Receptor

The receptor myostatin uses to put the brakes on muscle growth. Every myostatin inhibitor works by keeping the ligand off this receptor rather than by acting on it directly.

Amylin is released alongside insulin and signals fullness through a different brain pathway than GLP-1. That is the whole argument for cagrilintide: two satiety routes at once rather than a bigger dose of one.

The receptor every anabolic-androgenic steroid is designed to hit. Binding moves it into the nucleus where it switches on genes for muscle protein synthesis, and in other tissues for hair loss, prostate growth and oil production.

The fat-cell adrenergic receptor. Activating it releases stored fat and raises heat production without the heart-rate effect of beta-1. It is the claimed target of the GH fragments that are supposed to burn fat without growing anything.

The other main dopamine receptor family, tied to reward learning and drive. Altered receptor density is one of the more reproducible findings in animal studies of nandrolone.

The dopamine receptor that holds prolactin down and carries reward and motivation signalling. Losing D2 tone raises prolactin and flattens drive and sexual response.

Drives epithelial cells to divide and migrate over a wound. It is one of the several targets BPC-157 is credited with, and it is also a well-known oncology target, which is the reason the growth-signal caution exists.

Where EPO tells the bone marrow to make red cells. Separating this from EPO's tissue-protective signalling is the entire design goal of ARA-290: repair without raising haematocrit.

The estrogen receptor that dominates breast tissue, liver and the pituitary feedback loop. Gynecomastia and much of the negative feedback on LH run through it.

The second estrogen receptor, common in brain, bone and vascular tissue. Part of why estradiol is needed for mood, libido and bone density rather than being purely a side effect to crush.

Fibroblast growth factor's receptor. In the brain, NCAM signals through it to grow new neurites, which is the route FGL is designed to take.

The receptor that tells inflammation to stop and start clearing up, rather than blocking it from starting. Humanin and LL-37 both act here.

The brain's main calming channel. Some androgen metabolites sit on it as neurosteroids and change anxiety and sleep quality without touching the androgen receptor at all.

What ghrelin binds to make the pituitary release growth hormone, and what every GHRP and MK-677 is built to hit. It also carries the hunger signal, which is why some GH secretagogues make you ravenous and others do not.

The other half of the GH release switch. GHRH sets how big a growth hormone pulse can be; the ghrelin receptor sets whether one fires. Hitting both at once is why a GHRH analog and a GHRP stack rather than duplicate.

The second incretin receptor. Adding it to GLP-1 agonism is what separates tirzepatide from semaglutide: more energy expenditure and a direct effect on fat tissue, on top of the appetite drop.

The incretin receptor behind semaglutide and every drug in that class. Three separate effects run through it: appetite suppression in the brain, slower stomach emptying, and glucose-dependent insulin release from the pancreas.

Glucagon's receptor. Agonising it raises energy expenditure and burns liver fat, which is why the triple agonists add it. It also raises blood glucose, which is the tension every dual and triple agonist has to balance.

The cortisol receptor. Some androgens bind it too, and whether they act as agonist or blocker at a given tissue is a large part of why compounds with similar AR affinity feel so different.

The pituitary receptor that decides whether LH and FSH are released. It only responds to PULSES. A steady signal desensitises it and shuts the axis down completely, which is why the same drug can restart testicular function or chemically castrate depending on how it is dosed.

The shared signalling subunit a large family of inflammatory cytokines runs through, IL-6 included. Humanin's cytoprotective effect is described as working through this complex.

Where growth hormone itself acts. Binding pairs the receptor and fires JAK2/STAT5, which in the liver means IGF-1 output and in fat means lipolysis. Injected GH works here; secretagogues work one step upstream.

Hepatocyte growth factor's receptor. In the brain it drives new synapse formation, which is the mechanism claimed for dihexa.

The receptor that carries almost all of growth hormone's anabolic effect, one step downstream of it. It is also the reason the IGF-1 analogs are the peptides with the most serious theoretical cancer question: the same signal that grows muscle grows anything already growing.

One step above GnRH. Kisspeptin neurons are the master switch that tells the hypothalamus to release GnRH at all, which is why acting here produces a physiologic LH pulse rather than overriding the axis.

The pigment receptor on melanocytes. Activating it makes the skin produce eumelanin, which is the tanning effect of the melanotans. The same receptor family also damps inflammation, which is what KPV uses it for.

A central melanocortin receptor involved in energy balance and sexual arousal. It is one of the two receptors PT-141 works through.

The melanocortin receptor that controls appetite and central sexual arousal. It is why the melanotans suppress hunger and cause spontaneous erections, and why PT-141 works in the brain rather than in the blood vessels the way a PDE5 inhibitor does.

The melanocortin receptor on sebaceous and other exocrine glands. Pan-melanocortin agonists hit it, which is part of why they can trigger oil production and acne alongside the tan.

The aldosterone receptor in the kidney. When a steroid activates it, sodium and water are held onto, which shows up as blood pressure and smooth-over-the-muscle bloat.

Oxytocin's receptor, and it is not only in the brain. The uterus, heart, gut and T-cells all carry it, which is why an intranasal dose taken for mood also has cardiovascular and gut effects.

The progesterone receptor. 19-nor steroids are structurally close enough to progesterone to activate it, which is why nandrolone and trenbolone produce progestogenic side effects that an aromatase inhibitor cannot touch.

What prolactin acts through, including in breast tissue. It is the reason a progestogenic compound can produce gyno with a perfectly normal estradiol reading.

A serotonin receptor involved in mood, impulse control and aggression. Androgen exposure shifts serotonergic signalling in animal work, which is the mechanistic case behind steroid irritability.

Part of how the immune system recognises a bacterial surface. Thymosin alpha-1 acts through it and TLR9 to push dendritic cells and T-cells toward a coordinated response.

Recognises bacterial and viral DNA inside the cell. The second of the two toll-like receptors thymosin alpha-1 is described as working through.

Nerve growth factor's receptor. It keeps sensory and cholinergic neurons alive and drives neurite outgrowth, which is what the porcine brain-extract peptides are claimed to mimic.

What BDNF binds. It is the main receptor behind the claim that a nootropic peptide improves learning or protects neurons: almost all of them are described as raising BDNF, which means acting here.

The main receptor for new blood vessel growth. Healing peptides that speed up tendon and gut repair are described as acting here, because tissue cannot repair faster than it can be supplied.

VIP's two receptors. They open airways, widen vessels, move the gut and damp cytokine output, which is why one peptide is studied for conditions as unrelated as pulmonary hypertension and inflammatory bowel disease.