed following treatment with Bisdemethoxycurcumin, indicating that Bisdemethoxycurcumin may promote apoptosis in tumors via mitochondrial modulation. The growth of SGC 7901 gastric cancer cells was inhibited and arrested at G1 phase. Specific indicators of mitochondrial dysfunction, a reduction in adenosine triphosphate generation, the inner mitochondrial membrane potential, augmentation of reactive oxygen species production and cytochrome c were also detected in the mitochondria following treatment with Bisdemethoxycurcumin. These results indicate that Bisdemethoxycurcumin attenuates gastric adenocarcinoma growth by inducing mitochondrial dysfunction.|
Pharmacol Rep. 2013;65(3):700-9.
|Bisdemethoxycurcumin suppresses MCF-7 cells proliferation by inducing ROS accumulation and modulating senescence-related pathways.[Pubmed: 23950593]|
|Bisdemethoxycurcumin significantly inhibited MCF-7 breast cancer cell proliferation, while a rapid rise of the intracellular ROS level accompanied with a reduction of Dym were observed. In addition, Bisdemethoxycurcumin activated the pro-apoptotic protein p53 and its downstream effector p21 as well as the cell cycle regulatory proteins p16 and its downstream effector retinoblastoma protein (Rb). All of these Bisdemethoxycurcumin-induced effects were counteracted with the pre-incubation of the antioxidant N-acetylcysteine (NAC).|
Mol Nutr Food Res. 2013 Sep;57(9):1611-8.
|Bisdemethoxycurcumin inhibits PDGF-induced vascular smooth muscle cell motility and proliferation.[Pubmed: 23554078]|
|Bisdemethoxycurcumin elicited a concentration-dependent inhibition of PDGF-stimulated phosphorylation of PDGF receptor-β, Akt and Erk as well as the PDGF-stimulated SMC migration and proliferation. Bisdemethoxycurcumin was more potent than curcumin in inhibiting migration and proliferation and suppressing PDGF-signaling in SMCs. Both compounds were equipotent in inhibiting PDGF-stimulated generation of intracellular reactive oxygen species.|
Phytomedicine. 2009 Apr;16(4):342-51.
|Comparative antiulcer effect of bisdemethoxycurcumin and curcumin in a gastric ulcer model system.[Pubmed: 19188055 ]|
|The antiulcer effect of Bisdemethoxycurcumin, a yellow pigment found mainly in rhizomes of Curcuma longa, was compared with curcumin in gastric ulcer model systems to validate its clinical application as a remedy for peptic ulcer. Western blot analysis of mouse macrophage cell line RAW 264.7 activated with lipopolysaccharide showed that Bisdemethoxycurcumin inhibited inducible nitric oxide synthase (iNOS) production significantly but had no effect on tumor necrosis factor-alpha (TNF-alpha) production, whereas curcumin showed stronger suppression of iNOS protein production and inhibited TNF-alpha protein production significantly. However, Bisdemethoxycurcumin and curcumin possessed similar potency in scavenging nitric oxide generated from mouse macrophage cell line RAW 264.7. Reverse-transcriptase polymerase chain reaction (RT-PCR) analysis showed that both curcuminoids inhibited the induction of iNOS dose-dependently at the transcriptional level and curcumin also appeared to inhibit the induction of TNF-alpha at post-transcriptional level. These results indicated that Bisdemethoxycurcumin directly accelerates gastric ulcer healing with potency equal to curcumin. Its antiulcer effect might be due to its properties of decreasing gastric acid secretion and enhancing the mucosal defensive mechanism through suppression of iNOS-mediated inflammation.|
Carcinogenesis, 2007, 28(8):1765-73.
|Curcumin, demethoxycurcumin, bisdemethoxycurcumin, tetrahydrocurcumin and turmerones differentially regulate anti-inflammatory and anti-proliferative responses through a ROS-independent mechanism[Pubmed: 17522064]|
|Curcumin, a component of turmeric (Curcuma longa), has been shown to exhibit chemopreventive activity. Whether analogs of curcumin (Cur), such as Demethoxycurcumin (DMC), Bisdemethoxycurcumin (BDMC), tetrahydrocurcumin (THC) and turmerones, modulate inflammatory signaling and cell proliferation signaling to same extent as curcumin was investigated. The results indicate that the relative potency for suppression of tumor necrosis factor (TNF)-induced nuclear factor-kappaB (NF-kappaB) activation was Cur > DMC > BDMC; thus suggesting the critical role of methoxy groups on the phenyl ring. THC, which lacks the conjugated bonds in the central seven-carbon chain, was completely inactive for suppression of the transcription factor. Turmerones also failed to inhibit TNF-induced NF-kappaB activation. The suppression of NF-kappaB activity correlated with inhibition of NF-kappaB reporter activity and with down-regulation of cyclooxygenase-2, cyclin D1 and vascular endothelial growth factor, all regulated by NF-kappaB.|