62645-28-7
Chemical Structure
Ro 106-9920
- CAS. Nr.: 62645-28-7
- Formula:C10H7N5OS
- Molecular Weight:245.26
IUPAC Name: 6-(phenylsulfinyl)tetrazolo[1,5-b]pyridazine
InChIKey: JFSXSNSCPNFCDM-UHFFFAOYSA-N
SMILES: O=S(C1=CC=CC=C1)C2=NN3N=NN=C3C=C2
Biological Activity: 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 AT1A 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].
| Art. -Nr. | Produktname | Reinheit | Beschreibung | Pricing | |||||||||||||||||||
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Ro 106-9920 | 97.70% | 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 AT1A 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. | ||||||||||||||||||||
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References
- [1]. Hsieh KY, et al. Golden berry 4β-hydroxywithanolide E prevents tumor necrosis factor α-induced procoagulant activity with enhanced cytotoxicity against human lung cancer cells. Sci Rep. 2021 Feb 25;11(1):4610.
- [2]. Wang M, et al. Suppression of nF-κB by ro 106-9920 alleviates ischemia/reperfusion-induced renal dysfunction and inflammation via modulation of neutrophil extracellular trap formation in acute kidney injury mice. Renal failure. 2025 Dec;47(1):2545983. [Content Brief]
- [3]. Li H, et al. Neutrophil Extracellular Trap Formation Suppressed by Ro 106-9920 Enhances Diabetic Wound Healing by Blocking NLRP3 Inflammasome Activation. Frontiers in bioscience (Landmark edition). 2025 May 19;30(5):37393. [Content Brief]
- [4]. Mazière C, et al. Oxidized low density lipoprotein enhanced RANKL expression in human osteoblast-like cells. Involvement of ERK, NFkappaB and NFAT. Biochimica et biophysica acta. 2013 Oct;1832(10):1756-64.
- [5]. Morinelli TA, et al. Angiotensin II activates NF-κB through AT1A receptor recruitment of β-arrestin in cultured rat vascular smooth muscle cells. American journal of physiology. Cell physiology. 2013 Jun 15;304(12):C1176-86.
- [6]. Malaver E, et al. NF-kappaB inhibitors impair platelet activation responses. J Thromb Haemost. 2009 Aug;7(8):1333-43. [Content Brief]
