Lucidenic acid B

Lucidenic acid B is a triterpenoid compound. Lucidenic acid B inhibits the activities of ERK1/2, AP-1, NF-kB, and IKK, suppresses PMA (Phorbol 12-myristate 13-acetate) (HY-18739)-induced MMP-9 expression and cell invasion, and induces apoptosis in leukemia cells via the mitochondrial pathway. Lucidenic acid B inhibits the growth of various cancer cell lines without affecting normal lymphocytes and does not induce G1 phase arrest or necrosis. Lucidenic acid B can be used in research on hepatocellular carcinoma, human acute promyelocytic leukemia, and skin tumor promotion^[1][2][3]. IC50 & Target:Apoptosis^[1] In Vitro:Lucidenic acid B (LAB) (10-100 μM; 24 h) reduces PMA (Phorbol 12-myristate 13-acetate) (HY-18739)-induced invasion of HepG2 cells in a dose-dependent manner^[1].
Lucidenic acid B (10-100 μM; 24 h) suppresses PMA-induced MMP-9 expression in HepG2 cells at the transcriptional level^[1].
Lucidenic acid B (10-100 μM; 24 h) suppresses PMA-induced MMP-9 activity in HepG2 cells^[1].
Lucidenic acid B (10-100 μM; 24 h), in combination with an IKK inhibitor, synergistically suppresses PMA-induced MMP-9 expression in HepG2 cells^[1].
Lucidenic acid B (10-100 μM; 24 h) suppresses the PMA-induced phosphorylation of ERK1/2 in HepG2 cells without affecting Akt phosphorylation^[1].
Lucidenic acid B (10-100 μM; 24 h) enhances IκBα protein expression in PMA-stimulated HepG2 cells, which prevents NF-κB activation^[1].
Lucidenic acid B (10-100 μM; 24 h) strongly inhibits the PMA-stimulated NF-κB and AP-1 DNA-binding activities in HepG2 cells in a dose-dependent manner^[1].
Lucidenic acid B (10-100 μM; 24 h) dose-dependently reduces the nuclear protein levels of NF-κB, c-Jun, and c-Fos in PMA-stimulated HepG2 cells^[1].
Lucidenic acid B (25-500 µM; 24-72 h) potently inhibits the growth of HL-60 human acute promyelocytic leukemia cells with an IC₅₀ of 19.3 µM, while exhibiting weaker growth inhibition against COLO 205, HepG2, and HT-29 cells, and no effect on normal human peripheral blood lymphocytes^[2].
Lucidenic acid B (25-100 µM; 24-72 h) does not induce G1 cell cycle arrest in HL-60 cells but causes a time- and dose-dependent increase in the sub-G1 apoptotic cell population^[2].
Lucidenic acid B (5-100 µM; 24-72 h) induces apoptotic nuclear morphological changes in HL-60 cells in a time- and dose-dependent manner, with visible apoptotic bodies at 50 µM after 24 h^[2].
Lucidenic acid B (5-100 µM; 72 h) induces dose-dependent early and late apoptosis in HL-60 cells after 72 h of treatment, with negligible necrosis^[2].
Lucidenic acid B (5-100 µM; 3-12 h) induces a time- and dose-dependent loss of mitochondrial membrane potential in HL-60 cells^[2].
Lucidenic acid B (5-25 µM; 3-6 h) modulates Bcl-2 family protein expression (increasing pro-apoptotic Bax, Bak, Bad and decreasing anti-apoptotic Bcl-2, Bcl-X_L) and induces cytochrome c release from mitochondria in HL-60 cells in a time- and dose-dependent manner^[2].
Lucidenic acid B (5-25 µM; 3-6 h) induces caspase-9 and caspase-3 activation and PARP cleavage in HL-60 cells in a time- and dose-dependent manner^[2].
Lucidenic acid B induced cell death in HL-60 cells is prevented by inhibition of caspase-9 or caspase-3, confirming the functional requirement of these caspases in the apoptotic pathway^[2].