[{"from": "human", "value": "Please give me some details about this molecule. [C][C][=C][N][=C][Branch2][Ring1][Ring1][N][=C][Ring1][=Branch1][C][=C][N][Branch1][Branch1][N][=C][Ring1][Branch1][C][Branch1][C][C][C][N][C][=C][C][=Branch2][Ring1][=Branch2][=C][Branch1][Branch1][C][=C][Ring1][=Branch1][N][C][C][C][Branch1][Branch1][C][C][Ring1][=Branch1][N][Branch1][C][C][C][C][O][F].[O][S][=Branch1][C][=O][=Branch1][C][=O][O]"}, {"from": "gpt", "value": "The molecule is the maleate salt form of flonoltinib, an orally bioavailable dual inhibitor of both Janus-associated kinase 2 (JAK2) and of FMS-like tyrosine kinase 3 (FLT3; CD135; STK1; FLK2), with potential anti-inflammatory, immunomodulating and antineoplastic activities. Upon oral administration, flonoltinib targets, binds to and inhibits the activity of both JAK2 and FLT3. This prevents the activation of the JAK/signal transducer and activator of transcription (STAT) signaling pathway and the activation of STAT3 and STAT5 as well as FLT3-mediated signaling. This may lead to an induction of apoptosis and a decrease in proliferation of tumor cells in which JAK2 and FLT3 are overexpressed. In addition, as JAK2 and FLT3 play a key role in the regulation of the inflammatory response and dendritic cell (DC) proliferation, differentiation and function, inhibition of JAK2- and FLT3-mediated signaling may suppress the generation and differentiation of DCs, and may regulate inflammatory and immune responses. JAK2, often upregulated or mutated in a variety of cancer cells, mediates STAT3 activation and plays a key role in tumor cell proliferation and survival. FLT3, a class III receptor tyrosine kinase (RTK), is overexpressed or mutated in most B-lineage neoplasms and in acute myeloid leukemias."}]