Methodology

How the estimate actually works.

Every "estimated level" shown across Peptide Plug — in the Half-Life Visualizer, the in-app Estimated Levels feature, and the compound-specific calculators — is built from the same public reference data and the same basic pharmacokinetic math. This page explains exactly how, in plain language.

The Model

Two related models are used across the site, both built on the same first-order pharmacokinetic principles.

In-app Estimated Levels. Uses a single-compartment, first-order exponential decay model: every logged dose decays independently as amount × 0.5^(hours elapsed ÷ half-life). This is a lightweight model suited to a daily-tracking view built from your actual logged dose history. Standard first-order elimination kinetics — the textbook "half-life" concept.
Half-Life Visualizer. Uses a two-phase Bateman equation that adds an absorption phase on top of elimination: Level(t) = Dose × [ka/(ka−ke)] × (e^(−ke·t) − e^(−ka·t)), where ke is derived from elimination half-life and ka from absorption half-life. This produces a curve that rises to a peak after injection rather than assuming an instant peak. One-compartment model with first-order absorption and elimination — standard in pharmacokinetics texts (e.g. Rowland & Tozer, Clinical Pharmacokinetics and Pharmacodynamics).
Multiple doses (superposition). Both models handle a repeated dosing schedule the same way: the total estimated level at any moment is the sum of the still-active contribution from every dose logged or scheduled up to that point. This is standard for any linear (first-order) pharmacokinetic system. Linear pharmacokinetics superposition principle.

Where the Half-Life Data Comes From

Every compound is tagged with an evidence level so you can see how solid the underlying number actually is — never presented with more confidence than the source supports.

FDA label. The compound has an FDA-approved product with a package insert stating a specific half-life from that product's own clinical pharmacology studies. This is the highest-confidence tier. FDA prescribing information / package inserts.
Clinical trial data. The compound is investigational but has published Phase 2/3 trial pharmacokinetic data. Published clinical trial protocols and results.
Published PK study. A peer-reviewed pharmacokinetic study exists in humans, independent of a specific drug-approval trial. Peer-reviewed pharmacokinetics literature.
Limited human data. Some human data exists but is sparse or shows a wide range across small studies. Small or limited-scope published studies.
Not characterized in humans. No solid human plasma PK study was identified. Any number circulating online for these compounds typically traces back to animal studies, structural analogy to a related molecule, or informal sources — not human trial data. Absence of published human PK literature.

What This Model Does NOT Do

Being direct about the limits of a public-data estimate matters as much as explaining how it works.

It is not a clinical pharmacokinetic model. It does not account for your individual absorption rate, metabolism, body composition, kidney or liver function, drug interactions, or any of the many factors that make real-world pharmacokinetics vary meaningfully between people. —
It cannot know your actual blood concentration. The output is a relative estimate built from public population-level data and the dose/timing you enter — not a measurement. Two people taking an identical dose on an identical schedule can have genuinely different blood levels. —
It is built entirely from public reference data. Nothing about your specific physiology feeds into this model. It is, at best, a reasonable population-average estimate — useful for understanding general shape and timing, not for precision. —

Estimate only — not medical advice. Individual variation in how compounds are absorbed and cleared can be significant. This estimate is not a substitute for actual blood testing, and nothing produced by this model should be used to make dosing decisions. Talk to a licensed clinician about your protocol and any lab work you're considering.

Frequently Asked Questions

Is this the same math a doctor or pharmacist would use?

The underlying concepts (half-life, first-order decay, the Bateman equation) are standard pharmacokinetics taught in medical and pharmacy education — but a clinical assessment would also incorporate your actual lab results, medical history, and individual factors this public-data model has no access to.

Why do two tools on this site use slightly different math?

The in-app Estimated Levels feature uses a simpler single-exponential model suited to a lightweight daily view built from your real logged doses. The standalone Half-Life Visualizer uses the more detailed Bateman equation with an absorption phase, better suited to exploring "what if" schedules in detail. Both share the same half-life reference data and the same superposition principle for multiple doses.

Can I trust the exact numbers this produces?

Trust them as a rough, order-of-magnitude estimate for understanding timing and shape — not as a precise or clinical figure. The evidence tag shown for each compound tells you how much confidence the underlying half-life number itself deserves; many research peptides carry a "limited" or "not characterized" tag specifically to avoid overstating what's known.

Why does the model need an absorption half-life at all?

An injected dose isn't instantly present in the bloodstream — it's absorbed from the injection site over some period first. Ignoring this (as a pure elimination-only model does) makes the peak appear instantly at the moment of injection, which isn't realistic. The Bateman equation's absorption phase corrects for that, even though the specific absorption-rate number is usually an estimate rather than a cited figure.

Does a longer half-life mean a compound is "stronger"?

No — half-life describes clearance speed, not potency or effect strength. A compound with a long half-life simply stays present longer and requires less frequent dosing to maintain a steady level; it says nothing about how strong its effect is at any given level.

Where can I see this same methodology applied to a specific compound?

Every entry in the Half-Life Data Table uses this exact framework, and the Half-Life Visualizer lets you apply it to any compound with your own dose and schedule.