Myrislignan

Myrislignan is a PI3K/AKT/NF-κB inhibitor that can cross the blood-brain barrier. Myrislignan exerts anticancer activity by inducing apoptosis and ferroptosis. Myrislignan inhibits the replication and invasion of Toxoplasma gondii; it induces reactive oxygen species (ROS) imbalance, autophagy, and the death of Toxoplasma gondii tachyzoites. Myrislignan inhibits mitochondrial function and ERK1/2 phosphorylation to improve ovariectomy-induced osteoporosis. Myrislignan can be used in studies related to gastric cancer, glioblastoma, osteoporosis, and toxoplasmosis^[1][2][3][4]. In Vitro:Myrislignan (50-200 μM; 48-72 h) inhibits the viability of human gastric cancer SGC-7901 cells in a dose-dependent manner^[1].
Myrislignan (50-200 μM; 48 h) promotes apoptosis of human gastric cancer SGC-7901 cells in a dose-dependent manner^[1].
Myrislignan (50-200 μM; 48 h) downregulates the protein expression of PI3K and AKT in a dose-dependent manner in human gastric cancer SGC-7901 cells in vitro, and upregulates the protein expression of BAX, Caspase-3 and Caspase-9^[1].
Myrislignan (5-60 μg/mL; 24-48 h) inhibits the growth of human glioblastoma cell lines U87 and U251, as well as human low-grade glioma cell lines SHG44, HS683, and SW1088 in a dose- and time-dependent manner, while a low dose (30 μg/mL) shows no toxicity to the human normal astrocyte cell line NHA^[2].
Myrislignan (5-30 μg/mL; 24 h) inhibits the migration and invasion abilities of human glioblastoma cell lines U87 and U251 in a dose-dependent manner^[2].
Myrislignan (5-30 μg/mL; 48 h) dose-dependently impairs the wound healing capacity of human glioblastoma cell lines U87 and U251^[2].
Myrislignan (5-30 μg/mL) dose-dependently regulates the expression of EMT-related proteins in human glioblastoma cell lines U87 and U251, and inhibits the activation of the NF-κB pathway by reducing the levels of p-p65 and p-IκB-α^[2].
Myrislignan (5-30 μg/mL; 48 h) dose-dependently inhibits the activity of the NF-κB signaling pathway in human glioblastoma cell lines U87 and U251^[2].
Myrislignan (15 μg/mL) reduces the levels of nuclear and total phosphorylated p65 in the human glioblastoma cell line U87 without altering the total p65 level^[2].
Myrislignan (10 μg/mL) induces growth inhibition of the human glioma cell line U87 via ferroptosis. This effect is reversed by the ferroptosis inhibitor Fer-1 (HY-100579) and enhanced by the GPX4 inhibitor RSL3 (HY-100218A)^[2].
Myrislignan (5-15 μg/mL) dose-dependently induces lipid peroxidation and reduces the levels of antioxidant molecules without affecting the labile iron pool in the human glioblastoma cell line U87^[2].
Myrislignan (5-15 μg/mL) induces dose-dependent ultrastructural changes of mitochondria associated with ferroptosis in the human glioblastoma cell line U87^[2].
Myrislignan (5-15 μg/mL) downregulates the protein level of SLC7A11 in the human glioblastoma cell line U87 in a dose-dependent manner, without altering the expression levels of Nrf2, TFR1 or GPX4^[2].
Myrislignan (0-80 μM; 48-96 h) exerts no effect on the viability of primary mouse bone marrow macrophages and does not induce their apoptosis even at concentrations up to 80 μM and treatment durations as long as 96 h^[3].
Myrislignan (0-30 μM; 7 days) inhibits RANKL-induced osteoclast differentiation of primary mouse bone marrow macrophages in a dose-dependent manner, and its inhibitory effect peaks at the middle stage of differentiation (days 3-4) at a concentration of 30 μM^[3].
Myrislignan (15-30 μM; 7 days) inhibits the formation of podosome belts-a key cytoskeletal feature of mature osteoclasts-in primary mouse bone marrow macrophages treated with RANKL for 7 days^[3].
Myrislignan (15-30 μM; 2 days) impairs the bone resorption function of mature osteoclasts derived from primary mouse bone marrow macrophages^[3].
Myrislignan (15-30 μM; 7 days) dose-dependently inhibits the expression of osteoclast-specific genes in RANKL-treated primary mouse bone marrow macrophages^[3].
Myrislignan (15-30 μM; 3-7 days) inhibits mitochondrial function in primary mouse bone marrow macrophages treated with RANKL, reduces mtROS production on day 3, and decreases mitochondrial membrane potential on day 7^[3].
Myrislignan (30 μM; 60 min) specifically inhibits RANKL-induced phosphorylation of ERK in primary mouse bone marrow macrophages without affecting other MAPK or NF-κB pathway proteins; meanwhile, it blocks H₂O₂-induced ERK activation at a concentration of 30 μM^[3].
Myrislignan (30 μM; 60 min-7 days) inhibits osteoclastogenesis in primary mouse bone marrow macrophages by suppressing ERK phosphorylation and downstream protein expression; this effect is partially reversed by the ERK agonist LM22B-10 (HY-104047) at a concentration of 30 μM^[3].
Myrislignan (32-70 mg/mL; 24 h) alters the gene expression of tachyzoites of the RH strain of Toxoplasma gondii; differentially expressed genes (DEGs) are enriched in redox processes and the oxidative phosphorylation pathway^[4].
Myrislignan (32-70 mg/mL; 8-24 h) induces a statistically significant time-dependent increase in ROS activity in tachyzoites of the RH strain of Toxoplasma gondii^[4].
Myrislignan (32-70 mg/mL) induces a statistically significant increase in SOD activity in tachyzoites of the RH strain of Toxoplasma gondii, but SOD levels do not increase over time^[4].
Myrislignan (32-70 mg/mL; 16-24 h) induces the formation of autophagosome-like structures in tachyzoites of Toxoplasma gondii RH strain within infected Vero cells, followed by subsequent degeneration after treatment at 32 or 70 mg/mL for 16 or 24 h^[4].
Myrislignan (32-70 mg/mL; 16 h) induces autophagosome formation in tachyzoites of the RH strain of Toxoplasma gondii^[4].
Myrislignan (16-70 mg/mL; 16 h) upregulates the autophagy marker TgATG8-PE in a dose-dependent manner in tachyzoites of the RH strain of Toxoplasma gondii^[4].
Myrislignan (32-70 mg/mL; 24 h) induces concentration-dependent cell death in tachyzoites of the RH strain of Toxoplasma gondii^[4]. In Vivo:Myrislignan (5 mg/kg; i.p.; every 3 days; 21 days) suppresses glioblastoma progression in an intracranial xenograft model, improving mouse survival, reducing tumor weight, and modulating EMT and ferroptosis-related protein expression^[2].
Myrislignan (15-30 mg/kg; i.p.; daily; 6 weeks) dose-dependently reduces ovariectomy-induced bone loss in female C57BL/6J mice^[3].