Stattic has been used to inhibit signal transducer and activator of transcription 3 (STAT3) activity in various cell lines and culture.[1][2][3]
Stattic was used to study Stat3-mediated cell signaling in human lung carcinoma cells.5
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Stattic (Stat3 three inhibitory compound) alters the SH2 domain of Stat3 and indirectly inhibits with phosphopeptide binding. It is readily transported across the cell membrane compared to other phosphopeptides.2 Stattic induces increased formation of ROS and negatively affects the cardiomyocyte mitochondrial function,3 and sensitizes nasopharyngeal carcinoma cells to chemoradiotherapy.4
Stattic is an irreversible STAT3 activation inhibitor.
Signal transducers and activators of transcription (STATs) are a family of latent cytoplasmic transcription factors that transmit signals from the cell membrane to the nucleus. One family member, STAT3, is constitutively activated by aberrant upstream tyrosine kinase activities in a
Regulation of human airway smooth muscle cells (HASMC) by cytokines contributes to chemotactic factor levels and thus to inflammatory cell accumulation in lung diseases. Cytokines such as the gp130 family member Oncostatin M (OSM) can act synergistically with Th2 cytokines
Nasopharyngeal carcinoma (NPC) is an Epstein-Barr virus-associated malignancy most common in East Asia, Africa and Alaska. Radiotherapy and cisplatin-based chemotherapy are the main treatment options. Unfortunately, disease response to concurrent chemoradiotherapy varies among patients with NPC, and many cases are
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