A quick-reference chart comparing the reported plasma half-lives of 12 commonly studied research peptides, from compounds measurable in plasma for only minutes to engineered molecules that persist for days, with the evidence basis for each value.
In pharmacokinetic (PK) research, half-life (t½) is the time required for the plasma concentration of a compound to decrease by 50% from its peak. For peptides, this parameter is shaped by enzymatic degradation, renal clearance, molecular size, and structural modifications designed to extend circulation time.
Half-life is central to interpreting concentration-time data. It determines when a compound reaches steady state under repeated exposure in a study model, when it is considered eliminated, and how time-course observations should be read. A peptide with a half-life of minutes behaves very differently in an experimental system from one engineered to circulate for a week.
The values below are approximate plasma half-lives drawn from published preclinical and clinical pharmacokinetic literature. Reported values vary with species, route, assay method and study design, and for several smaller peptides the published data are limited. Each row states the basis for its value. These figures are a research reference only.
| Peptide | Reported plasma half-life | Category | Evidence basis | Research notes | Links |
|---|---|---|---|---|---|
| GLP-1 | ~7 days (≈168 h) | Long | Clinical PK | Fatty acid acylation enables reversible albumin binding, which greatly reduces renal clearance. Longest-acting compound in this chart. | Guide |
| GLP-3 | ~6 days | Long | Clinical PK (Phase 1) | Triple GLP-1/GIP/glucagon receptor agonist with a C20 fatty acid modification; extended profile comparable to other acylated incretins. | Product · Guide |
| GLP-2 | ~5 days | Long | Clinical PK | Dual GLP-1/GIP receptor agonist with a C20 fatty diacid enabling albumin binding. | Product · Guide |
| IGF-1 LR3 | ~20–30 hours | Long | Preclinical, limited | The Long R3 variant carries a 13-amino-acid N-terminal extension and an Arg→Glu substitution that reduce affinity for IGF-binding proteins; reported to persist far longer than native IGF-1 (minutes). | Product · Guide |
| TB (Thymosin-B fragment) | Hours | Medium | Limited published data | A 43-amino-acid actin-sequestering peptide. Direct plasma half-life measurements are sparse; the original chart listed ~6–8 h. | Comparison |
| MOTS | Hours (estimated) | Medium | Limited, rodent estimates | Mitochondrial-derived 16-amino-acid peptide. Pharmacokinetic data are limited; estimates come from rodent studies. | Product · Guide |
| Ipamorlin | ~2 hours | Medium | Clinical PK | Selective growth-hormone secretagogue (ghrelin receptor agonist). | Product · Comparison |
| Tesa | ~26–38 minutes | Short | Clinical PK | GHRH analog with a trans-3-hexenoic acid modification. Short plasma half-life; the growth hormone response it triggers is reported to last hours. | Product · Guide |
| Serma | ~10–20 minutes | Short | Clinical PK | GHRH(1-29) fragment; rapidly degraded by plasma proteases. | Product · Guide |
| GHK | Minutes | Short | Limited direct PK | Copper-binding tripeptide. Rapid clearance is reported; gene-expression changes are described persisting well after exposure. | Product · Guide |
| Semx | Minutes | Short | Limited, rodent | Synthetic ACTH(4-10) analog with a Pro-Gly-Pro extension; rapid plasma degradation reported in rodent work. | Product |
| Body Protection Compound 157 | Minutes | Short | Limited published PK | Pentadecapeptide of gastric origin. Very rapid plasma clearance is reported; direct human PK data are limited. | Product · Guide |
Evidence basis: "Clinical PK" = published human pharmacokinetic data; "Preclinical" = animal studies; "Limited" = few or no direct plasma half-life measurements in the peer-reviewed literature, values are estimates or ranges commonly cited in reviews. Categories: short < 1 hour, medium 1–12 hours, long > 12 hours.
Bars are proportional to reported duration on a compressed scale, grouped by category. Where the literature gives only an order of magnitude, the bar shows that magnitude and the label says so.
Half-life is derived from the elimination phase of a concentration-time curve: plasma samples are collected at intervals after exposure, the intact peptide is quantified (typically by immunoassay or LC-MS/MS), and the rate of decline is fitted. Three points matter when reading the numbers in the chart:
Half-life also frames how time-course data are interpreted. A biological response observed 24 hours after exposure to a peptide with a 2-minute half-life points to downstream signalling or tissue-level effects rather than continued receptor occupancy by the parent molecule.
One of the most common misreadings of pharmacokinetic data is to equate plasma half-life with duration of biological effect. They are distinct measurements:
For example, GHK has a plasma half-life reported in minutes, yet gene-expression studies describe changes across thousands of genes detectable 24 hours or more after exposure. Tesa has a plasma half-life of roughly half an hour, while the growth hormone response it triggers is reported to last several hours.
The dissociation is most pronounced for peptides that act as signalling triggers rather than sustained receptor occupants: the peptide initiates a cascade, and the cascade continues independently.
Several mechanisms described in the literature explain how short-lived peptides can produce prolonged effects in laboratory models:
For this reason plasma PK data alone are insufficient for predicting experimental outcomes. Tissue distribution, receptor-occupancy assays and downstream biomarker measurements give a more complete picture of a peptide's functional timeline.
Plasma half-life (t½) is the time it takes for the concentration of a peptide in blood plasma to fall by half after its peak. It is a pharmacokinetic measurement derived from concentration-time curves. For peptides it is shaped by enzymatic degradation, renal clearance, protein binding, molecular size, and structural modifications such as fatty acid acylation or PEGylation that slow clearance.
Among the compounds in this chart, the acylated incretin analogs have the longest reported plasma half-lives: GLP-1 at roughly 7 days, GLP-3 at roughly 6 days and GLP-2 at roughly 5 days in published clinical pharmacokinetic studies. The values reflect deliberate molecular engineering, principally fatty acid acylation that enables reversible albumin binding and shields the peptide from renal clearance and enzymatic breakdown.
Short peptides without protective modifications, such as GHK, Serma or Body Protection Compound 157, are exposed to circulating proteases and are small enough to be filtered rapidly by the kidneys. Without a fatty acid chain, an albumin-binding domain or other stabilising change, the intact molecule is typically measurable in plasma for only minutes in the studies that have reported it.
No. Half-life and potency are independent pharmacological parameters. Half-life describes how long the intact peptide remains in circulation; potency describes the concentration needed to produce a defined effect at a receptor in an assay. A peptide with a plasma half-life of minutes can show measurable activity in laboratory models, and a long half-life only means the compound persists longer, not that it is more active.
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Browse Products Certificates of AnalysisDisclaimer: All compounds referenced in this article are intended for laboratory research use only. They are not approved for human or veterinary use by the FDA or any regulatory agency. Half-life values are approximate, are drawn from the published literature cited above, and vary with species, route, assay and study design. Nothing in this article is medical advice, and it does not describe or recommend any use, administration or dosing of these compounds.