[{"from": "human", "value": "Please give me some details about this molecule. [C][C][=Branch1][C][=O][N][C][C][C][C][=C][C][=Branch2][Ring2][C][=C][Branch2][Ring1][N][C][=Branch2][Ring1][=Branch1][=C][Ring1][=Branch1][C][=C][C][=C][Branch1][O][C][=Branch1][C][=O][C][=C][Ring1][P][Ring1][Branch2][O][C][O][C][O][C][O][C]"}, {"from": "gpt", "value": "The molecule is only found in individuals that have used or taken this drug. It is a major alkaloid from Colchicum autumnale L. and found also in other Colchicum species. Its primary therapeutic use is in the treatment of gout, but it has been used also in the therapy of familial Mediterranean fever (periodic disease). The precise mechanism of action has not been completely established. In patients with gout, colchicine apparently interrupts the cycle of monosodium urate crystal deposition in joint tissues and the resultant inflammatory response that initiates and sustains an acute attack. Colchicine decreases leukocyte chemotaxis and phagocytosis and inhibits the formation and release of a chemotactic glycoprotein that is produced during phagocytosis of urate crystals. Colchicine also inhibits urate crystal deposition, which is enhanced by a low pH in the tissues, probably by inhibiting oxidation of glucose and subsequent lactic acid production in leukocytes. Colchicine has no analgesic or antihyperuricemic activity. Colchicine inhibits microtubule assembly in various cells, including leukocytes, probably by binding to and interfering with polymerization of the microtubule subunit tubulin. Although some studies have found that this action probably does not contribute significantly to colchicine's antigout action, a recent in vitro study has shown that it may be at least partially involved."}]