N-(2-Bromophenyl)-9-Methyl-9-Azabicyclo[3.3.1]Nonan-3-Amine (also known as AT-1001) is a high-affinity and highly selective ligand at α3β4 nicotinic cholinergic receptors (nAChRs) that was reported to decrease nicotine self-administration in rats. AT-1001 has a single-digit nanomolar binding affinity for the α3β4 nAChR and over 100-fold selectivity over the α4β2 nAChR and α7 nAChR in competition binding experiments. In electrophysiological experiments, AT-1001 had partial agonist activity at the α3β4 nAChR, evoking 35% of maximum ACh response, and at the same doses, produced desensitization of the ACh response, effectively acting as a functional antagonist at the α3β4 nAChR. Interestingly, AT-1001 also selectively decreased self-administration of cigarette smoke extract (CSE), an aqueous extract of cigarette smoke components, without altering natural food intake, when administered systemically to rats trained to self-administer CSE

AC-2592 (glucagon-like peptide 1, or GLP-1) was being in development by Amylin Pharmaceuticals for the treatment of severe congestive heart failure. AC-2592 is a glucagon like peptide 1 receptor agonist.

Anaritide (Auriculin-Registered Trademark) is a 25-amino-acid synthetic form of atrial natriuretic peptide. Scios Nova was developing anaritide acetate for use in the treatment, prevention and diagnosis of acute renal failure, heart failure and hypertension. Scios suspended development of AURICULIN® anaritide based upon the results of an interim analysis of data from a 250-patient Phase III study in oliguric acute renal failure. The study was suspended due to the low probability that a positive outcome could be obtained with respect to its primary clinical endpoint, dialysis-free survival.

Delcasertib is a peptide inhibitor of protein kinase C-delta, developed by KAI Pharmaceuticals. Delcasertib disrupts binding of delta-PKC to its receptor for activated C kinase, thereby preventing localization of delta-PKC to the mitochondria during periods of myocardial ischemia and reperfusion. In preclinical studies, when given as a single intracoronary dose, delcasertib reduced infarct size, enhanced early recovery of regional left ventricular contractility, and improved microvascular patency and function in animal models of acute myocardial infarction. The compound diminished myocardial necrosis and improved reperfusion in a pilot study during the primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI). In a larger clinical trial, however, intravenous infusion of delcasertib during PCI for acute STEMI in a population of patients treated according to the contemporary standard of care did not reduce biomarkers of myocardial injury.