Sinapultide is a synthetic peptide used to mimic human lung surfactant protein B, the most important surfactant protein for a proper functioning of the respiratory system. Protein B lowers surface tension at the air-liquid interface of the alveolar surfaces during respiration and stabilizes the alveoli against collapse at resting transpulmonary pressures. A deficiency of pulmonary surfactant in premature infants results in respiratory distress syndrome. Sinapultide compensates for the deficiency of surfactant and restores surface activity to the lungs of these infants. Sinapultide was originally developed in the Scripps Research Institute and then licensed to Windtree Therapeutics (formerly Discovery Laboratories, Inc.). Sinapultide is the active ingredient of Lucinactant, a liquid medication to treat infant respiratory distress syndrome. Lucinactant was approved by the FDA in 2012 and sold under the trademark Surfaxin, but in 2015 it was discontinued by Discovery Laboratories, Inc in favor of Aerosurf, another drug containing Sinapultide.

Desirudin (Iprivask), a recombinant hirudin, is a parenteral direct thrombin inhibitor approved to prevent venous thromboembolism in patients undergoing elective hip replacement surgery. Desirudin is a potent inhibitor of both clot-bound and freely circulating thrombin. Desirudin acts independently of anti-thrombin, forming a noncovalent irreversible complex with both the active site of thrombin as well as the fibrinogen binding site. This Desirudin–thrombin complex prevents fibrinogen cleavage and other thrombin catalyzed reactions such as the activation of clotting factors V, VIII and XIII, and thrombininduced platelet activation, resulting in a dose-dependent prolongation of activated partial thromboplastin time (aPTT). Desirudin is highly selective and has no effect on plasmin, factors IXa and Xa, tissue plasminogen activator, activated protein C, trypsin, chymotrypsin or complement activation pathways. Bleeding complications reported with the use of desirudin in patients undergoing hip-replacement surgery are similar to those reported with heparin and enoxaparin.

Lepirudin is a direct thrombin inhibitor obtained by recombinant technology from the medicinal leech and used for treatment of heparin-induced thrombocytopenia (HIT). Lepirudin was the first direct thrombin inhibitor approved and most frequently used for the treatment of patients with HIT. The efficacy of lepirudin for HIT has been shown to improve general outcomes in patients with HIT, reducing a primary composite endpoint of new thrombosis, all-cause amputation, and all-cause death. Lepirudin forms a stable non-covalent complex with alpha-thrombin, thereby abolishing its ability to cleave fibrinogen and initiate the clotting cascade. It is a highly potent, selective, and essentially irreversible inhibitor of thrombin and clot-bond thrombin. Lepirudin is identical to natural hirudin except for substitution of leucine for isoleucine at the N-terminal end of the molecule and the absence of a sulfate group on the tyrosine at position 63.

Elcatonin is a physio-chemically stable calcitonin derivative in which the disulfide bond between cysteine residues at positions 1 and 7 of eel calcitonin has been replaced by an ethylene bond. The primary pharmacological effect of Elcatonin is its activity at specific osteoclast receptors, resulting in diminished osteoclast activity at extremely low concentrations. Elcatonin inhibits the bones autolysis and renal calcium, phosphorus, and sodium reabsorption thus keeps blood calcium at a normal level. In clinical settings, once-weekly intramuscular injection of elcatonin has been shown to significantly increase bone mineral density within 6 months and to alleviate post-fracture pain and improve Quality of life in osteoporosis