Pharmacokinetics
Standard one-compartment model. Each dose adds the full amount, decays exponentially with k = ln(2) / half-life, and total plasma concentration is the sum of all contributions. Useful for seeing when steady state is reached, and how peak-trough swings change with dosing interval.
Decay constant k
0.0289 /hr
half-life 24h
Predicted Css peak
2.00 mg
long-term steady state
Predicted Css trough
1.00 mg
peak-to-trough ratio 2.00x
For sustained-action peptides (semaglutide ~7-day half-life, tirzepatide ~5-day, tesamorelin ~26 minutes IV but rapid receptor binding), steady-state plasma concentration is the relevant target. Once you reach steady state, peak-to-trough fluctuation is small and the receptor sees roughly constant signal.
For pulsatile-action peptides (CJC-1295 without DAC, Ipamorelin), steady state is exactly what you don't want. The receptor desensitizes under continuous exposure; the trick is to dose so plasma rises sharply, triggers the GH pulse, then falls back to baseline before the next dose. Long half-lives blunt this entirely — which is why CJC-1295 with DAC is mechanistically different from plain CJC-1295 despite sharing most of the structure.
BPC-157 has a short circulating half-life but appears to have tissue-specific actions that persist much longer than plasma half-life would predict. The one-compartment model below gives plasma kinetics, not effect duration. Useful approximation for dosing-interval reasoning, not for predicting clinical effect.
Educational only — uses arbitrary mg unit since we don't know volume of distribution. Real clinical PK requires Vd, clearance, bioavailability, and absorption-rate modelling.