Neoprzewaquinone A

Neoprzewaquinone (NEO) is an orally active phenanthraquinone derivative isolated from Salvia miltiorrhiza Bunge. Neoprzewaquinone A inhibits IL-15Rα, blocks the ROCK2/STAT3 pathway to impair the migration and invasion abilities of triple-negative breast cancer cells; induces apoptosis of hepatocellular carcinoma cells by inhibiting the PI3K-AKT pathway; suppresses LPS-induced inflammation via binding to TLR4/MD2, and inhibits IL-15-induced proliferation, migration and phagocytosis of microglial cells; protects osteoblasts from mitochondrial dysfunction and apoptosis in diabetic osteoporosis by activating PRKD2 and the ELF5/PRKD2/PI3K/AKT/mTOR axis. Neoprzewaquinone A can be used in the research of diseases including rheumatoid arthritis, hepatocellular carcinoma, diabetic osteoporosis and triple-negative breast cancer^{[1][2][3][4][6][7]}. In Vitro:Neoprzewaquinone A (NEO) forms stable complexes with purified IL-1β, IL-6, and TNF-α proteins^[1].
Neoprzewaquinone A (1-80000 nM) dose-dependently inhibits the in vitro binding of IL-1β to IL-1R1, IL-6 to IL-6R, and TNF-α to TNFR1^[1].
Neoprzewaquinone A (5-20 μM; 24 h) dose-dependently inhibits the viability, migration, invasion capacity and cytotoxicity of MH7A rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS)^[1].
Neoprzewaquinone A (5-20 μM; 24 h) dose-dependently downregulates the expressions of IL-1β, IL-6, and TNF-α in MH7A rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS)^[1].
Neoprzewaquinone A (5-20 μM; 24 h) does not alter the cell cycle distribution of MH7A rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS)^[1].
Neoprzewaquinone A (5-20 μM; 24 h) dose-dependently inhibits the activation of the MAPK pathway in MH7A rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS)^[1].
Neoprzewaquinone A (20 μM; 24 h) modulates gene expression in primary RA-FLS^[1].
Neoprzewaquinone A (5-20 μM; 24 h) dose-dependently inhibits the viability of primary RA-FLS and increases the cytotoxicity of primary RA-FLS^[1].
Neoprzewaquinone A (0.3125-10 μM; 150 s) binds to purified PRKD2 protein, with a K_D value of 6.39 × 10^-6 M^[3].
Neoprzewaquinone A (0.012-6.250 μM; 60 s binding, 60 s dissociation) specifically binds to recombinant IL-15Rα protein, with a dissociation constant (K_D) of 0.62 μM^[5].
Neoprzewaquinone A binds to the IL-15/IL-15Rα protein complex with a K_D value of 0.6203 μM^[6].
Neoprzewaquinone A (5-20 μM; 24 h) dose-dependently induces apoptosis of MH7A rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS)^[1].
Neoprzewaquinone A (1-20 μM) inhibits the viability of HepG2, Huh7 and Hepa1-6 hepatocellular carcinoma cells in a dose-dependent manner^[2].
Neoprzewaquinone A (5-20 μM; 24 h) inhibits the migration of HepG2 and Huh7 hepatocellular carcinoma cells in a dose-dependent manner^[2].
Neoprzewaquinone A (5-20 μM; 3 days followed by 2 weeks of normal culture) inhibits colony formation of HepG2 hepatocellular carcinoma cells in a dose-dependent manner^[2].
Neoprzewaquinone A (0.3-10 μM; 24-72 h) potently inhibits the viability of MDA-MB-231 triple-negative breast cancer cells, with an IC₅₀ of 4.69 μM at 72 h^[4].
Neoprzewaquinone A (0.5-1 μM; 7 days) inhibits the colony-forming ability of MDA-MB-231 triple-negative breast cancer cells^[4].
Neoprzewaquinone A potently and selectively inhibits purified PIM1 kinase with an IC₅₀ of 0.56 μM^[4].
Neoprzewaquinone A (10 μM) directly binds to PIM1 in MDA-MB-231 triple-negative breast cancer cells^[4].
Neoprzewaquinone A (5-20 μM; 20 h) inhibits the PIM1/ROCK2/STAT3 signaling pathway in MDA-MB-231 triple-negative breast cancer cells, reduces the levels of phosphorylated and total ROCK pathway proteins, but does not alter the total PIM1 level^[4].
Neoprzewaquinone A (5-20 μM; 20 h) dose-dependently inhibits the EMT process in MDA-MB-231 triple-negative breast cancer cells, upregulates E-cadherin levels and downregulates Vimentin levels^[4].
Neoprzewaquinone A (10-20 μM) protects MC3T3-E1 mouse preosteoblasts against HGPA-induced mitochondrial dysfunction and apoptosis by restoring the activation of the ELF5/PRKD2 and PI3K/AKT/mTOR pathways, reducing ROS, and improving mitochondrial function^[3].
Neoprzewaquinone A (1-3 μM; 24 h) inhibits the migration of MDA-MB-231 triple-negative breast cancer cells^[4].
Neoprzewaquinone A (1-3 μM; 24 h) inhibits the invasion of MDA-MB-231 triple-negative breast cancer cells^[4].
Neoprzewaquinone A (5-20 μM; 24 h) induces G₀/G₁ phase arrest, apoptosis and autophagy in triple-negative breast cancer MDA-MB-231 cells^[4].
Neoprzewaquinone A inhibits the proliferation of IL-15-stimulated Mo7e cells, with an IC₅₀ value of 1.075 μM^[6].
Neoprzewaquinone A (5-20 μM; 24 h) regulates the expression of autophagy-related proteins in MDA-MB-231 triple-negative breast cancer cells, upregulating Beclin1 and LC3B while downregulating ATG5^[4].
Neoprzewaquinone A (0.18-5.40 μM; 72 h) inhibits IL-15-induced proliferation of the human megakaryocytic leukemia cell line Mo7e, with an IC₅₀ value of 1.075 μM^[5].
Neoprzewaquinone A (0.3 μg/mL; 24-72 h) inhibits basal proliferation and migration, as well as IL-15-induced proliferation and migration, of human microglial cells HMC3^[6].
Neoprzewaquinone A (0.3 μg/mL; 3-48 h) inhibits both basal phagocytosis and IL-15-induced phagocytosis in human microglial HMC3 cells^[6].
Neoprzewaquinone A inhibits the binding of lipopolysaccharide (LPS) to the TLR4/MD2 receptor on the cell membrane^[7].
Neoprzewaquinone A inhibits LPS-mediated dimerization of TLR4 and MD2 in cells^[7].
Neoprzewaquinone A inhibits the phosphorylation of NF-κB p65 in LPS-stimulated cells^[7].
Neoprzewaquinone A (0.3 μg/mL) inhibits multiple parameters of glycolysis and mitochondrial respiration in human microglial HMC3 cells, and partially reduces the non-mitochondrial respiration level and respiratory capacity of HMC3 cells treated with IL-15^[6].
Neoprzewaquinone A inhibits the secretion of NO, TNF-α, IL-6 and IL-1β in LPS-stimulated cells^[7]. In Vivo:Neoprzewaquinone A (0.1875-0.75 mg/kg; intravenous injection; once daily for 35 consecutive days) dose-dependently alleviates rheumatoid arthritis symptoms and joint damage in mice with collagen-induced arthritis^[1].
Neoprzewaquinone A (0.1875-0.75 mg/kg; intravenous injection; once daily for 13 consecutive days) inhibits hepatocellular carcinoma progression in a dose-dependent manner in BALB/c nude mice^[2].
Neoprzewaquinone A (2.3-3.8 mg/kg; p.o.; once daily for 4 consecutive weeks of observation) alleviates diabetic bone loss in male C57BL/6 mice, and improves bone mineral density, trabecular bone structure and mechanical strength^[3].
Neoprzewaquinone A (0.1-1.0%; single oral administration) reduces intraocular pressure in normotensive NZW rabbits in a dose-dependent manner^[4].