Peptide Library

Appears to promote blood-vessel formation and tissue repair — mostly shown in rodents.

Profile in production — references being resolved.

Binds actin to regulate cell movement, supporting wound closure and reduced scarring.

Carries copper into cells and shifts gene expression toward repair.

Dampens inflammatory signalling (NF-κB) inside immune and gut-lining cells, partly by being carried into cells through the PepT1 transporter, without the pigmentation effects of full α-MSH

Activates the "innate repair receptor" (a pairing of the EPO receptor with the β-common receptor CD131) that is switched on in injured tissue, producing EPO's tissue-protective effects without stimulating red blood cell production

Punches holes in bacterial membranes directly and acts as an immune signal — recruiting white cells, binding bacterial endotoxin, promoting wound closure and new blood vessels

Buffers acid in muscle, scavenges reactive oxygen species and reactive aldehydes, chelates metals, and blocks the formation of advanced glycation end-products (AGEs) that stiffen and damage proteins

Boosts the maturation and function of T cells, dendritic cells and natural killer cells, largely by acting on Toll-like receptors (TLR2 and TLR9), and helps rebalance an over- or under-active immune response

Proposed to restore T-cell maturation and balance immune function, and — per the bioregulator hypothesis — to influence gene expression in thymus and immune cells; mechanism is poorly characterised by Western standards

Proposed to activate telomerase, normalise melatonin rhythm and act as a "pineal bioregulator" that resets age-related changes in gene expression; the telomerase claim rests on cell-culture data

Proposed to enter neurons and alter gene expression (e.g. of proteins involved in cell division and ageing), reduce oxidative stress and protect neurons from hypoxia and excitotoxicity; mechanism is from cell culture and molecular modelling

Protects cells from stress-induced death by blocking the pro-death protein Bax, binding IGFBP-3, and signalling through cell-surface receptors (FPRL1/FPR2 and a CNTFR/WSX-1/gp130 complex) — shown in cells and rodents

Acts as a metabolic stress signal: activates AMPK in muscle, alters the folate–methionine cycle, and under stress moves into the nucleus to switch on stress-response genes

Binds cardiolipin in the inner mitochondrial membrane, stabilising cristae structure and the electron-transport chain so cells make more ATP and leak fewer free radicals

Breaks the grip between FOXO4 and p53 inside senescent ("zombie") cells, freeing p53 to trigger their self-destruction while sparing normal cells

Donates electrons to neutralise reactive oxygen species and detoxify compounds via glutathione-S-transferases; recycled by glutathione reductase

Activates the GHRH receptor on the pituitary, stimulating growth hormone synthesis and release; with DAC the stimulus is continuous, without DAC it produces a short pulse

Triggers a pulse of growth hormone with little effect on cortisol or prolactin.

Activates the pituitary GHRH receptor to stimulate synthesis and pulsatile release of the body's own growth hormone

Stimulates the pituitary GHRH receptor to increase pulsatile growth hormone release, which raises IGF-1 and preferentially mobilises visceral (deep abdominal) fat

Mimics ghrelin at pituitary and hypothalamic receptors to release a large pulse of growth hormone, and also raises cortisol, ACTH and prolactin and stimulates appetite

Activates the ghrelin receptor in the pituitary and hypothalamus, releasing a pulse of growth hormone; also raises appetite, cortisol and prolactin

Releases a large pulse of growth hormone via the ghrelin receptor; the most potent injectable GHRP, but also raises cortisol and prolactin and desensitises with repeated use

Activates the IGF-1 receptor like native IGF-1 but barely binds the IGF-binding proteins that normally buffer it, so more stays free and active for longer

Proposed to activate muscle satellite (stem) cells and delay their differentiation, expanding the pool available for repair — through a receptor that has never been identified

Traps myostatin and activin before they can reach their receptors, removing a brake on muscle growth and altering reproductive and metabolic signalling

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

Raises brain-derived neurotrophic factor (BDNF) and other trophic signals, modulates dopamine and serotonin turnover, and dampens inflammatory gene expression after brain injury — without ACTH's hormonal effect on cortisol

Appears to modulate GABA-A receptor signalling, slow the breakdown of the brain's enkephalins, and shift serotonin and inflammatory cytokine balance — producing anxiety reduction without sedation in animal and small human studies

Reported to bind hepatocyte growth factor (HGF) and strongly amplify signalling through its receptor c-Met, driving the formation of new synapses in the hippocampus

Claimed to mimic the actions of neurotrophic factors (nerve growth factor, BDNF, CNTF) — supporting neuron survival, reducing inflammation and excitotoxic damage after injury — though no single active component has been identified

Reported to raise BDNF expression in the brain and inhibit the LIF/STAT signalling branch of CNTF, boosting new neuron formation and synaptic protein levels without the growth-factor side effects of CNTF itself

Unclear

Activates melanocortin receptors (mainly MC4R) in brain regions involved in sexual arousal; it is not a blood-vessel drug like sildenafil

Activates the MC1R receptor on pigment cells, driving production of eumelanin (the dark, UV-protective pigment) without needing UV exposure; also antioxidant and anti-inflammatory effects in skin

Darkens skin through MC1R on pigment cells and, because it also hits brain melanocortin receptors, triggers erections, appetite loss, nausea and yawning

Fires the hypothalamic GnRH neurons, which release LH and FSH from the pituitary, which in turn drive testosterone or oestrogen and ovulation — it sits one step above GnRH in the reproductive axis

Signals the pituitary to release LH and FSH in a pulse; given in pulses it drives the gonads, given continuously it shuts them down

Acts as a long-lasting stand-in for LH at the LH/CG receptor: in men it drives the testes to make testosterone and supports sperm production; in women it triggers final egg maturation and ovulation and supports the corpus luteum

Contracts the uterus and milk ducts via the oxytocin receptor; in the brain, modulates social attention, bonding, stress and sexual response

Relaxes smooth muscle (blood vessels, airways, gut), stimulates secretion, and is one of the body's main anti-inflammatory and immune-balancing neuropeptides; in the lung it protects the surfactant-producing cells

Proposed to compete with SNAP-25 in the "SNARE" complex, slightly reducing acetylcholine release at the nerve–muscle junction and so softening expression lines — a very mild, reversible version of what botulinum toxin does, if it penetrates…

Acts on the GHRH receptor in the pituitary to trigger a pulse of growth hormone; the four substitutions slow enzymatic clearance so the pulse is larger and longer than with native GHRH

Mimics ghrelin at the pituitary and hypothalamus to release a pulse of growth hormone, with the GHRP-6-type side effects on appetite, cortisol and prolactin

Mimics ghrelin to release a pulse of growth hormone from the pituitary; like hexarelin it also produces small rises in prolactin, ACTH and cortisol

Binds the GH receptor on liver, muscle, bone and fat; drives IGF-1 production and acts directly to promote growth, protein synthesis, fat breakdown and reduced insulin sensitivity

Activates the IGF-1 receptor like IGF-1 but binds far more weakly to IGF-binding proteins, so more of it is free and active — roughly 10 times as potent as IGF-1 in cell culture

Signals through the IGF-1 receptor and the A isoform of the insulin receptor to promote growth and survival, while a third receptor (IGF2R) mops it up; in adults it is mainly a fetal and tissue-level growth factor rather than a GH-driven…

Mimics ghrelin to trigger a measured pulse of growth hormone from the pituitary; a weak pulse indicates GH deficiency

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

Slows the division of blood-forming stem cells and dampens TGF-β-driven scarring; broken down by ACE, so ACE inhibitors raise its level several-fold

Acts locally in the gut lining to stop tight junctions between cells from loosening, so fewer gluten fragments and other large molecules slip through

Blocks nicotinic acetylcholine receptors on adrenaline-releasing cells, so less catecholamine is released; also lowers blood pressure, calms the heart, improves insulin signalling and kills some microbes in animal and cell studies

Proposed to enter cells and alter gene expression in immune and other tissues, nudging ageing cells toward a more active state; mechanism rests on cell-culture and modelling work

Proposed to alter gene activity in liver and immune cells by loosening condensed chromatin; based on cell-culture work from one group

Reported to normalise T-cell numbers and function and to inhibit angiogenesis; the molecular target is not established

A genuine thymic hormone that helps T cells mature and keeps immune signalling balanced; in rodents it also damps inflammation and pain

Claimed to be neuroprotective and "nootropic" — reducing glutamate toxicity, oxidative stress and inflammation and supporting neuron survival — but the active components are not identified

Claimed to protect and stimulate retinal pigment epithelium and photoreceptors and to improve retinal metabolism; active components not identified

Proposed to stimulate cell activity in testicular and pituitary tissue and restore hormone output in ageing males via gene-expression effects; evidence is in vitro and from one group

Proposed to enter cells, bind DNA at gene-promoter regions and nudge expression of genes involved in cardiomyocyte survival and fibroblast activity — shown only in cell and rodent work from one group

Proposed to regulate gene expression in bronchial and gastric epithelium — including antioxidant and anti-inflammatory genes — via DNA binding; cell and rodent data from one group

Proposed to bind DNA in bronchial epithelial cells and alter expression of genes for proliferation, differentiation and mucin/antioxidant function; shown in culture and rodents by one group

Proposed to regulate gene expression in vascular endothelium and smooth muscle — and, in later work, in neurons — through DNA binding; cell and rodent evidence from one group

Proposed to regulate gene expression in hepatocytes and gut epithelium — proliferation, antioxidant and detoxification genes — via DNA binding; evidence from one group, cell and rodent

Mimics humanin — binds a cell-surface receptor complex (CNTFR/WSX-1/gp130) and intracellular pro-apoptotic proteins (Bax, IGFBP-3), protecting cells from stress and death — but roughly 1,000 times more potent than the natural peptide in…

Cytoprotective and metabolic signalling similar to humanin — reduces apoptosis and oxidative stress, improves mitochondrial function and insulin sensitivity in rodents; recent work points to hypothalamic action and to chaperone-like effects…

Reported to restore age-declined melatonin secretion, normalise circadian hormone rhythms, raise antioxidant enzyme activity and, in the group's reports, lengthen telomeres — mostly from one research group over four decades

Membrane Klotho is the co-receptor for FGF23 (phosphate and vitamin D control); soluble Klotho acts hormonally — dampening insulin/IGF-1 and Wnt signalling, protecting against oxidative stress, and enhancing synaptic function in animals

Binds activin type II receptors (ActRIIA/B) with ALK4/5/7 and signals through SMAD2/3 — the same pathway as myostatin, which is why its effects on muscle are contested

Broken down in the body to cycloprolylglycine, a dipeptide the brain makes itself; in rodents it raises NGF and BDNF in the hippocampus, protects neurons from oxidative and amyloid-related damage and modulates glutamate signalling

Assumed to be the same as Semax — raises BDNF and NGF signalling in the brain, modulates gene expression after ischaemia and dampens enkephalin breakdown — with the end-caps intended to slow enzymatic degradation

Assumed identical to Selank — modulation of GABA-related signalling, inhibition of enkephalin-degrading enzymes and shifts in immune and inflammatory gene expression — with the caps intended to slow enzymatic breakdown

Proposed to enter cells and bind DNA/histones to shift gene expression toward neuronal survival and repair, and to support regeneration of injured nerves — shown only in rodents and cell culture by one group

Stabilises microtubules inside neurons by interacting with microtubule end-binding proteins, which in cells and animals reduces tau tangling, protects synapses and improves survival under stress

Activates orexin receptors OX1R and OX2R on arousal-promoting brain circuits to sustain wakefulness, suppress REM sleep, and raise appetite, reward drive and sympathetic tone

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…

Proposed, by analogy with the rest of the family, to enter bladder-wall cells and modulate gene expression toward normal tissue function and repair; no published experiment demonstrates this for Vesilute itself

Activates the kisspeptin receptor (KISS1R, formerly GPR54) on hypothalamic GnRH neurons, which releases GnRH and therefore LH and FSH from the pituitary

Initially stimulates, then desensitises pituitary GnRH receptors, shutting down LH/FSH and so testosterone or oestrogen to castrate/post-menopausal levels within 2–4 weeks

After an initial surge, continuously occupies pituitary GnRH receptors and desensitises them, suppressing LH/FSH and so testosterone or oestrogen to castrate/post-menopausal levels

Competitively blocks pituitary GnRH receptors, so LH and FSH fall within hours, with no initial flare and rapid reversal when stopped

Competitively blocks pituitary GnRH receptors, suppressing LH (and to a lesser extent FSH) within hours, without flare, reversible within 1–2 days of stopping

Selectively activates vasopressin V2 receptors: in the kidney this concentrates urine and retains water; in blood vessels it releases stored von Willebrand factor and factor VIII

Activates V1a receptors (blood-vessel constriction, brain social circuits), V1b receptors (pituitary ACTH release) and V2 receptors (water retention in the kidney, vWF release)

After a brief stimulation, desensitises pituitary GnRH receptors and suppresses LH/FSH, taking oestrogen (or testosterone) to post-menopausal/prepubertal levels

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

Activates melanocortin receptors MC1R (skin pigmentation, anti-inflammatory), MC3R and MC4R (appetite, energy balance, sexual function) and MC5R (sebaceous and exocrine glands)

A "matrikine" — a fragment of a matrix protein that signals to fibroblasts to make more collagen, fibronectin and glycosaminoglycans, as if repairing a wound

pal-GHK is proposed to signal collagen and matrix rebuilding; pal-GQPR is proposed to damp the skin's production of the inflammatory messenger interleukin-6, which otherwise accelerates matrix breakdown

Proposed to compete with SNAP-25 in the SNARE complex that nerve endings use to release acetylcholine, slightly reducing the muscle signal that forms expression lines — a far milder, reversible version of what botulinum toxin does

Proposed to block the muscle-type nicotinic acetylcholine receptor on the muscle side of the junction, so the muscle responds less to nerve signals — the opposite side of the junction from Argireline-type peptides

Proposed to activate enkephalin (opioid) receptors on nerve endings, which lowers calcium entry and so reduces the amount of acetylcholine released at the neuromuscular junction

Reversibly inhibits tyrosinase, slowing production of new melanin so that existing pigment fades with normal skin turnover — without killing pigment cells

Blocks CXXC5 from binding Dishevelled, removing a natural brake on Wnt/β-catenin signalling in hair follicles and skin, which in mice re-activates follicle growth and wound-induced hair formation

The body's own ligand for the growth hormone secretagogue receptor (GHS-R1a): triggers GH release from the pituitary, stimulates appetite via the hypothalamus, speeds stomach emptying and raises blood glucose by restraining insulin

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…

Absorbed Pro-Hyp and Hyp-Gly appear to act as signals to fibroblasts and chondrocytes, increasing collagen, elastin and proteoglycan synthesis; also supplies glycine and proline as building blocks

Different fragments do different things: some inhibit ACE (blood-pressure enzyme), some stimulate insulin and GLP-1, some act as weak opioid or antimicrobial peptides; GMP is a phenylalanine-free protein source

IPP/VPP inhibit ACE; casomorphins are weak opioid-receptor agonists; CPP bind calcium; α-casozepine binds GABA-A receptors in vitro (benzodiazepine-like)

Binds de-acetylated histones and inhibits histone acetylation in cell nuclei (an epigenetic brake), inhibits core-histone acetylation and integrin signalling; also reported to reduce HMG-CoA reductase expression

Fractions inhibit ACE and DPP-4 in vitro, modulate lipid metabolism (β-conglycinin-derived peptides lower hepatic fat in rodents), and act as fast-absorbed amino-acid sources for muscle

Marine collagen acts like other collagen peptides (Pro-Hyp / Hyp-Gly signalling to fibroblasts); FPH fractions inhibit ACE, modulate bile acids and may improve glucose handling — mostly animal data

Buffer acid, chelate metals, quench reactive carbonyls and aldehydes, and (anserine) resist breakdown by serum carnosinase better than carnosine, so may deliver HCD activity to tissues

A "matrikine" — a fragment that mimics a piece of broken-down collagen and signals fibroblasts to make new collagen, fibronectin and hyaluronic acid

Reported to dampen production of interleukin-6 (IL-6), an inflammatory messenger that rises with age and UV exposure and drives collagen breakdown

Designed to mimic the part of thrombospondin-1 that switches on latent TGF-β, the main growth factor that tells fibroblasts to make collagen; also claimed to inhibit collagen-degrading MMPs

Reported to inhibit angiotensin-converting enzyme (ACE) locally, improving microcirculation and fluid drainage under the eye, and to reduce glycation of collagen

GHK: signals fibroblast repair and binds copper already present in skin; GPO: acts as a collagen "building block" and matrikine signal to fibroblasts

Reported to delay cellular senescence in fibroblasts and keratinocytes and to increase firmness-related matrix proteins; marketed as a "firming" and "anti-ageing" peptide

Activates MC1R on melanocytes to increase melanin (especially the brown-black eumelanin) and, in the same pathway, dampens inflammatory signalling and supports DNA-repair responses

Both reduce melanin production upstream of tyrosinase: oligopeptide-68 by lowering MITF (the master pigment-gene switch); nonapeptide-1 by stopping α-MSH from binding its receptor

Peptides are meant to anchor and nourish the follicle (matrix proteins, microcirculation); the plant partners (apigenin, oleanolic acid; biochanin A) are meant to reduce DHT formation and inflammation around the follicle

EGF drives keratinocyte and fibroblast proliferation and migration via the EGF receptor; bFGF drives fibroblast proliferation, collagen synthesis and new blood-vessel growth via FGF receptors

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

TRH tells the pituitary to release TSH (and prolactin); in the brain it acts as a neuromodulator that increases arousal, motor activity and cerebellar output — taltirelin was built to exploit the brain effects with minimal thyroid effect

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 somatostatin receptors (mainly SSTR2, also SSTR5) to switch off secretion of growth hormone, many gut hormones and tumour peptides, and to slow gut motility and splanchnic blood flow

Activates somatostatin receptors SSTR2 and SSTR5 to suppress growth hormone and gut/tumour hormone secretion and to slow neuroendocrine tumour growth

Activates four of the five somatostatin receptors (SSTR1, 2, 3 and especially SSTR5) to suppress ACTH from pituitary corticotroph tumours and GH from somatotroph tumours that respond poorly to octreotide or lanreotide

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…

Activates the natriuretic peptide receptor B (NPR-B) on growth-plate cartilage cells, raising cGMP, which switches off the overactive FGFR3–MAPK signalling that stops bone growth in achondroplasia

Activates GC-C receptors on the surface of the intestinal lining, raising cGMP, which drives chloride and bicarbonate (and therefore water) into the gut lumen to soften stool and speed transit, while cGMP leaking from the cells quietens…

Binds thrombin directly at two sites and blocks it from making fibrin; thrombin then slowly cleaves the peptide, so the block is short-lived and reversible

Reversibly occupies the platelet glycoprotein IIb/IIIa receptor so fibrinogen cannot cross-link platelets — the final common step of platelet clumping

Binds the viral gp41 protein while it is in the middle of fusing with a cell, locking it open so the virus cannot enter

Blocks N-type (CaV2.2) voltage-gated calcium channels on pain-nerve terminals in the spinal cord, stopping release of pain neurotransmitters

Competitively blocks the bradykinin B2 receptor so the excess bradykinin produced in an HAE attack cannot make blood vessels leak

Activates guanylate cyclase-C on the gut lining, raising cGMP, which pushes chloride and water into the bowel and softens stool; cGMP also damps visceral pain nerves

Activates natriuretic peptide receptor-A, raising cGMP, which widens arteries and veins, lowers filling pressures, and promotes salt and water loss through the kidney

Binds cyclophilin inside T cells; the complex blocks calcineurin, so T cells cannot switch on IL-2 and other activation genes

In the presence of calcium it inserts its fatty tail into the bacterial cell membrane, forms clusters, and lets ions leak out, killing the cell quickly without lysing it

The boron atom reversibly binds the active site of the 26S proteasome (mainly the β5 "chymotrypsin-like" subunit), stopping cells from disposing of unwanted proteins; myeloma cells, which make huge amounts of antibody protein, cannot cope…

Cationic peptides that disrupt microbial membranes (partly via binding the cell-wall precursor lipid II) and also signal to the immune system, recruiting and activating immune cells

A detergent-like peptide that inserts into and lyses cell membranes — this is behind both its antimicrobial/anticancer activity in the lab and its toxicity and pain

Cationic peptides that bind and disrupt microbial membranes and sequester iron bacteria need; the parent protein also modulates immunity

Cationic membrane-disrupting peptide that permeabilises bacterial membranes, giving broad activity and a low tendency to select resistance

Cationic membrane-active peptide with antibacterial and antifungal activity, applied topically for skin and catheter-site indications

Binds lipid II (the bacterial cell-wall building block), both blocking wall synthesis and using lipid II as a docking point to punch pores in the membrane

Forms head-to-head dimer ion channels in the bacterial membrane that let Na⁺/K⁺ leak through, collapsing the ion gradients the cell needs

Their positive charge binds lipid A of lipopolysaccharide in the Gram-negative outer membrane, disrupting it and the inner membrane and killing the cell

Reproduces the active site of thymopoietin, promoting maturation and regulation of T lymphocytes — a "two-way" immune modulator

Thought to shift the immune response away from attacking myelin — inducing regulatory/anti-inflammatory T cells and acting as a decoy resembling myelin basic protein

Binds calcitonin-receptor-like receptor paired with RAMP2 or RAMP3, raises cAMP, widens blood vessels and — importantly — stabilises the barrier between blood and tissue

Activates the APJ receptor to increase heart contractility without raising oxygen cost much, widen blood vessels via nitric oxide, and oppose the angiotensin II arm of the renin–angiotensin system

Acts chiefly at the Mas receptor to oppose angiotensin II: widening vessels, reducing fibrosis and inflammation, and limiting cell proliferation

Activates the RXFP1 receptor to widen blood vessels, increase blood flow to the kidney, and suppress fibrosis — a hormone that remodels connective tissue

Urocortin 1 activates both CRF receptors (CRF-R1 and R2); urocortins 2 and 3 act selectively at CRF-R2, which in the heart and vessels means vasodilation and increased contractility rather than a stress response

Acts at three G-protein-coupled receptors (GalR1–3), mostly inhibitory: it quietens neuronal firing, suppresses insulin release, dampens pain signalling and limits seizure spread

Acts at Y-family receptors: via Y1 and Y5 in the hypothalamus it is the body's most powerful appetite stimulant; via Y1 on blood vessels it constricts; via Y2 it acts as a presynaptic brake, and in the amygdala it promotes stress resilience

Activates the NK1 receptor to transmit pain signals in the spinal cord, trigger neurogenic inflammation in tissue, dilate vessels and drive the vomiting reflex in the brainstem

Acts at the CLR/RAMP1 receptor to produce the most potent microvascular vasodilation known in humans, and to transmit and sensitise trigeminal pain signalling — the central mechanism of migraine

Acts at five receptors (SSTR1–5) to inhibit secretion almost universally — growth hormone, TSH, insulin, glucagon, gastrin and pancreatic enzymes — and to reduce splanchnic blood flow

Released by duodenal S cells when acid arrives; tells the pancreas to pour out bicarbonate-rich fluid and the stomach to release gastrin in people with gastrinoma — the basis of its diagnostic uses

Released by duodenal I cells after a fatty or protein-rich meal; contracts the gallbladder, drives pancreatic enzyme secretion, slows stomach emptying and signals fullness to the brain via the vagus nerve

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

Mimics the gut hormone GLP-2: thickens and lengthens the intestinal lining, increases blood flow and nutrient absorption, and slows transit — so people with very short bowels absorb more from what they eat and need less intravenous feeding

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

Released when the heart is stretched by too much blood volume or pressure; act on the kidney to excrete sodium and water, relax blood vessels, and switch off the renin–angiotensin–aldosterone and sympathetic systems — the heart's own…

The most powerful vasoconstrictor the body makes: a local signal that tightens blood vessels, thickens their walls over time and drives fibrosis — overactive in pulmonary hypertension, resistant hypertension and some kidney diseases

A local inflammatory mediator: dilates blood vessels, makes capillaries leak fluid (swelling), triggers pain nerves and causes cough and airway constriction — useful in tissue defence, harmful when overproduced as in hereditary angioedema

The body's own morphine-like messengers: released by neurons and the pituitary to dampen pain signals, blunt the stress response, shape reward and mood, and regulate gut, breathing and hormone release — acting on the same receptors that…

Does not act on the IGF-1 receptor; appears to normalise synaptic development and dampen neuroinflammation, with effects on microglia, astrocytes and dendritic morphology in Rett models — exact receptor unknown

Enhances cellular zinc uptake and acts on zinc-dependent pathways; activates Nrf2 antioxidant responses; modulates dopamine and appetite signalling in rodents; recently described as a modulator of the chloride channel CLIC1

Potently and selectively inhibits the neutrophil enzymes elastase and proteinase 3, limiting tissue destruction; also has antimicrobial, anti-inflammatory (NF-κB-dampening) and immune-modulating actions

Binds selectively to glioma and several other tumour cell surfaces — the target is generally attributed to a matrix metalloproteinase-2 complex and chloride channel components — and carries whatever is attached to it (a fluorescent dye, a…

Block acid-sensing ion channels (ASIC1a and ASIC1b) rather than opioid receptors, producing analgesia in rodents that naloxone does not reverse

Each family blocks or modulates a specific ion channel or receptor with unusual precision — nicotinic receptors (α), voltage-gated sodium channels (μ), calcium channels (ω), noradrenaline transport (χ) — which is why they are the standard…

Selectively blocks small-conductance calcium-activated potassium channels (SK channels, principally SK2/KCa2.2), removing the afterhyperpolarisation that normally limits repetitive firing in neurons and other excitable cells

Act at the bombesin receptor family — principally GRP receptor (BB2/GRPR) and neuromedin B receptor (BB1) — which in normal physiology drives gastrin release, gut motility, satiety and itch, and which is heavily over-expressed on several…

Bivalent, essentially irreversible direct thrombin inhibitor — one end occupies thrombin's active site, the other its fibrinogen-binding exosite — blocking clot formation without needing antithrombin and without being neutralised by…

Crotalphine produces long-lasting analgesia in rodents by activating peripheral opioid receptors (kappa and delta) and engaging cannabinoid signalling; crotamine is a muscle toxin that happens also to be an efficient cell-penetrating and…

Hi1a is a potent and selective inhibitor of acid-sensing ion channel 1a (ASIC1a), the channel that drives cell death when tissue pH falls during loss of blood supply; ProTx-II is a potent inhibitor of the voltage-gated sodium channel…

Strongly cationic and amphipathic — bind anionic bacterial membranes and lipopolysaccharide, permeabilise the membrane and kill rapidly; the same physical chemistry makes them cytotoxic to mammalian cells and red cells at higher…

The peptide binds somatostatin receptor subtype 2 (SSTR2) on neuroendocrine tumour cells and is internalised; Ga-68 emits positrons that a PET camera detects, while Lu-177 emits short-range beta particles that irradiate the tumour from…

Binds SSTR2 (and SSTR5 to a lesser degree) on neuroendocrine tumour cells; the attached radiometal images or irradiates them

The Glu-urea-Lys head binds the active site of PSMA, an enzyme over-expressed on the surface of most prostate cancer cells; the complex is internalised and the attached isotope images (Ga-68) or irradiates (Lu-177) the cell

Binds SSTR2 (and SSTR5) on neuroendocrine tumour cells; indium-111 gamma rays are detected by a gamma camera at 4 and 24 hours

Binds SSTR2 without activating or internalising it; because antagonists recognise many more receptor conformations than agonists, far more molecules bind per tumour cell, delivering more radiation or a brighter image

Binds FAP, a protease on the surface of cancer-associated fibroblasts in the stroma of most solid tumours (and in some fibrotic and inflamed tissues); the isotope images or irradiates the tumour's supportive tissue rather than the cancer…

RGD is the three-amino-acid sequence that extracellular-matrix proteins use to grip integrin receptors; cyclic RGD peptides bind integrin αvβ3 (and αvβ5) on tumour blood vessels and some tumour cells, either blocking them (cilengitide) or…

Binds the GLP-1 receptor, which is expressed at extremely high density on insulinomas (and on normal pancreatic beta cells), and is internalised; the isotope lets a PET or SPECT camera find tumours that are often under 1 cm and invisible to…

Tilmanocept's mannose groups bind CD206 (the mannose receptor) on macrophages and dendritic cells inside lymph nodes, so it is retained in the first ("sentinel") nodes draining a tumour

Binds the chemokine receptor CXCR4, which is over-expressed on many haematological cancers (myeloma, lymphoma, leukaemia), some solid tumours, aldosterone-producing adrenal adenomas and activated immune cells; the isotope images or…

Binds pituitary GnRH receptors far more durably than natural GnRH; a brief surge of LH/FSH is followed by receptor desensitisation and a sustained shutdown of testosterone or oestrogen production

Continuous GnRH-receptor stimulation desensitises the pituitary, shutting down LH/FSH and therefore testosterone or oestrogen production after an initial flare

Continuous low-level GnRH-receptor stimulation from a hydrogel reservoir desensitises the pituitary and suppresses LH, FSH and sex steroids for a full year

Blocks pituitary GnRH receptors directly, so LH, FSH and testosterone fall within days with no initial surge

Slowly cleaved in the body to lysine-vasopressin, which constricts splanchnic (gut) arteries via V1 receptors, lowering portal pressure and redirecting blood to the kidneys

Activates uterine oxytocin receptors like oxytocin but resists breakdown, so a single dose keeps the uterus contracted for an hour or more after delivery

Blocks oxytocin from binding its receptor on uterine muscle, lowering intracellular calcium and reducing contraction frequency

CRH stimulates pituitary corticotrophs to release ACTH; ACTH(1-24) stimulates the adrenal cortex (MC2 receptor) to release cortisol — each is used to test the next link in the chain

Activates AT1 receptors on blood-vessel muscle to constrict arteries and raise blood pressure; also prompts aldosterone and vasopressin release and sympathetic activation

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

Binds complement protein C3 and its fragment C3b, blocking all three complement activation pathways at their convergence point

Binds complement C5 at two sites, preventing its cleavage into C5a and C5b and so stopping formation of the membrane-attack complex that damages the neuromuscular junction

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

Non-competitively inhibit β-(1,3)-D-glucan synthase, an enzyme fungi need to build their cell wall and humans do not have, causing fungal cell lysis

Bind the D-alanyl-D-alanine end of peptidoglycan precursors, physically blocking the enzymes that build the bacterial cell wall; lipoglycopeptides additionally anchor to and disrupt the membrane

Activates kappa-opioid receptors on peripheral sensory nerves and immune cells to suppress itch signalling and inflammation, while barely entering the brain, so it avoids the sedation, euphoria and dysphoria of brain-acting opioids

Mimics hepcidin, the liver hormone that controls iron: it triggers degradation of ferroportin, trapping iron in gut cells and macrophages, which lowers the iron available to the bone marrow and so restrains red-cell overproduction

Blocks the CXCR4 receptor on haematopoietic stem cells, breaking the CXCL12 (SDF-1) "anchor" that holds them in the bone marrow so they spill into the blood where they can be collected

Presents a melanoma-associated peptide to the immune system in a strongly adjuvanted depot so that CD8+ "killer" T cells specific for gp100-bearing melanoma cells expand

Expands HER2-specific CD8+ T cells so they can recognise and kill residual HER2-expressing breast-cancer cells after surgery and chemotherapy

Presents a telomerase fragment to helper (CD4+) T cells, which in turn support CD8+ responses against the telomerase-positive cells found in most cancers; the same peptide also has direct anti-inflammatory and cell-penetrating properties…

Raises CD8+ and CD4+ T-cell and antibody responses against survivin, a protein that blocks cell death and is strongly expressed by glioblastoma and many other cancers but almost absent from normal adult tissue

Immunises the patient against their own EGF so that antibodies mop up circulating EGF and starve EGFR-driven tumours of their growth signal — an antibody-mediated "ligand deprivation" strategy, not a T-cell vaccine

Vaccinates against many tumour antigens at once so that losing any single antigen does not allow the tumour to escape, with cyclophosphamide pre-treatment intended to deplete regulatory T cells first

Raises T cells against the specific mutated KRAS protein driving the patient's tumour — a true tumour-specific target, since the mutation does not exist in normal tissue

Vaccinates each patient against the specific mutations in their own tumour, so the targets are sequences that exist nowhere in normal tissue and against which the immune system has not been tolerised

Delivers only the T-cell-recognised parts of an allergen, deliberately too short to be cross-linked by IgE on mast cells, so the immune system can be re-educated toward tolerance without triggering an allergic reaction

Delivers the autoantigen epitope under conditions designed to induce regulatory rather than effector T cells, aiming to switch off the specific autoimmune attack while leaving the rest of the immune system intact

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

Activates the GLP-2 receptor in the gut to increase villus height, mucosal surface area and nutrient absorption, so people on intravenous nutrition can reduce it

Activates the intestinal GLP-2 receptor to expand absorptive mucosal surface, reducing the intravenous nutrition and fluid people with short bowel syndrome need

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

Binds PCSK9 in the circulation and blocks it from degrading LDL receptors, so the liver clears more LDL cholesterol from the blood

The lipophilic peptide carries melphalan rapidly into cells, where aminopeptidases cleave it and trap a high concentration of active alkylator inside — especially in myeloma cells, which are rich in those enzymes

The Angiopep-2 peptide binds LRP1 on brain capillary endothelium and is carried across the blood-brain barrier by receptor-mediated transcytosis, taking its chemotherapy payload with it

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