Gamma-oryzanol is a naturally occurring component in rice bran and rice germ, which consists of a mixture of ferulic acid esters of sterols and triterpene alcohols. The mechanism of action of gamma-oryzanol is believed to be involved in the metabolism of catecholamine in the hypothalamus. The antioxidant effect of gamma-oryzanol was well documented and excellent in inhibiting lipid peroxidation. Isolation, extraction, and purification of gamma oryzanol were first reported in the mid-1950s. It has been sold in Japan as a medicine since 1962, first to treat anxiety and later in menopause. Gamma oryzanol and rice bran oil therapy have been used to manage elevated cholesterol and triglyceride levels since the late 1980s. No human clinical studies reported adverse effects of rice bran or its fiber fraction.

Semaglutide (trade name Ozempic) is a pharmaceutical drug in development by a Danish company Novo Nordisk for the treatment of type 2 diabetes. Semaglutide is a once-daily glucagon-like peptide-1 analog that differs to others by the presence of an acyl group with a steric diacid at Lys26 and a large synthetic spacer and modified by the presence of a α-aminobutyric acid in position 8 which gives stability against the dipeptidylpeptidase-4. Semaglutide is a GLP-1 analogue with 94% sequence homology to human GLP-1. Semaglutide acts as a GLP-1 receptor agonist that selectively binds to and activates the GLP-1 receptor, the target for native GLP-1. GLP-1 is a physiological hormone that has multiple actions on glucose, mediated by the GLP-1 receptors. The principal mechanism of protraction resulting in the long half-life of semaglutide is albumin binding, which results in decreased renal clearance and protection from metabolic degradation. Furthermore, semaglutide is stabilized against degradation by the DPP-4 enzyme. Semaglutide reduces blood glucose through a mechanism where it stimulates insulin secretion and lowers glucagon secretion, both in a glucose-dependent manner. Thus, when blood glucose is high, insulin secretion is stimulated and glucagon secretion is inhibited. The mechanism of blood glucose lowering also involves a minor delay in gastric emptying in the early postprandial phase.

Liraglutide is an acylated human Glucagon-Like Peptide-1 (GLP-1) receptor agonist with 97% amino acid sequence homology to endogenous human GLP-1(7-37). GLP-1(7-37) represents <20% of total circulating endogenous GLP-1. Like GLP-1(7-37), liraglutide activates the GLP-1 receptor, a membranebound cell-surface receptor coupled to adenylyl cyclase by the stimulatory G-protein, Gs, in pancreatic beta cells. Liraglutide increases intracellular cyclic AMP (cAMP) leading to insulin release in the presence of elevated glucose concentrations. This insulin secretion subsides as blood glucose concentrations decrease and approach euglycemia. Liraglutide also decreases glucagon secretion in a glucose-dependent manner. The mechanism of blood glucose lowering also involves a delay in gastric emptying. GLP-1(7-37) has a half-life of 1.5-2 minutes due to degradation by the ubiquitous endogenous enzymes, dipeptidyl peptidase IV (DPP-IV) and neutral endopeptidases (NEP). Unlike native GLP-1, liraglutide is stable against metabolic degradation by both peptidases and has a plasma half-life of 13 hours after subcutaneous administration. The pharmacokinetic profile of liraglutide, which makes it suitable for once daily administration, is a result of self-association that delays absorption, plasma protein binding and stability against metabolic degradation by DPP-IV and NEP. Liraglutide, a subcutaneous, once-daily GLP-1 agonist, is approved for the treatment of type 2 diabetes in the United States and Europe. It also has been studied for weight loss. Liraglutide helps to induce and sustain weight loss in patients with obesity. Its efficacy is comparable to other available agents but it offers the unique benefit of improved glycemic control.

Pramlintide is an analog of human amylin. Amylin is co-secreted with insulin from pancreatic beta cells and acts centrally to slow gastric emptying, suppress postprandial glucagon secretion, and decrease food intake. These actions complement those of insulin to regulate blood glucose concentrations. Amylin is relatively deficient in patients with type 2 diabetes, depending on the severity of beta-cell secretory failure, and is essentially absent in patients with type 1 diabetes. Through mechanisms similar to those of amylin, pramlintide improves overall glycemic control, reduces postprandial glucose levels, and reduces bodyweight in patients with diabetes using mealtime insulin. SYMLIN® (pramlintide acetate) is indicated for patients with type 1 or type 2 diabetes who use mealtime insulin and have failed to achieve desired glycemic control despite optimal insulin therapy.

Taspoglutide is a glucagon-like peptide-1 agonist was studied in phase III clinical trials for the treatment patients with type 2 diabetes. However, in September 2010 Roche halted Phase III clinical trials due to gastrointestinal intolerability and serious hypersensitivity reactions experienced by some trial participants.

Elsiglutide (ZP 1846) is a synthetic 39-amino acid glucagon-like peptide-2 (GLP-2) analogue. Upon subcutaneous administration, elsiglutide binds to GLP-2 receptors and thereby promotes proliferation of epithelial cells. Elsiglutide prevents or reduces the occurrence of gastrointestinal damage caused by chemotherapeutic agents, including gastrointestinal mucositis and chemotherapy-induced diarrhea (CID). Elsiglutide is being developed by Helsinn Healthcare, for the prevention of chemotherapy-induced diarrhoea.

Davalintide (AC-2307) is a second-generation mimetic of a pancreatic peptide hormone amylin, developed by Amylin Pharmaceuticals. In preclinical models, davalintide possessed enhanced pharmacological properties and was able to reduce food intake. Safety, tolerability, and effect on body weight of subcutaneous davalintide were investigated in obese or overweight subjects. The results of the clinical trial were not reported, but Amylin decided to discontinue davalintide in 2010.