Fibrinogen is a key molecular contributor to a wide range of illnesses including cardiovascular diseases and bleeding disorders. Variation in fibrinogen structure or its circulating antigenic level are two of the mechanisms by which this important clotting protein can predispose to disease. In this thesis, we characterized new mutations in the fibrinogen genes identified in patients with abnormal antigenic and/or functional levels of fibrinogen, and searched for chemical modulators of fibrinogen production. In silico modelling or in vitro functional analyses proved causality for the genetic modifications identified in hypo- (FGB c.882G>C, c.1298G>T, c.1329C>G and FGA c.1078_1084del) or dysfibrinogenemia (FGB c.402_410del). Screening 1,280 small molecules uncovered two compounds that modulate fibrinogen production in vitro and in vivo, using human hepatocyte-derived cells and zebrafish larvae, respectively. Anthralin decreases fibrinogen levels while retinoic acid increases them. Both drugs affected laser-induced venous thrombosis in zebrafish larvae, which correlated with their effects on fibrinogen production.