Ro 106-9920

Ro 106-9920 is an orally active NF-κB inhibitor. Ro 106-9920 prevents ubiquitination of IκBα, blocks nuclear translocation of NF-κB, and inhibits NF-κB activation. Ro 106-9920 suppresses TNF-α-induced tissue factor expression and procoagulant activity, enhances TNF-α-mediated cytotoxicity against cancer cells, and eliminates the formation of neutrophil extracellular traps. Ro 106-9920 inhibits NLRP3 inflammasome activation, reduces inflammatory cytokine secretion, decreases myeloperoxidase activity, attenuates renal cell apoptosis, and improves renal function. Ro 106-9920 blocks ANG II (Angiotensin II human) (HY-13948)-induced nuclear localization of p65, internalization of AT_1A receptor, colocalization of β-arrestin-2, and expression of COX-2, and alters the formation of β-arrestin endosomes. Ro 106-9920 can be used in research related to non-small cell lung cancer, acute kidney injury, diabetes mellitus, and osteoporosis^{[1][2][3][4][5][6]}. IC50 & Target:NF-kappaB^[1] In Vitro:Ro 106-9920 (10 μM; 1 h pre-incubation prior to 12 h TNF-α exposure) prevents TNF-α-induced tissue factor protein expression in human non-small cell lung cancer H1299 and A549 cells^[1].
Ro 106-9920 (10 μM; 1 h pre-incubation prior to 48 h TNF-α exposure) enhances TNF-α-mediated cytotoxicity against human non-small cell lung cancer H1299 and A549 cells^[1].
Ro 106-9920 (10 μM; 1 h pre-incubation prior to 24 h TNF-α exposure) reverses TNF-α-induced procoagulant activity, restored to control levels, in human non-small cell lung cancer H1299 and A549 cells^[1].
Ro 106-9920 (1 μM; 3 days) reduces CuLDL-stimulated cell-associated RANKL expression in MG63 human osteoblast-like cells^[4].
Ro 106-9920 (10 μM; 30 min) potently reduces ANG II-induced AT₁A receptor internalization in rat aortic vascular smooth muscle cells (RASMC), lowering internalization from ~70% to ~20%^[5].
Ro 106-9920 (10 μM; 30 min) blocks ANG II-induced internalization of AT₁A/GFP receptors in HEK-293 cells, preventing movement from the plasma membrane to the nuclear membrane area^[5].
Ro 106-9920 (10 μM; 30 min) inhibits ANG II- and SII-ANG II-induced β-arrestin-2 recruitment to the human AT₁ receptor in CHO-K1 cells, reducing recruitment to basal levels^[5].
Ro 106-9920 (10 μM; 60 min) inhibits ANG II-induced colocalization of AT₁A/GFP receptors with β-arrestin-2/RFP in HEK-293 cells, preventing the approximately fourfold increase in colocalization seen with ANG II alone^[5].
Ro 106-9920 (10 μM; 60 min) alters ANG II-induced β-arrestin-2 endosome formation in HEK-293 cells, producing significantly larger endosomes compared to ANG II alone^[5].
Ro 106-9920 (6.25-25 μM; 1 min pre-incubation) dose-dependently inhibits thrombin-induced IκBα degradation without altering IκBα phosphorylation in human leukocyte-free washed platelets^[6].
Ro 106-9920 (12.5 μM; 1 min pre-incubation) reduces thrombin-induced fibrinogen binding to αIIbβ3 integrin in human washed platelets^[6].
Ro 106-9920 (12.5 μM; 1 min pre-incubation) inhibits thrombin-induced platelet spreading on immobilized fibrinogen in human washed platelets^[6].
Ro 106-9920 (12.5 μM) does not alter thrombin-induced intracellular Ca²⁺ mobilization in human washed platelets^[6].
Ro 106-9920 (12.5 μM) inhibits thrombin-induced ATP release but does not affect Arachidonic acid (HY-109590)-induced ATP release in human washed platelets^[6].
Ro 106-9920 (12.5 μM) reduces thrombin-induced P-selectin expression in human washed platelets^[6].
Ro 106-9920 (25 μM) inhibits thrombin-induced cPLA₂ activity in human washed platelets^[6].
Ro 106-9920 (12.5-25 μM; 1 min pre-incubation) dose-dependently inhibits thrombin-induced ERK2 phosphorylation in human washed platelets^[6].
Ro 106-9920 (2.5 μM; 12 h) inhibits NET formation and NLRP3 inflammasome activation in mouse neutrophil-RAW264.7 macrophage cocultures, and mitigates NET-induced impairments in viability, migration, and angiogenic function of NIH/3T3 fibroblasts, HaCaT keratinocytes, and HUVEC endothelial cells^[3].
Ro 106-9920 (1 μM; 1 h) reduces CuLDL-stimulated NFkappaB DNA binding activity in MG63 human osteoblast-like cells^[4].
Ro 106-9920 (10 μM; 30 min) inhibits ANG II (Angiotensin II human) (HY-13948)- and TNFα-induced p65 NF-κB nuclear localization in rat aortic vascular smooth muscle cells (RASMC)^[5].
Ro 106-9920 (1-10 μM; 30 min) inhibits ANG II-induced COX-2 protein expression in rat aortic vascular smooth muscle cells (RASMC) in a concentration-dependent manner, reducing the sixfold increase in COX-2 expression to baseline at 10 μM^[5]. In Vivo:Ro 106-9920 (5-20 mg/kg/day; i.g.; daily; 7 days) provides dose-dependent protection against ischemia/reperfusion-induced acute kidney injury in male C57BL/6J mice, with the 20 mg/kg daily intragastric dose yielding the strongest efficacy, including reducing serum creatinine AUC_0-t to 205.088, renal histopathological score to 1.000, and renal Cit-H3 protein expression to 0.522 relative units by inhibiting apoptosis, inflammation, NF-κB activation, and NETosis^[2].
Ro 106-9920 (5 mg/kg; s.c.) enhances diabetic wound healing by suppressing neutrophil extracellular trap formation and NLRP3 inflammasome activation, while promoting angiogenesis and re-epithelialization without altering blood glucose levels or causing organ toxicity^[3].