AZD4017, a 11β-hydroxysteroid dehydrogenase type 1 inhibitor, has been developed by AstraZeneca for the treatment of obesity, raised intraocular pressure (IOP) and type 2 diabetes. Inhibition of 11β-HSD1 is an attractive mechanism for the treatment of obesity and other elements of the metabolic syndrome. However, studies were discontinued due to safety and efficacy reasons. Besides, specific inhibition of 11β-HSD1 can decrease intracranial pressure and consequently treat patients with Idiopathic Intracranial Hypertension (IIH), thus AZD4017 participated in phase II clinical trials to treat this disease. IIH, also known as benign intracranial hypertension or pseudotumor cerebri, is a condition of unknown etiology characterized by elevated intracranial pressure (ICP) and papilledema. In addition, AZD4017 in combination with prednisolone participated in phase II clinical trials for patients with Iatrogenic Cushing's Disease. It was postulated that the adverse metabolic effects of prednisolone could be reduced by co-administration of AZD4017.

ACT-281959 (molecular weight 850.9 g/mol), the di-ester prodrug of ACT-246475 (molecular weight 618.6 g/mol), was developed to improve absorption after oral dosing and is rapidly converted by esterases in vivo to ACT-246475 in two-steps via the formation of ACT-409100 (molecular weight 734.7 g/mol), the mono-ester prodrug. ACT-281959 is a novel potent and selective P2Y12 receptor antagonist with a wider therapeutic window. ACT-281959 showed antithrombotic efficacy after oral administration in the rat ferric chloride model. ACT-281959 entered clinical studies in healthy volunteers. ACT-281959 had been in phase I clinical trials by Actelion for the treatment of thrombosis. But there is no development reported for this study recently.

MDCO 700 (formerly ABP 700) is hypnosedative and anaesthetic agent that was being developed by The Medicines Company for the induction of general anesthesia and procedural sedation. It is a positive allosteric modulator of the GABAA receptor. It is a second generation analogue of etomidate, developed to retain etomidate's beneficial haemodynamic and respiratory profile but diminishing its suppression of the adrenocortical axis. Infusions of ABP-700 showed a dose-dependent hypnotic effect, and did not cause severe hypotension, severe respiratory depression, or adrenocortical suppression. The drug development for anaesthesia has been discontinued.

Vaccenic acid (VA) (t11 octadecenoic acid) is a positional and geometric isomer of oleic acid (c9-octadecenoic acid), and is the predominant trans monoene in ruminant fats (50%–80% of total trans content). Dietary VA can be desaturated to cis-9,trans-11 conjugated linoleic acid (c9,t11-CLA) in ruminants, rodents, and humans. Hydrogenated plant oils are another source of VA in the diet, and it has been recently estimated that this source may contribute to about 13%–17% of total VA intake. In contrast to suggestions from the epidemiological studies, the majority of studies using cancer cell lines (Awad et al. 1995; Miller et al. 2003) or rodent tumors (Banni et al. 2001; Corl et al. 2003; Ip et al. 1999; Sauer et al. 2004) have demonstrated that VA reduces cell growth and (or) tumor metabolism. Animal and in vitro studies suggest that the anti-cancer properties of VA are due, in part, to the in vivo conversion of VA to c9,t11-CLA. However, several additional mechanisms for the anti-cancer effects of VA have been proposed, including changes in phosphatidylinositol hydrolysis, reduced proliferation, increased apoptosis, and inhibition of fatty acid uptake. In conclusion, although the epidemiological evidence of VA intake and cancer risk suggests a positive relationship, this is not supported by the few animal studies that have been performed. The majority of the studies suggest that any health benefit of VA may be conferred by in vivo mammalian conversion of VA to c9,t11-CLA. VA acts as a partial agonist to both peroxisome proliferator-activated receptors (PPAR)-α and PPAR-γ in vitro, with similar affinity compared to commonly known PPAR agonists. Hypolipidemic and antihypertrophic bioactivity of VA is potentially mediated via PPAR-/-dependent pathways.