Peptide Library

Mimics GLP-1: more insulin when glucose is high, slower stomach emptying, less appetite.

Activates both of the gut's main incretin receptors: boosts glucose-dependent insulin release, lowers glucagon, slows stomach emptying and strongly reduces appetite, with GIP activity possibly improving fat-tissue handling and tolerability

Combines the appetite and insulin effects of GLP-1/GIP agonism with glucagon-receptor activation, which raises energy expenditure and liver fat burning

Mimics the gut hormone GLP-1: glucose-dependent insulin release, lower glucagon, slower gastric emptying and reduced appetite via the brain

Mimics amylin, the hormone co-released with insulin, to increase fullness, slow gastric emptying and reduce food intake through brainstem and hypothalamic pathways that are distinct from GLP-1 — which is why the two combine well

Reduces appetite and improves glucose handling through GLP-1 receptor activation while raising energy expenditure and liver fat breakdown through glucagon receptor activation

Proposed to copy the fat-mobilising region of growth hormone — increasing fat breakdown and reducing fat storage — without GH's effects on growth, IGF-1 or blood sugar

Homes to the blood vessels that supply white fat and kills them, starving fat tissue so it shrinks — a "vascular targeting" approach borrowed from cancer research

Activates the GLP-1 receptor: more insulin when glucose is high, less glucagon, slower stomach emptying, less appetite

Activates the GLP-1 receptor: glucose-dependent insulin release, lower glucagon, slower gastric emptying, reduced appetite; the antibody fragment keeps it in the blood for days

Activates the GLP-1 receptor with a pronounced slowing of gastric emptying, so its main effect is on post-meal glucose; also reduces appetite

GLP-1 activity lowers appetite and glucose; added glucagon-receptor activity raises energy expenditure and drives liver fat breakdown

Replaces the hormone amylin that beta cells normally release with insulin: slows gastric emptying, suppresses post-meal glucagon, and reduces appetite

Activates amylin receptors (calcitonin receptor + RAMP complexes) in the brainstem and hypothalamus to increase fullness, reduce food intake and slow gastric emptying — reported to be a balanced amylin/calcitonin receptor agonist rather…

Activates amylin receptors in the brainstem and hypothalamus to increase fullness and reduce food intake, with a slower gastric emptying effect

Acts in the hypothalamus and brainstem to suppress food intake independently of leptin, raises blood pressure and sympathetic tone, improves glucose handling in rodents, and increases anxiety-like behaviour — through a receptor that has…

Re-activates the MC4R appetite pathway in the hypothalamus that is broken downstream of leptin in POMC, PCSK1, LEPR and Bardet-Biedl syndrome obesity, reducing hunger and body weight

Signals the brain how much body fat exists; when leptin is very low (starvation, lipodystrophy, genetic deficiency) replacing it restores appetite control, metabolic rate, reproductive hormones and insulin sensitivity — when leptin is…

Binds the human GLP-1 receptor and mimics the gut hormone GLP-1 — glucose-dependent insulin release, less glucagon, slower stomach emptying, reduced appetite — but resists the enzyme that destroys GLP-1 in minutes

Given as a once-daily pulse, briefly activates the PTH1 receptor on bone cells, which stimulates osteoblasts (bone-building cells) more than osteoclasts — the opposite of what continuously high PTH does

Activates the same PTH1 receptor as teriparatide but binds preferentially to a short-lived receptor conformation, producing a briefer signal that favours bone formation with less bone resorption and less calcium release

Binds calcitonin receptors on osteoclasts and shuts down bone resorption within minutes; also increases kidney calcium excretion and has a separate central pain-relieving effect

Activates the glucagon receptor on liver cells, triggering release of stored glucose (glycogenolysis) and new glucose production; raises blood sugar within 10–15 minutes provided liver glycogen stores exist

Binds the insulin receptor (a tyrosine kinase) on muscle, fat and liver cells, driving glucose uptake and storage, switching off liver glucose output and fat breakdown, and promoting protein synthesis — the body's main anabolic and…

Released from L cells of the lower gut after eating, in proportion to calories; PYY3-36 acts on Y2 receptors in the hypothalamus, brainstem and vagal nerves to reduce appetite and slow gut transit

Activates both the GLP-1 receptor (less eating, more insulin) and the glucagon receptor (more energy expenditure, more fat burning in the liver) — a combination that lowers weight more than appetite suppression alone and improves fatty…

Released with every insulin pulse after a meal; slows stomach emptying, suppresses glucagon and signals fullness through the brainstem — the "third beta-cell hormone" that smooths the post-meal glucose rise

Activates the GLP-1 receptor to boost glucose-dependent insulin release, suppress glucagon, slow gastric emptying and reduce appetite; the Fc carrier extends half-life to allow weekly or less frequent dosing

Standard GLP-1 receptor agonism (glucose-dependent insulin release, lower glucagon, slower gastric emptying, reduced appetite), with the albumin fusion giving a roughly five-day half-life

Blocks the GLP-1 receptor, blunting the exaggerated insulin surge that causes low blood sugar after meals in people who have had gastric bypass surgery

Binds albumin reversibly so that only a small fraction circulates free at any moment, giving one injection a week of basal insulin receptor activity

Fc fusion gives the insulin molecule an antibody-like circulating lifetime, so one weekly injection provides flat basal insulin receptor activity

GLP-1 activity suppresses appetite and improves glucose handling while glucagon receptor activity raises energy expenditure and drives fat out of the liver

Both activate the GLP-1 receptor to increase glucose-dependent insulin release, suppress glucagon, slow gastric emptying and reduce appetite; they differ almost entirely in how long they last

Ring closure locks the peptide's shape, hides its backbone from proteases and reduces its polar surface — which gives protein-like target binding with drug-like stability and, in some cases, oral absorption