Half-life
The time it takes for the concentration of a compound in the body to fall by half. It sets dosing frequency and time to steady state. It does not set duration of effect.
Half-life is the time required for the concentration of a compound in blood to fall by half. If a compound has a six-hour half-life, then six hours after it peaks roughly half remains, at twelve hours a quarter, at eighteen hours an eighth. The decline is exponential rather than linear, which is why the same interval removes half of whatever is left rather than a fixed amount.
It is the single most useful number for reasoning about a dosing schedule, and it is regularly asked to answer questions it cannot.
What it sets: how often, and how long until steady
The practical consequence of half-life is accumulation. If you dose again before the previous dose has cleared, concentration builds. It keeps building until the amount cleared between doses equals the amount going in, which is steady state.
The arithmetic is reliable. After one half-life you are at 50 percent of the eventual steady-state level, after two 75 percent, after three 87.5, after four roughly 94, after five roughly 97. Five half-lives is the conventional working answer for reaching steady state, and the same figure describes washout: five half-lives after stopping, roughly 97 percent has cleared.
This is why a compound with a long half-life takes a long time to show what it does. Semaglutide's half-life is about a week, so steady state is roughly five weeks out. Judging it at week two means judging a level that is still climbing.
The half-life calculator does this arithmetic, including accumulation ratio and how much remains at the next dose.
What it does not set: how long the effect lasts
The most common error is treating half-life as duration of action. They are different quantities and they can diverge sharply.
Half-life is pharmacokinetics, what the body does to the compound. Duration of effect is pharmacodynamics, what the compound does to the body. A molecule that binds its receptor irreversibly can produce an effect lasting long after it has cleared, because the effect depends on the receptor recovering rather than on the drug still being present. Conversely a compound can circulate for days while producing very little, if the concentration sits below the threshold where anything happens.
So "it has a long half-life" and "it works for a long time" are two claims. The first is measurable and usually published. The second requires outcome data, which for most research peptides does not exist.
Where the numbers come from, and how firm they are
A published half-life comes from measuring blood concentrations over time in a defined population, by a defined route. Change any of those and the number moves. Subcutaneous and intravenous administration give different curves for the same molecule, because absorption from under the skin is itself a rate-limiting step.
Half-life also varies between people, with kidney and liver function, and sometimes with dose. Published figures are usually a mean or a range from a specific study, not a constant.
For approved drugs these figures come from registration trials and are firm. For most research peptides they come from small studies, animal models, or nowhere at all. Where this site lists a half-life the compound library also grades how much research sits behind it, and the honest answer for many compounds is very little.
Two half-lives, and why the route matters
Published figures often distinguish a distribution phase from a terminal phase. Immediately after a dose, concentration falls quickly as the compound moves out of blood into tissue. Later it falls more slowly, governed by elimination. The terminal half-life is the second, slower number, and it is usually the one quoted, which is why a compound can feel like it has faded long before its stated half-life has elapsed.
Route matters more for injectable peptides than it does for most oral drugs. When a compound is absorbed from under the skin more slowly than the body clears it, the measured half-life stops describing elimination and starts describing absorption. The curve is then set by how fast the depot under the skin releases, not by how fast the kidneys and liver remove. This is why the same molecule can show a markedly longer apparent half-life given subcutaneously than intravenously, and why a half-life quoted without a route is close to meaningless.
It is also why formulation changes half-life without changing the molecule. Attaching a fatty acid chain so the peptide binds albumin, or conjugating it to a larger carrier, extends circulation time by slowing clearance. Semaglutide and the earlier GLP-1 agonists differ enormously in half-life while acting on the same receptor.
Related terms: steady state, pharmacokinetics, titration.
