For research and educational purposes only. Not medical advice. Values reflect best available published data from animal studies, limited human pharmacokinetic trials, and validated clinical prescribing information where applicable. Where human data is absent, values are estimated from preclinical models and detection window analysis.
TL;DR
Half-life determines how long a compound stays active, and every dosing decision flows from it. Getting it wrong means either inadequate exposure or dangerous accumulation. This guide covers half-life, bioavailability, duration of active effect, steady-state timing, washout periods, and dosing frequency for 75 peptides, bioregulators, and research compounds across 13 functional categories. Key takeaways: it takes 4–5 half-lives to reach steady-state and 4–5 half-lives to wash out; Khavinson bioregulators have 15-minute plasma half-lives but months-long biological effects; Noopept is a prodrug and the parent plasma half-life is irrelevant for timing; GLP-1 compounds require 4–5 weeks of weekly dosing before readers are measuring steady-state effects. The listed research text specifies using the searchable reference table below to find any compound instantly.
Why This Guide Exists
If readers have spent any time in the research peptide space, they have encountered this scenario. Someone is three weeks into a protocol, frustrated that they are not observing the effects they expected, and they start questioning the vendor or the compound. The peptide COA is clean. The vendor is vetted. The sourcing is legitimate.
The problem is not the compound. The problem is the pharmacokinetics.
They are running a compound with a 7-day half-life and measuring outcomes at week two: during the accumulation phase before steady-state has been reached. Or they are timing doses based on the plasma half-life of a prodrug rather than the active metabolite. Or they are stacking two compounds with dramatically different half-lives and attributing effects to the wrong variable.
These are not exotic research errors. They are the most common protocol design failures in the research peptide community, and every one of them is preventable with basic pharmacokinetic literacy. This post covers the foundational concepts and then delivers the complete reference data for 75 compounds across 13 functional categories.
The Foundational Concepts Every Researcher Needs to Understand
What Half-Life Actually Means
Half-life is the time required for the concentration of a compound in the body to decrease by 50 percent. It is a property of the compound, the route of administration, and the individual’s metabolic function. It is not a fixed number that tells you how long the compound works: it tells you how quickly the body eliminates it.
That distinction matters because the biological effect of a compound often outlasts its plasma half-life by a significant margin. A peptide that stimulates BDNF upregulation may clear from circulation in 30 to 60 minutes while the BDNF elevation it triggered persists for 6 to 8 hours. A bioregulator peptide may have a 15-minute plasma half-life while the gene expression changes it triggers persist for months. Reading the half-life number without understanding what it actually measures will produce systematically incorrect protocol design.
The Steady-State Principle
Steady-state is the point at which the amount of compound entering the body with each dose exactly equals the amount being eliminated between doses. It takes approximately 4 to 5 half-lives to reach steady-state regardless of the compound.
For ipamorelin with a 2-hour half-life and twice-daily dosing, steady-state is reached within 8 to 10 hours (essentially day one). For semaglutide with a 7-day half-life and once-weekly dosing, steady-state is reached at 4 to 5 weeks. A researcher measuring outcomes at week two is measuring the build-up phase, not the stable therapeutic exposure level. For CJC-1295 with DAC and a 6 to 8 day half-life, the same principle applies: researchers who report no meaningful IGF-1 elevation after two weeks of weekly injections may simply not have reached steady-state.
The Washout Calculation
Washout follows the same 4 to 5 half-life rule. It takes 4 to 5 half-lives to eliminate approximately 97 percent of a compound from systemic circulation.
For ipamorelin with its 2-hour half-life, meaningful washout is complete within 8 to 10 hours. For semaglutide at 7 days, meaningful washout takes 4 to 5 weeks. For tesofensine with its 8 to 12 day half-life, washout extends 6 to 10 weeks. Researchers who design protocols with insufficient washout periods are not starting each cycle from a clean baseline: they may effectively be running a continuous protocol rather than the discrete cycles they intended.
The Prodrug Problem
Several compounds in common research use are prodrugs. The parent compound that is administered is not the biologically active species: it is converted to the active compound after administration, and it is the active compound’s half-life that determines protocol timing, not the parent compound’s.
Noopept is the most important example. The parent compound N-Phenylacetyl-L-Prolylglycine Ethyl Ester has a plasma half-life of approximately 30 to 60 minutes. It is metabolized in the brain to cycloprolylglycine, the AMPA receptor-modulating species that produces the cognitive effects. The active metabolite has a CNS residence time of approximately 2 to 4 hours. Researchers who time their dosing based on the 30-minute parent compound half-life are dosing based on irrelevant pharmacokinetic data.
The Plasma vs. Effect Disconnect
For compounds that operate by triggering downstream signaling cascades rather than by continuously occupying a receptor, the duration of biological effect is almost always longer than the plasma half-life suggests.
BPC-157 has an estimated plasma half-life of 7.9 to 30 minutes in animal models. Its documented duration of biological effect in tissue-level signaling is estimated at 6 to 8 hours. The most extreme version of this disconnect is the Khavinson bioregulator class, where short-chain peptides with plasma half-lives of 10 to 30 minutes trigger gene expression changes at the chromatin level that persist for weeks to months (a difference not of degree but of orders of magnitude).
Route of Administration and Half-Life
The same compound administered by different routes will display meaningfully different pharmacokinetic behavior. IV administration produces immediate peak concentration followed by rapid decline. SubQ administration produces a delayed, lower peak with a more prolonged absorption curve that extends the functional duration beyond what the elimination half-life alone predicts.
Intranasal administration for CNS-active compounds like Semax and Selank partially bypasses systemic circulation through the olfactory nerve pathway, meaning plasma half-life measurements underrepresent the actual duration of CNS exposure. This is why cross-study comparisons of the same compound via different routes can produce apparently contradictory results. The pharmacokinetic environment is genuinely different.
The Complete Reference Table: 75 Compounds Across 13 Categories
All 75 compounds are organized into 13 functional categories. Each row links to the compound’s full encyclopedia entry and, where pharmacokinetic data is sufficient, to the Half-Life Visualizer for a graphical plasma decay curve. Search by compound name or filter by category to navigate the table.
Five Advanced Pharmacokinetic Concepts That Separate Good Protocols From Great Ones
One: Receptor Saturation Is a Ceiling, Not a Floor
For receptor-mediated compounds, more is not more above the saturation threshold. Ipamorelin at the GHS-R1a receptor is the clearest example: doses above the point of complete receptor saturation produce no additional GH pulse amplitude while creating unnecessary peptide burden and increasing desensitization risk. Research protocols designed around maximum tolerated dose rather than receptor saturation threshold are not optimizing the compound; they are wasting it.
Two: Tissue Distribution Changes Everything for Lipophilic Compounds
Compounds that distribute extensively into adipose and other lipid-rich tissues have total body residence times that far exceed their plasma half-lives. Cardarine and tesofensine are the clearest examples: tissue accumulation means the washout period required is multiple times longer than the plasma half-life calculation alone would suggest. Researchers who use plasma half-life alone to calculate washout windows for lipophilic compounds will systematically underestimate residual compound burden at the start of their next protocol cycle.
Three: Combining Compounds With Different Half-Lives Creates Interpretation Challenges
Stacking compounds with dramatically different half-lives means they are at completely different points in their concentration curves at any given measurement time. The most common version of this in the research peptide community is the CJC-1295 with DAC plus ipamorelin stack. Ipamorelin’s 2-hour half-life produces acute pulsatile GH stimulation against a background of sustained pituitary sensitization from CJC-1295 with DAC’s 6 to 8 day half-life. Attributing measured effects to one compound versus the other in this environment is not straightforwardly possible without compound-specific washout designs.
Four: Measurement Timing Is Research Methodology
Any biomarker measurement must be recorded with the time post-dose, the dose number within the cycle, and whether steady-state had been reached at the time of measurement. A GH measurement at peak concentration is not the same data point as a GH measurement at trough. Comparing results across researchers who measured at different pharmacokinetic phases is a core driver of the reproducibility problems that have plagued peptide research for years.
Five: The Bioregulator Half-Life Paradox Requires a Different Mental Model
For Khavinson bioregulators, the standard pharmacokinetic mental model breaks down entirely. A 15-minute plasma half-life and a months-long gene expression change are simultaneously true. The plasma half-life tells readers when to schedule the next dose within a cycle. The gene expression persistence tells readers when to measure outcomes and how to design cycle spacing. Applying only one of these data points to protocol design while ignoring the other will produce either inadequate dosing frequency within cycles or incorrect outcome measurement timing between cycles.
Thymalin, Epitalon (Epithalon), and Thymosin Alpha-1 are the most studied examples of this class where the biological effect and pharmacokinetic windows require completely separate mental frameworks. Thymalin mortality studies from Khavinson’s group document effects at annual follow-up from a compound that clears from plasma in minutes. Understanding both timescales simultaneously is non-negotiable for anyone designing a meaningful bioregulator research protocol.
For vetted vendors carrying research compounds with documented third-party COA verification and current coupon codes, visit the vendor directory. For a graphical plasma decay curve for any compound in this table, use the Half-Life Visualizer.
For research and educational purposes only. Not medical advice. Research peptides and bioregulators are not FDA-approved for human use unless specifically noted as approved pharmaceuticals above.