Dexindoprofen is a non-steroidal drug that has analgesic and anti-inflammatory properties. Dexindoprofen is the dextrorotatory stereo-isomer of indoprofen, to which it has a similar adverse effect pattern. Gastrointestinal and nervous system effects and skin reactions are the most frequent. Following reports of severe gastrointestinal bleeding and carcinogenicity in animals indoprofen was withdrawn from the market worldwide.

Enrasentan is an orally active mixed endothelin A/B receptor antagonist with a 100-fold greater affinity for the endothelin A receptor. In an animal model of hypertension and cardiac hypertrophy the drug has reduced blood pressure, prevented cardiac hypertrophy and preserved myocardial function. In rats with hyperinsulinemia and hypertension enrasentan normalized blood pressure and prevented cardiac and renal damage. In rats with stroke the drug reduced the ischemic area in the brain. Enrasentan had been in phase II clinical trial for the treatment of heart failure but the results suggested that enrasentan does not appear to have favorable effects on ventricular remodeling.

Etersalate is a derivative of aspirin exerting antiplatelet, analgesic, anti-inflammatory and antipyretic properties. Etersalate has potential to prevent oligomerization of amyloid beta (Aβ) peptides.

Cefcanel is a semisynthetic third-generation cephalosporin with antibacterial activity. Cefcanel is active against the species E. coli, K. aerogenes and Proteus mirabilis; H. influenzae and M. catarrhalis has reasonable susceptibility. Cefcanel inhibits 90% of S. aureus strains at 2 µg/ml, irrespective of the presence of a β-lactamase. Cefcanel binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.

Livoletide (AZP-531) is an analog of unacylated ghrelin, a naturally occurring hormone that is thought to counteract the effects of acylated ghrelin. The drug was designed to improve glycaemic control and reduce weight. Livoletide participated in pivotal phase 2b/3 clinical study for the treatment of Prader-Willi syndrome. In addition, the drug was studied in patients with type 2 diabetes mellitus (T2D). Its pharmacokinetic profile, suitable for once daily dosing, and metabolic effects support further clinical development for T2D.

Omecamtiv mecarbil (CK-1827452) is a specific cardiac myosin activator and a clinical drug for left ventricular systolic heart failure (in Phase 2 of development). Omecamtiv mecarbil is an inotropic agent that prolongs systolic ejection time and increases ejection fraction through myosin ATPase activation.

Fasobegron is an agonist of β3-adrenoreceptor.

Ciadox is Quinoxaline 1,4-dioxide derivative with antimicrobial and promoting activities. Cyadox supplied as premix in the final feed in Eastern Europe and may be used in pigs up to four months of age. Some evidence demonstrated that the mechanism of Ciadox for improving pig growth performance was correlated with several metabolic hormones and growth factors. Cyadox also did not show any adverse effects in carcinogenicity tests with rats and long-term toxicity tests with mice and rats. Cyadox subchronic oral toxicity evaluation shows mild toxicity in non-rodents animals. Metabolic transformation of Ciadox leads to three major metabolites, including 1,4-bisdesoxycyadox, 4-desoxycyadox, and quinoxaline-2-carboxylic acid. Ciadox and metabolites shows virtually no toxic effects in the acute and subchronic oral toxicity study and no mutagenic, carcinogenic activivt.

Tucaresol, a substituted benzaldehyde, was being developed by Glaxo Wellcome for the prevention of sickle cell disease. Tucaresol was designed to interact with haemoglobin to increase oxygen affinity and has been shown to inhibit sickling in vitro. Tucaresol is also a low-molecular-weight compound that enhances co-stimulatory signaling to CD4 cells. Immune induction is dependent on transient covalent bonding (Schiff base formation) between carbonyls and amines expressed on antigen presenting cell (APC) and T-cell surfaces. Tucaresol substitutes for the natural donor of carbonyl groups to mimic the transient bonding that is essential for T-cell activation. In preliminary studies, tucaresol has been shown to stimulate HIV-specific cytotoxic T lymphocyte responses and generation of naive T cells via thymopoiesis in patients receiving ART who have suppressed viremia. Tucaresol appears to specifically increase type 1 cytokine production. Tucaresol has been used in trials studying the treatment of HIV infections. However, the development of tucaresol for HIV, Hepatitis B and sickle cell diseas treatment has been discontinued.