Bisdemethoxycurcumin

Bisdemethoxycurcumin stably binds to purified human SRC, EGFR, AKT1, and PIK3R1 proteins, with the strongest binding affinity to AKT1 (-9.2 kcal/mol)^[1].
Bisdemethoxycurcumin (1-256 μM; 24-48 h) exhibits no cytotoxicity against ATDC5 chondrocytes at concentrations ≤ 8 μM within 24 h or 48 h, with a 48 h CC₅₀ value of 14.62 μM^[2].
Bisdemethoxycurcumin (2-8 μM; 7 days) dose-dependently reverses TBHP-induced reduction in the area of ATDC5 chondrocytes after 7 days of high-density culture^[2].
Bisdemethoxycurcumin (2.5-40 μM; 48 h) shows no cytotoxicity against RAW264.7 cells at concentrations of 2.5 μM and 5 μM after 48 h of incubation, but induces significant cytotoxicity at concentrations ≥ 10 μM^[1].
Bisdemethoxycurcumin (2.5 μM; 25 h) inhibits LPS-induced phosphorylation of Akt, PI3K and p38 proteins in RAW264.7 cells, but has no effect on the phosphorylation of ERK1/2 or JNK^[1].
Bisdemethoxycurcumin exhibits favorable pharmacokinetic properties and targets the PI3K/AKT signaling pathway, in which PDK1 serves as a key potential mediator of its anti-atherosclerotic effects^[3].
Bisdemethoxycurcumin (2.5 μM; 25 h) reduces the mRNA expression levels of IL-6, IL-1β, TNF-α and MCP-1 in LPS (HY-D1056)-induced RAW264.7 cells^[1].
Bisdemethoxycurcumin (2-8 μM; 48 h) reverses TBHP-induced extracellular matrix (ECM) degradation in ATDC5 chondrocytes in a dose-dependent manner by upregulating type II collagen and aggrecan, and downregulating ADAMTS4 and MMP3^[2].
Bisdemethoxycurcumin (2-8 μM; 48 h) activates the Nrf2/HO-1 pathway in a dose-dependent manner, and inhibits pyroptosis in TBHP-stimulated ATDC5 chondrocytes by upregulating Nrf2 and HO-1, and downregulating NLRP3, GSDMD, Caspase 1 and IL-1β, with a treatment duration of 48 h^[2].
Bisdemethoxycurcumin (8 μM; 24 h) significantly reduces the TBHP-induced upregulation of ADAMTS5 and NLRP3 protein expressions in ATDC5 chondrocytes^[2].
Bisdemethoxycurcumin (10-40 μM; 12 h) reduces lipid accumulation in mouse aortic vascular smooth muscle cells stimulated by oxidized low-density lipoprotein (ox-LDL) (HY-NP013) and promotes cholesterol efflux^[3].
Bisdemethoxycurcumin (20 μM; 12 h) promotes autophagy and reduces lipid deposition in ox-LDL-stimulated mouse aortic vascular smooth muscle cells by inhibiting the PDK1/Akt/mTOR signaling pathway^[3].
The autophagy-promoting and lipid-lowering effects of Bisdemethoxycurcumin (20 μM; 12 h) in ox-LDL-stimulated mouse aortic vascular smooth muscle cells depend on the downregulation of PDK1^[3].
Bisdemethoxycurcumin (10 µmol; 18 h) inhibits LPS-induced inflammatory responses and oxidative stress in primary mouse peritoneal macrophages by suppressing NF-κB p65 activation and restoring the levels of redox balance markers^[4].
Bisdemethoxycurcumin (10 µmol; 18 h) protects primary mouse peritoneal macrophages against LPS-induced inflammation and oxidative stress by activating AMPKα^[4].
Combination treatment with bisdemethoxycurcumin (40 μM) and potassium iodide achieves a maximum reduction of 3.5 log₁₀ CFU/mL in Candida albicans ATCC 10231 biofilms at 1 hour post-irradiation^[6].
When Bisdemethoxycurcumin (20-80 μM) is used alone, the amount of hydroxyl radicals it generates shows a strong correlation with the reduction degree of Candida albicans ATCC 10231 biofilms; however, when it is used in combination with potassium iodide, the correlation is only moderate after irradiation^[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.