Lenomorelin (Ghrelin) is a pleiotropic hormone, whose effect on growth hormone secretion, through the growth hormone secretagogue (GHS) receptor, is one of its many actions. It is synthesized principally in the stomach. Ghrelin-producing cells constitute a distinct group of endocrine cells dispersed throughout the gastric mucosa and to a lesser extent in the small intestine and the endocrine pancreas. Ghrelin plasma levels rise during fasting and chronic caloric restriction to stimulate food intake and fat storage and to prevent life-threatening falls in blood glucose. Plasma ghrelin levels decrease after a meal is consumed and in conditions of energy surplus (such as obesity). Ghrelin has emerged as a key player in the regulation of appetite and energy homeostasis. It stimulates food intake and transduces signals to hypothalamic regulatory nuclei that control energy homeostasis. Ghrelin levels are negatively correlated with body mass index (BMI) and insulin resistance. Lenomorelin is a peptide of 28 amino acids, in which the serine 3 residue is n-octanoylated, which is necessary for biological activity.

Forigerimod (also known as IPP-201101) a phosphopeptide is being investigated for the treatment of Lupus Erythematosus, Systemic. This drug is completed phase III clinical trials and is ready for licensing.

Dirucotide (MBP 8298) is a synthetic myelin basic protein (MBP) peptide designed to decrease type 2 helper T cells (TH2)-mediated B-cell signalling of auto-reactive T-cells thereby reducing the production of specific antibodies that target endogenous MBP. MBP is the dominant site of attack in patients with multiple sclerosis and haplotype (HLA) DR2 or DR4. Dirucotide did not meet the primary endpoint of delaying disease progression, as measured by the Expanded Disability Status Scale (EDSS), during the two-year MAESTRO-01 Phase III trial in patients with secondary progressive multiple sclerosis (SPMS). In addition, there were no statistically significant differences between dirucotide and placebo on the secondary endpoints of the study. After disappointing trial results, development of the drug was ended in 2009.

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.

Ularitide is a recombinant form of urodilatin, a natriuretic peptide synthesized in the distal tubular cells of the kidney. It regulates renal sodium and water excretion through binding to natriuretic peptide type A receptors, increasing intracellular cyclic guanosine monophosphate (cGMP) levels. While these effects, as well as others such as vasodilation, are also exhibited by other natriuretic peptides, urodilatin has a terminal extension that brings resistance to biological inactivation by neutral endopeptidase, whose activity is increased in decompensated heart failure. Animal studies have demonstrated enhanced diuresis and natriuresis and reduced PCWP (pulmonary capillary wedge pressure) and systemic vascular resistance relative to atrial natriuretic peptide (ANP [99-126], the active circulating isoform). When injected into the blood, ularitide appears to cause diuresis (urine output) and natriuresis (sodium excretion), as well as vasodilation. Ularitide is currently in Phase 3 development as a potential treatment for patients with acute decompensated heart failure (ADHF).

FERTIRELIN is an analog of luteinizing hormone releasing factor. The drug has been used since 1981 in Japan to treat various types of reproductive failure in cattle.