Peptides work by locking onto receptors on cells and passing on one instruction. That might be to release a hormone, slow digestion or speed up repair.
Messengers, not materials
The most useful mental model: a peptide is a message, not a building material.
When a peptide binds a receptor on a cell surface, it triggers a cascade of events inside that cell: upregulating gene expression, stimulating growth factors, modulating inflammation, or prompting the release of other hormones. The peptide itself is rarely consumed or incorporated into anything. It delivers an instruction and leaves.
This is why dose-response curves for peptides often behave strangely compared to, say, a vitamin. More message is not always more effect, and sometimes it is less. DSIP is the clearest example in this course: our sources describe no added benefit above 300 mcg, and one describes it worsening the sleep it improves at 200.
The six things peptides are asked to do
Depending on the amino acid sequence, a peptide can instruct the body to:
Release hormones. Growth hormone-releasing peptides such as tesamorelin, CJC-1295 and ipamorelin signal the pituitary gland to produce and release growth hormone. They do not supply the hormone; they ask for it.
Regulate appetite and blood sugar. GLP-1 peptides such as semaglutide, tirzepatide and retatrutide target metabolic pathways, reducing appetite and slowing gastric emptying.
Accelerate tissue repair. BPC-157 and TB-500 promote healing in muscle, tendon and gut tissue through angiogenesis and cell migration respectively.
Improve sleep. DSIP modulates delta-wave sleep architecture rather than sedating.
Boost metabolism. MOTS-C activates AMPK, the same metabolic switch triggered by exercise and fasting.
Support skin and repair. GHK-Cu stimulates collagen synthesis and influences over 4,000 genes.
Secretagogue versus replacement
One distinction runs through the whole growth hormone section of this library and is worth understanding before you get there.
A secretagogue tells your body to make more of something. Tesamorelin binds GHRH receptors on the anterior pituitary and prompts the gland to produce and release your own growth hormone. Because the signal enters upstream, your natural pulsatile release pattern stays intact, and so does the somatostatin feedback loop, the brake your body uses to stop GH release when levels are high enough.
Replacement bypasses all of that. Injecting growth hormone directly overrides the pituitary's regulation, which is where supraphysiological exposure and its side effect profile come from.
That is the whole argument for tesamorelin over HGH, and it is a good example of how mechanism drives risk rather than potency alone.
Local versus systemic
The second distinction that changes how you actually use a compound.
BPC-157 concentrates its effect near the injection site. The angiogenic effect is local. So protocols specify injecting near the injury.
TB-500 protocols treat it as acting through the whole body, so the injection site does not follow the injury. That idea comes from its parent protein; it has not been tested for TB-500 in people.
GHK-Cu topical stays in the skin. GHK-Cu injected goes everywhere.
If a protocol tells you where to inject and you do not know why, that is the question to ask. The answer is almost always local versus systemic.
Effects build, mostly
Very few peptides produce an acute felt effect. DSIP takes 4 to 7 days before most people notice anything. Tesamorelin's visceral fat change is measured at 12 to 26 weeks. GHK-Cu produces nothing visible for the first four weeks.
The compounds that do produce a fast subjective effect, appetite suppression from a GLP-1 for instance, are the exception rather than the rule. Expecting week-one results is the single most common reason people abandon a protocol before it has had a chance to work.