Feedback Activation of STAT3 Is a Widespread Drug-Resistance Mechanism was written by Anonymous. And the article was included in Cancer Discovery in 2014.Reference of 219580-11-7 The following contents are mentioned in the article:
STAT3 activation contributes to resistance to a broad spectrum of targeted therapies in cancer. Receptor tyrosine kinase (RTK)/MEK inhibition induces autocrine STAT3 activation through FGFR and JAK kinases. Together with the observation that high STAT3 and FGFR expression was associated with poor response to EGFR-targeted therapy in a small group of patients with non-small cell lung cancer (NSCLC), these findings implicate feedback upregulation of STAT3 as a common cause of resistance to RTK/MEK-targeted therapy and provide a rationale for combination strategies including inhibitors of STAT3 or its upstream kinases. This study involved multiple reactions and reactants, such as 1-(tert-Butyl)-3-(2-((4-(diethylamino)butyl)amino)-6-(3,5-dimethoxyphenyl)pyrido[2,3-d]pyrimidin-7-yl)urea (cas: 219580-11-7Reference of 219580-11-7).
1-(tert-Butyl)-3-(2-((4-(diethylamino)butyl)amino)-6-(3,5-dimethoxyphenyl)pyrido[2,3-d]pyrimidin-7-yl)urea (cas: 219580-11-7) belongs to pyrimidine derivatives. Pyrimidine is an aromatic heterocyclic organic compound similar to pyridine. Drugs having the pyrimidine motif have manifested to exhibit gratifying biological activity like anticancer, antiviral, anti-inflammatory, antibacterial, and antihypertensive activities.Reference of 219580-11-7
Referemce:
Pyrimidine | C4H4N2 – PubChem,
Pyrimidine – Wikipedia