Brassinin

Brassinin is an indole derivative found in cruciferous plants. Brassinin acts as an IDO inhibitor (K_i = 97.7 μM). Brassinin inhibits angiogenesis and induces apoptosis, autophagy, paraptosis, ROS production, and ER stress. Brassinin selectively stimulates lysosomal degradation of Tie2 and promotes lysosomal and proteasomal degradation of FGFR1 in endothelial cells, downregulating AKT and ERK phosphorylation. Brassinin inhibits endothelial cell proliferation, migration, tube formation, spheroid sprouting, and angiogenesis. Brassinin inhibits PI3K/Akt/mTOR/S6K1 signaling, upregulates p21 and p27, and induces G1 phase cell cycle arrest through RB hypophosphorylation. Brassinin inhibits tyrosinase catalytic activity, reduces tyrosinase mRNA, and inhibits MITF nuclear translocation. Brassinin is used for research on triple-negative breast cancer, chronic myeloid leukemia, colon cancer, glioma, atherosclerosis, and skin cancer^{[1][2][3][4][5][6][7][8][9][10]}. In Vitro:Brassinin (2.5-100 µM; 48 h) preferentially reduces the viability of HUVECs and HDMECs compared with pericytes, fibroblasts, and breast cancer cells^[1].
Brassinin (25-100 µM; 6 h, then additional 18 h with BrdU (5-BrdU) (HY-15910)) inhibits HUVEC proliferation in a dose-dependent manner^[1].
Brassinin (25-100 µM; 24 h) inhibits HUVEC migration in a dose-dependent manner^[1].
Brassinin (25-100 µM; 24 h) inhibits HUVEC tube formation, causing a 78% reduction in tube network structures at 100 µM^[1].
Brassinin (25-100 µM; 24 h) inhibits HUVEC spheroid sprouting in a dose-dependent manner^[1].
Brassinin (25-100 µM; 2 h) selectively downregulates Tie2 and FGFR1 protein levels in HUVECs and inhibits AKT and ERK phosphorylation^[1].
Brassinin promotes the degradation of Tie2 and FGFR1 proteins in HUVECs, with only a slight effect on Tie2 mRNA and no effect on FGFR1 mRNA^[1].
Brassinin (100-400 μM; 24 h) does not affect basal proliferation but significantly reverses Ang II (Angiotensin II human) (HY-13948)-induced proliferation of mouse aortic SMCs^[6].
Brassinin (100 μM; 24 h) significantly attenuates Ang II-induced migration of mouse aortic SMCs without affecting basal migration^[6].
Brassinin (100 μM; 24 h) reverses the Ang II-induced decrease in SM α-actin and calponin expression in mouse aortic SMCs^[6].
Brassinin (100 μM; 24 h) significantly upregulates CSE protein expression in mouse aortic SMCs without affecting 3-MST levels^[6].
Brassinin (100 μM; 24 h) significantly induces CSE mRNA levels in mouse aortic SMCs^[6].
Brassinin (100 μM; 24 h) significantly enhances the binding of C/EBPβ to the CSE promoter in mouse aortic SMCs^[6].
Brassinin stimulates lysosomal degradation of Tie2 and both lysosomal and proteasomal degradation of FGFR1 in HUVECs^[1].
Brassinin (10-100 µM; 24 h) exhibits cytotoxicity against KBM5, KCL22, and LAMA84 CML cells, while showing low cytotoxicity toward PBMCs^[2].
Brassinin (50 µM; 24 h) reduces the viability of CML cells^[2].
Brassinin (10-100 µM; 24 h) activates the MAPK signaling pathway in KBM5, K562, KCL22, and LAMA84 CML cells^[2].
Brassinin (200 µM or higher; 24-72 h) inhibits the growth of human colon cancer HT-29 cells in a dose- and time-dependent manner^[3].
Brassinin (1-15 µM; 1 h pretreatment; 6 days stimulation) inhibits α-MSH (HY-P0252)-induced melanin accumulation in B16F10 cells^[7].
Brassinin (5-15 µM; 1 h pretreatment; 6 days stimulation) decreases cellular tyrosinase activity in α-MSH-stimulated B16F10 cells^[7].
Brassinin (5-15 µM; 1 h pretreatment; 6 days stimulation) decreases tyrosinase mRNA levels in α-MSH-stimulated B16F10 cells^[7].
Brassinin (5-15 µM; 1 h pretreatment; 6 days stimulation) inhibits the nuclear translocation of MITF in α-MSH-stimulated B16F10 cells^[7].
Brassinin (100-400 μM; 48 h) exhibits antiproliferative effects in U373, T98G, LN229, GBM-Y2, and GBM-Y5 glioma cells, with IC₅₀ values ranging from 200.8 to 547.5 μM at 48 h, but shows lower toxicity in normal HA1800 astrocytes^[8].
Brassinin (25-200 μM; 48 h) inhibits clonogenic proliferation of U373, LN229, and GBM-Y2 glioma cells^[8].
Brassinin (50-200 μM) inhibits the activity of the AMPKα-ULK1-beclin1 signaling pathway in U373 and LN229 glioma cells in a dose-dependent manner^[8].
Brassinin (10-50 µM; 24 h) induces apoptosis, autophagy, and paraptosis markers in KBM5, K562, KCL22, and LAMA84 CML cells^[2].
Brassinin (50 µM; 24 h) increases the sub G₁ phase cell population in CML cells^[2].
Brassinin (200-400 µM; 24 h) induces G1 phase arrest in human colon cancer HT-29 cells, with the maximum arrest effect observed at 300 µM^[3].
Brassinin (50-400 µM; 6-24 h) upregulates p21 and p27 proteins and inhibits RB protein phosphorylation in human colon cancer HT-29 cells^[3].
Brassinin (50-400 µM; 3-24 h) increases the amount of p21 mRNA in human colon cancer HT-29 cells by stabilizing p21 mRNA^[3].
Brassinin (300-400 µM; 24 h) at least partially contributes to its induced G1 phase arrest in HT-29 cells through the increase of p27 and/or p21^[3].
Brassinin (300-400 µM) induces G1 phase arrest in HT-29 cells, which involves the inhibition of the PI3K-Akt pathway^[3].
Brassinin (50-400 µM; 24 h) inhibits the PI3K-Akt signaling pathway in human colon cancer HT-29 cells, as evidenced by decreased phosphorylation levels of Akt, PDK1, and GSK-3β^[3].
Brassinin (50-200 μM; 48 h) blocks cell cycle progression by arresting U373 and GBM-Y2 glioma cells in the G1 phase^[8].
Brassinin (50 µM; 24 h) promotes early apoptosis in KBM5, K562, KCL22, and LAMA84 CML cells^[2].
Brassinin (50 µM; 24 h) induces autophagy in CML cells^[2].
Brassinin (50-200 μM) inhibits autophagosome formation in U373 and LN229 glioma cells, manifested as decreased LC3-II levels and increased p62 levels^[8].
Brassinin (50 µM; 12 h) induces ROS production in KBM5, K562, KCL22, and LAMA84 CML cells^[2].
Brassinin (50 µM; 24 h) causes GSH/GSSG imbalance in KBM5, K562, KCL22, and LAMA84 CML cells^[2].
Brassinin (50-200 μM; 48 h) induces excessive ROS production in U373 and LN229 glioma cells in a dose-dependent manner^[8].
Brassinin (50 µM; 24 h) causes loss of mitochondrial membrane potential in KBM5, K562, KCL22, and LAMA84 CML cells^[2].
Brassinin (50 µM; 24 h) induces ER stress and vacuolization in KBM5, K562, KCL22, and LAMA84 CML cells^[2].
Brassinin (200-400 μM; 60 min) is a moderate competitive inhibitor of purified recombinant human IDO at 37 °C, with a K_i of 97.7 μM^[5].
Brassinin (5-30 µM; 30 min) inhibits mushroom tyrosinase activity in a cell-free system^[7].
Brassinin binds to the active site of tyrosinase with a docking score of -6.7 kcal/mol, acting as a potent tyrosinase inhibitor^[7].
Brassinin (100 μM; 24 h) effectively attenuates Ang II-induced oxidative stress in mouse aortic SMCs without affecting basal ROS levels^[6].
Brassinin (1-50 µM; 4 min) exhibits antioxidant activity in cell-free FRAP assays^[7].
Brassinin (100 μM; 24 h) attenuates Ang II-induced upregulation of TNFα and IL6 and inhibits IL2 mRNA levels in mouse aortic SMCs^[6].
Brassinin (5-20 µM; 30 min) inhibits TNF-α-induced IL-8 mRNA expression in HUVECs in a dose-dependent manner^[9].
Brassinin (100 μM; 24 h) specifically reverses Ang II-induced AT1R mRNA expression without affecting AT2R, ACE, or ACE2 in mouse aortic SMCs^[6].
Brassinin (50-200 μM; 48 h) promotes apoptosis in U373 and LN229 glioma cells in a dose-dependent manner^[8].
Brassinin (50-200 μM) induces G₁ phase arrest in U373 and LN229 glioma cells by regulating cell cycle regulatory proteins, and alters apoptosis-related protein expression to promote apoptosis^[8].
Brassinin (100-200 μM; 48 h) inhibits autophagic flux in U373 and LN229 glioma cells^[8].
Brassinin (1-20 µM; 30 min) inhibits TNF-α-induced adhesion of U937 monocytes to HUVECs in a dose-dependent manner^[9].
Brassinin (1-20 µM; 30 min) inhibits TNF-α-induced protein expression of VCAM-1, ICAM-1, and E-selectin in HUVECs^[9].
Brassinin (5-20 µM; 30 min) inhibits TNF-α-induced nuclear translocation of NF-κB p65 and increases cytoplasmic IκB-α levels in HUVECs^[9].
Brassinin (1-20 µM; 30 min) inhibits TNF-α-induced cell surface expression of VCAM-1, ICAM-1, and E-selectin in HUVECs in a dose-dependent manner^[9].
Brassinin (30 min) reduces TNF-α-induced intracellular ROS production in HUVECs^[9]. In Vivo:Brassinin (100 µM; s.c.; single administration) reduces microvessel density by 40% in an in vivo Matrigel plug assay^[1].
Brassinin (180 mg/kg; i.p.; once daily; 14 days) significantly reduces TNBC tumor size and microvessel density while decreasing tumor cell proliferation without affecting apoptosis^[1].
Brassinin (75 mg/kg; i.p.; 5 days/week; 2 weeks) suppresses glioma growth in a subcutaneous xenograft model, reducing tumor volume and weight, inhibiting proliferation, and decreasing Bcl-2, p-AMPKα, and beclin1 signaling with good safety^[8].
Brassinin (75 mg/kg; i.p.; 5 days/week; 3 weeks) inhibits glioma growth in an intracranial xenograft model and extends the median survival of tumor-bearing mice from 29.5 days to 33.5 days^[8].