Licocoumarone

Licocoumarone (LC) (1.5-100 μM; 24 h) exhibits only extremely low cytotoxicity against RAW 264.7 macrophages even at concentrations as high as 100 μM^[1].
Licocoumarone (compound 5) potently inhibits the enzymatic activity of purified human recombinant DYRK1A, with an IC₅₀ of 12.56 μM and a K_d value of 14.90 μM; it protects purified human recombinant DYRK1A protein from pronase-induced proteolysis^[2].
Licocoumarone (1.5-50 μM; 1 h pretreatment followed by 24 h LPS stimulation) dose-dependently inhibits LPS-induced NO production in RAW 264.7 macrophages^[1].
Licocoumarone inhibits LPS-induced NF-κB activation in RAW 264.7 macrophages by reducing the phosphorylation level of p65 and suppressing IκBα degradation; it also inhibits TNF-α-induced NF-κB transcriptional activity in HeLa cells in a dose-dependent manner^[1].
Licocoumarone (3-50 μM; pretreated for 1 hour followed by LPS stimulation for 30 minutes) dose-dependently inhibits LPS-induced phosphorylation of ERK, JNK and p38 MAPKs in RAW 264.7 macrophages^[1].
Licocoumarone (3-50 μM; 1 h pretreatment, followed by LPS stimulation for mRNA/24 h for protein) inhibits LPS-induced mRNA and protein expression of iNOS, IL-1β, IL-6 and IL-10 in a dose-dependent manner in RAW 264.7 macrophages, but does not affect the expression of TNF-α^[1].
Licocoumarone (0-400 μM; 48 h) potently inhibits the viability of human pancreatic adenocarcinoma BxPC-3 cells, with an IC₅₀ of 50.77 μM after 48 h of treatment^[2].
Licocoumarone (25-50 μM; 2 h) significantly inhibits the proliferation of human pancreatic adenocarcinoma BxPC-3 cells, reducing the proportion of Edu-positive cells to 35.92% and 29.90%, respectively^[2].
Licocoumarone (25-50 μM; initial treatment for 48 h; 7-14 day growth period) significantly reduces the colony-forming ability of human pancreatic adenocarcinoma BxPC-3 cells^[2].
Licocoumarone (50 μM) significantly reduces the expression level of c-MET protein in human pancreatic adenocarcinoma BxPC-3 cells by inhibiting DYRK1A^[2].
Licocoumarone (25-50 μM; 48 h) significantly inhibits the migration of human pancreatic adenocarcinoma BxPC-3 cells; it induces apoptosis in human pancreatic adenocarcinoma BxPC-3 cells, with dose-dependent apoptotic morphological changes (chromatin condensation, nuclear fragmentation) observed^[2].
Licocoumarone (compound 18) (0.1-1000 μM) reversibly inhibits the neuraminidase in a non-competitive manner, with an IC₅₀ of 27.8 μM and a K_i of 12.1 μM^[3].
Licocoumarone (compound 13) selectively inhibits the growth of Bacillus cereus ATCC 11778 and Listeria monocytogenes ATCC 15313 with an MIC of 50 μM; it inhibits Candida parapsilosis ATCC 22019 with an MIC of 100 μM; and at concentrations up to 100 μM, it shows no activity against the tested Gram-negative bacteria, Staphylococcus aureus ATCC 25923, Candida albicans ATCC 10231 or Candida glabrata ATCC 90030^[4].
Licocoumarone (25-50 μM; 24-48 h) exhibits weak, concentration- and biofilm age-dependent activity against preformed Listeria monocytogenes ATCC 15313 biofilms: the maximum eradication rate reaches approximately 45% against 24 h preformed biofilms at 50 μM, while no eradication activity is observed against 48 h preformed biofilms even at the highest concentration of 50 μM^[4].

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