Peptide Half-Life Database: Research Reference Guide (2026)

Why Half-Life Matters in Peptide Research

Half-life determines how frequently a compound must be administered to maintain research concentrations, how long post-administration washout periods should be, and how to design dosing intervals in rodent study protocols. Short half-life peptides like BPC-157 require frequent dosing to sustain plasma levels. Long half-life compounds like Retatrutide (~6 days) allow weekly or less frequent administration. Understanding half-life is foundational to protocol design.

This database compiles half-life data from published preclinical and clinical research literature. All values are approximate — half-life varies by species, administration route, dose, and individual metabolic factors. Rodent values are not directly translatable to human pharmacokinetics.

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Peptide Half-Life Database

Recovery & Repair Peptides

Compound	Approximate Half-Life	Route	Notes
BPC-157	~1–4 hours	Subcutaneous / IM	Short half-life; frequent dosing in rodent studies. Oral bioavailability documented in animal models — GI stability is unusual for peptides.
TB-500 (Thymosin Beta-4 fragment)	~6–8 hours (biological activity)	Subcutaneous / IM	Biological activity window longer than plasma half-life due to tissue binding. Less frequent dosing in protocols than BPC-157.
GHK-Cu	~0.5–2 hours (plasma)	Subcutaneous / topical / IV	Short plasma half-life; tissue uptake is rapid. Topical formulations have different kinetics.
KPV	Very short — minutes	Subcutaneous / oral	Tripeptide — rapidly degraded. Oral stability in gut lining research is a key subject.

Metabolic & GLP-1 Class Peptides

Compound	Approximate Half-Life	Route	Notes
Semaglutide	~7 days	Subcutaneous	Weekly dosing in clinical trials. Albumin binding extends half-life. FDA-approved (Ozempic/Wegovy).
Tirzepatide	~5 days	Subcutaneous	Weekly dosing. C20 fatty acid modification enables albumin binding and extended half-life.
Retatrutide	~6 days	Subcutaneous	Weekly dosing in Phase 2 trials. Similar half-life to semaglutide despite triple receptor agonism.
Cagrilintide	~7 days	Subcutaneous	Long-acting amylin analogue. Paired with semaglutide in CagriSema combination trials.
Liraglutide	~13 hours	Subcutaneous	Daily dosing. Earlier GLP-1 agonist — shorter half-life than semaglutide.

Longevity & Mitochondrial Peptides

Compound	Approximate Half-Life	Route	Notes
MOTS-c	~2–4 hours (plasma)	Subcutaneous / IV	Short plasma half-life; nuclear translocation follows dosing. Exercise transiently raises endogenous levels.
SS-31 (Elamipretide)	~2–3 hours (plasma)	Subcutaneous / IV	Rapid tissue uptake — concentrates ~1000x in inner mitochondrial membrane. Biological effect persists beyond plasma clearance.
Humanin	~2–4 hours	Subcutaneous / IV	Mitochondrial-derived peptide. Declines with age. Limited published PK data.
Epithalon	~1–3 hours (estimated)	Subcutaneous / IV	Tetrapeptide telomere/longevity compound. Limited published human PK data.
NAD+	Rapidly metabolised (minutes to hours)	IV infusion	As a coenzyme, NAD+ is consumed and recycled continuously. IV infusion raises tissue levels transiently; precursor supplementation (NMN/NR) has longer kinetics.

Cognitive & Neuropeptides

Compound	Approximate Half-Life	Route	Notes
Semax	~20–25 minutes (plasma)	Intranasal / subcutaneous	Very short plasma half-life; CNS effects persist longer due to receptor binding. Russian-developed ACTH fragment.
Selank	~2–3 minutes (plasma)	Intranasal	Extremely short plasma half-life. Metabolites (including Thr-Lys-Pro) retain anxiolytic activity.
Dihexa	Extended — estimated days	Oral / subcutaneous	HGF mimetic. Unusually long activity for a peptide due to structural modifications. Limited published PK.
PT-141 (Bremelanotide)	~2.7 hours	Subcutaneous / intranasal	FDA-approved (Vyleesi). Published clinical PK available.

Growth Hormone Axis Peptides

Compound	Approximate Half-Life	Route	Notes
Ipamorelin	~2 hours	Subcutaneous	Selective GHRP. Short half-life used to time GH pulse research. Often paired with CJC-1295.
CJC-1295 (DAC)	~6–8 days	Subcutaneous	DAC modification creates covalent albumin binding. Weekly dosing in protocols.
CJC-1295 (no DAC / Mod GRF 1-29)	~30 minutes	Subcutaneous	Without DAC — short half-life mimics natural GHRH pulse. Often paired with ipamorelin.
GHRP-6	~2–3 hours	Subcutaneous	Growth hormone releasing peptide. Ghrelin receptor agonist. Increases appetite in models.
Hexarelin	~1–2 hours	Subcutaneous	GHRP — more potent GH release than GHRP-6. Also has cardiac receptor activity.
Tesamorelin	~26 minutes	Subcutaneous	FDA-approved (Egrifta). Daily dosing for HIV-associated lipodystrophy.

Immune Research Peptides

Compound	Approximate Half-Life	Route	Notes
Thymosin Alpha-1 (Tα1)	~2 hours	Subcutaneous	Immune modulator. FDA-approved in some markets (Zadaxin). Approved in 37+ countries.
LL-37	Very short — minutes	Topical / subcutaneous	Cathelicidin antimicrobial peptide. Rapid degradation limits systemic delivery in research.

Half-Life Factors: What Changes These Values

Species: Rodent metabolism is 5–10x faster than human. Rodent half-life values are shorter than equivalent human values.
Administration route: IV administration produces the fastest peak and often the shortest apparent half-life. Subcutaneous and IM injection result in slower absorption with different effective half-life kinetics.
Structural modifications: Fatty acid conjugation (GLP-1 class), PEGylation, and DAC modification all extend half-life by enabling albumin binding or slowing renal clearance.
Dose: At higher concentrations, clearance mechanisms can saturate, effectively extending half-life.
Protease susceptibility: Peptides are degraded by plasma and tissue proteases. D-amino acid substitutions, cyclisation, and other modifications reduce protease susceptibility and extend stability.

Half-Life vs Biological Activity Window

Plasma half-life and duration of biological effect are not the same. SS-31 concentrates in the inner mitochondrial membrane and exerts effects well beyond its ~2-3 hour plasma half-life. Selank’s metabolites retain anxiolytic activity after the parent peptide is cleared. BPC-157’s downstream gene expression changes persist after the compound itself is no longer detectable. When designing research protocols, biological effect duration is often more relevant than plasma half-life alone.

Frequently Asked Questions

What is peptide half-life?

Half-life (t½) is the time required for the plasma concentration of a compound to fall to half its initial value. For peptides, this is primarily determined by proteolytic degradation, renal filtration, and receptor-mediated clearance. It governs dosing interval design in research protocols.

Why do GLP-1 peptides have such long half-lives compared to recovery peptides?

GLP-1 class compounds (semaglutide, tirzepatide, retatrutide) are specifically engineered with fatty acid side chains that bind albumin in plasma. Albumin binding slows renal clearance and protects the peptide from degradation, extending half-life from hours to days. Recovery peptides like BPC-157 and GHK-Cu lack these modifications and are cleared rapidly.

How does route of administration affect half-life?

IV administration delivers the compound directly to plasma, producing the fastest peak concentration and typically the most measurable plasma half-life. Subcutaneous and IM injection produce slower absorption from the depot site, which can extend the effective exposure window even if the apparent elimination half-life is similar.

Are these half-life values applicable to human research?

Most half-life data for research peptides comes from rodent studies. Human pharmacokinetic data exists for FDA-approved compounds (semaglutide, tirzepatide, PT-141, tesamorelin, Tα1) but is limited or absent for non-approved research peptides. Rodent values are directionally useful but not directly translatable.

Related Research Tools at FenaLife

Use the FenaLife Peptide Calculator for reconstitution volumes and the Protocol Planner for research scheduling. See also: Peptide Storage Guide | How Long Do Reconstituted Peptides Last?

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