Halveringstidstabel for peptider

Genuine primary human PK exists — but read the identity caveat before applying it to a vial. Attie et al., Muscle Nerve 2013;47(3):416-423 (PMID 23169607) gave 48 healthy postmenopausal women a single subcutaneous dose of 0.02-3 mg/kg and reported a mean t1/2 of 10-15 days, with AUC(0-inf) and Cmax rising linearly with dose. That multi-week persistence is a property of the IgG1-Fc arm and its FcRn recycling, not of the receptor domain — and the Fc arm is what the grey market appears not to be selling. Reichel et al., Drug Testing and Analysis 2025;17(10):1934-1946 (PMID 40312924) ran SDS-/SAR-PAGE, Western blot and mass spectrometry on 14 black-market ACE-031 products: 12 contained full-length human activin receptor IIB (main band ~58.4 kDa) rather than the ActRIIB-IgG1-Fc fusion, with protease treatment confirming the Fc part was absent; one contained follistatin 344 instead; one contained no protein at all. Strip the Fc and the 10-15 day figure has nothing to attach to, so it should not be assumed to describe material bought as ACE-031. Scale is the second caveat: the lowest dose in Attie was 0.02 mg/kg, roughly 1.4mg for a 70kg adult, and the muscle signal (+3.3% total body lean mass by DXA, +5.1% thigh muscle volume by MRI at day 29) appeared only at 3 mg/kg, roughly 210mg — a 1mg vial sits below the smallest dose ever studied in humans. Development stopped for safety, not futility: Campbell et al., Muscle Nerve 2017;55(4):458-464 (PMID 27462804) halted the ambulatory Duchenne trial after the second dosing regimen over epistaxis and telangiectasias, bleeding and vascular signals attributed to broad activin-pathway ligand trapping. No approved product exists in any jurisdiction and the compound is prohibited under WADA List S4.3.

Lancet 2021 Phase 1b: half-life 159-195 h across 0.16-4.5 mg.

Fixed-dose co-formulation. No single half-life applies — the two components clear on their own schedules.

Teichman et al., J Clin Endocrinol Metab 2006: 5.8-8.1 days after single subcutaneous injection. The Drug Affinity Complex binds albumin, producing sustained elevation rather than a pulse.

Two-peptide blend — reported per component. The CJC in these blends is virtually always the no-DAC form, paired with a GHS-R1a agonist to drive a pulse.

Phase 1: half-life 310-366 h across 0.4-12 mg, subcutaneous. Longer than cagrilintide, and the basis for once-weekly dosing.

Cabrales et al., Eur J Pharm Sci 2013: elimination half-life 2.5 ± 1.1 h in nine healthy male volunteers after single IV bolus. Distribution half-life 7.6 min.

Measured, not folklore: Aebi/Assereto/Lauterburg 1991 infused 2 g/m² IV in 10 healthy volunteers and found an elimination half-life of 14.1 +/- 9.2 min (k = 0.063 +/- 0.027 min-1, Vd 176 +/- 107 mL/kg). Two caveats worth carrying: this is the clearance of *exogenous* glutathione from plasma, not the turnover of the endogenous intracellular pool, which is measured in days; and much of the dose is cleaved extracellularly by gamma-glutamyl transpeptidase, with plasma cysteine rising more than tenfold and urinary glutathione excretion roughly 300-fold within 90 minutes. Injected GSH behaves largely as a rapidly cleared cysteine delivery vehicle.

Synthetic GnRH (LHRH) decapeptide. Plasma distribution half-life ~2-10 min, terminal ~10-40 min — rapid endopeptidase degradation is exactly why physiological use is pulsatile. Established human PK.

Gobburu et al., Pharm Res 1999: terminal half-life 2 h after 15-minute IV infusion in healthy male subjects.

The two isoforms differ markedly and should not share a single number. Kisspeptin-54 approximately 27.6 min; kisspeptin-10 approximately 4 min in vivo.

Liraglutide injection label, clinical pharmacology: mean apparent clearance ~1.2 L/h with an elimination half-life of approximately 13 hours after subcutaneous dosing. Tmax 8-12 h, absolute bioavailability ~55%, plasma protein binding >98%, Vd/F ~13 L. One of the few compounds in this catalogue with genuine measured human PK; the 13 h figure is why it is dosed daily on a 0.6-3.0mg escalation rather than weekly, and it should not be compared milligram-for-milligram with the weekly GLP-1 ladder.

Phase 1b MAD trials: 150.9-403.5 h at 3-6 mg; 174.8-1075.7 h at 9-10 mg. The wide upper range likely reflects absorption-rate-limited kinetics rather than true terminal elimination, so a range is more honest than a point estimate.

Two different numbers for two different things. The peptide itself clears with a terminal phase of 0.8-1.7 h. The Scenesse slow-release implant shows an apparent half-life of ~15 h, which reflects the implant release rate, not intrinsic clearance.

FDA label (Pitocin): plasma half-life of about 1 to 6 minutes (IV/IM), decreased in late pregnancy and lactation. Intranasal oxytocin has different and less well-characterised kinetics — do not conflate the two.

FDA label (Vyleesi): mean terminal half-life approximately 2.7 h (range 1.9-4.0 h) after a single subcutaneous dose.

Urva et al., Lancet 2022 (Phase 1b): half-life approximately 6 days, dose-proportional. Investigational; no approved label.

FDA label states an elimination half-life of approximately 1 week (subcutaneous). Oral semaglutide is dosed daily for absorption reasons, not because the molecule clears faster.

FDA-approved Geref label: elimination half-life 11-12 min after IV or subcutaneous dosing. Mean absolute subcutaneous bioavailability approximately 6%.

Deliberately not given as a number. The commonly cited ~6 days is attributed to the Phase I programme (Jungnik 2023), but that full text is paywalled and no open-access source states a figure — only that the PK supports weekly dosing. We publish what is verifiable.

Identity caveat: the only human PK belongs to full-length 43-amino-acid Thymosin β4. What is sold as "TB-500" is often a synthetic 7-mer fragment (Ac-LKKTETQ). These numbers should not be assumed to apply to it.

FDA label: 11 min after a single 1.28 mg subcutaneous dose; 7.8-13.2 min across other presentations. Absolute subcutaneous bioavailability under 4%.

Fixed 2:1 pre-mixed vial (10mg tesamorelin + 5mg ipamorelin) with no pharmacokinetic study of its own — no published human trial has tested this combination at all. Component values only, both from primary human sources: tesamorelin from the FDA Egrifta/Egrifta SV label (11 min after a single 1.28mg subcutaneous dose, 7.8-13.2 min across presentations, absolute subcutaneous bioavailability under 4%), ipamorelin from Gobburu et al., Pharm Res 1999;16(9):1412-1416 (terminal half-life 2 h after a 15-minute IV infusion in healthy male subjects). The roughly tenfold gap matters for a fixed-ratio blend: the GHRH arm has cleared long before the secretagogue arm, so the 2:1 ratio in the powder is not the ratio present in circulation over time. The GHRH-plus-GHRP synergy the blend is sold on is class-level extrapolation (Bowers et al., JCEM 1990), not a measured property of this vial.

Rost et al. 1999: elimination half-life under 3 h after 900 µg/m² subcutaneous dosing. No accumulation on repeat dosing.

FDA label: elimination half-life of approximately 5 days, enabling once-weekly dosing.

Domschke et al., Gut 1978: average disappearance half-time of one minute in healthy volunteers after infusion. Consistent with rapid DPP-IV and neutral endopeptidase degradation.

Animal only. Six human trials were run but none published a numeric human half-life. Rapid clearance is mechanistically consistent for a 16-amino-acid hGH fragment, but any human figure is extrapolation.

No human pharmacokinetic study exists. Rat IV 15.2 min; dog IV 5.27 min. Figures presented elsewhere as settled human data are silent extrapolations from these animal numbers.

Vendor combination with no pharmacokinetic study of its own. Component values only; both component caveats apply.

Rat only, and the source paper is flagged. The 12.68 d IV / 8.83 d IP serum half-lives come from McCoy et al., J Pharmacol Exp Ther 2013;344:141-154, which carries a 2021 Notice of Concern from the journal (J Pharmacol Exp Ther 2021;378:313) following the Washington State University misconduct investigation into co-author Leen Kawas; the sibling 2014 HGF/c-Met mechanism paper (JPET 351:390-402) was fully retracted in April 2025. No human pharmacokinetic study and no human trial exists. Vendor and nootropic copy repeats '12.8 days' as though it were an established human figure, and some pages also float an unsourced 'oral half-life of 2-3 hours' with no paper behind it at all.

Blend with no pharmacokinetic study of its own. Typically GHK-Cu + BPC-157 + TB-500; one of the three components has no half-life data at all.

No human PK. Boghen et al., Peptides 1995: 120 min terminal half-life in dogs. Human studies report GH pharmacodynamics only. The "~55 min" and "~70 min" human figures circulating online appear to conflate the GH response curve with drug clearance.

Blend with no pharmacokinetic study of its own. Typically GHK-Cu + BPC-157 + TB-500 + KPV; two of the four components have no half-life data at all.

Rodent only. No human pharmacokinetic or dosing study exists; human evidence is limited to functional imaging work with no blood levels.

Rodent only: rapid brain penetration and fast blood clearance. No human concentration-time study exists; human evidence is older EEG and clinical-effect work.

Important distinction: this is an ex-vivo enzymatic degradation rate from brain homogenate, not a measured plasma half-life. No controlled human dosing PK study exists. The "7-8 min plasma half-life" seen online is a distortion of this figure.

This is CJC-1295 WITHOUT DAC (Mod GRF 1-29). No dedicated human PK trial exists for the no-DAC form; ~30 min is a consensus estimate. Critically, the published human trials bearing the name "CJC-1295" tested the DAC form only and must not be cited here — that is how a 30-minute peptide ends up mislabelled with an 8-day half-life.

DES(1-3) IGF-1 lacks the first three N-terminal residues, reducing IGFBP binding while keeping a short systemic half-life — studied for potent, local, short-lived action. No human elimination half-life is established; the ~20-30 min figure is an estimate.

The Long R3 modification (Arg3 substitution plus a 13-residue N-terminal extension) sharply reduces binding to IGF-binding proteins, greatly extending action versus native IGF-1 (~10-20 min). No elimination half-life has been measured in humans; the ~20-30 h figure is an estimate from the reduced IGFBP binding.

No dedicated PK study exists for PDA. It is the arginate-salt form of BPC-157 — the same pentadecapeptide sequence — so its clearance is expected to mirror BPC-157 (rat IV ~15 min). There is no human data, and the "more stable than BPC-157" claim is a vendor position, not established fact.

ARA-290 (cibinetide) is an 11-amino-acid Helix-B surface peptide derived from erythropoietin. It is non-erythropoietic and cleared rapidly; a precise validated human half-life for the research peptide is not established here.

No measured half-life exists for Acetyl Hexapeptide-8 in any species. It is a topically applied cosmetic peptide with no published pharmacokinetic study — the 2025 IJMS review of AH-8 skin permeability and efficacy (PMC12193160) contains no PK data at all, and no regulatory label exists because it is a cosmetic ingredient, not a drug. Percutaneous penetration data are contradictory (roughly 30% into the stratum corneum in 2h in one study vs 0.22% over 24h in Kraeling et al., with nothing reaching the receptor fluid), so even a skin residence estimate is unsupported. The peptide web widely repeats a '~4 hour topical half-life' figure, propagated by dosing-calculator sites and vendor pages; it traces to no primary source and should not be used.

No in-vivo pharmacokinetic study exists, human or animal. The "~30 min" and "~3 h" figures in circulation are inferences from generic "short linear tetrapeptides degrade quickly" reasoning, not measurements.

No established human elimination half-life for the injected FST-344 isoform as a research peptide. Endogenous follistatin turnover is rapid, but a dedicated PK figure for the sold compound is not published.

FOXO4-DRI is a D-retro-inverso peptide designed to disrupt the FOXO4-p53 interaction in senescent cells. No established human elimination half-life; the D-amino-acid backbone resists proteases, but no validated human PK figure exists.

In no species. Figures quoted online span 1 minute to 4 hours — a spread that is itself evidence none of them trace to a real study. The frequently repeated "25-35 min" appears in no journal.

Despite approval in Japan as a diagnostic agent, no published human plasma PK study reports a measured elimination half-life. Good pharmacodynamic data exists (GH peaks 15-30 min post-dose) but a hormone response curve is not a drug half-life — conflating the two is where the circulating "15-30 min" figure comes from.

The raw C-terminal fragment (residues 176-191 of GH) has no established human elimination half-life; the widely-quoted "~30 min" figure traces to no dedicated pharmacokinetic study. The stabilised analog AOD-9604 is the version that reached human trials.

Humanin is a mitochondrial-derived peptide (MDP). No established human elimination half-life for the native peptide or the potent S14G analog (HNG); reported figures are model-dependent and not from a validated human PK study.

No pharmacokinetic study exists in any species. The primary literature covers PepT1-mediated uptake and colitis efficacy, not plasma kinetics.

Real human trials exist but they are topical wound-healing studies reporting no plasma half-life. The widely cited "90-120 min" murine radiolabel study does not appear to exist.

No human pharmacokinetic study exists; the 1996 Phase I trial reports tanning and adverse effects but no PK parameters. The circulating "30-60 min" (and a garbled "33 hours") have no traceable source.

MGF (IGF-1Ec) is a mechanically-induced splice variant of IGF-1 with a very short systemic half-life (minutes) — it acts locally on muscle satellite cells. No elimination half-life is established; the pegylated form (PEG-MGF) is the systemic version.

No concentration-time study exists in any species — not even in rodents. The functional and metabolic papers report no half-life. The circulating "30-60 min" has no source.

Not a meaningful quantity here. NAD+ is an endogenous coenzyme, continuously synthesised, salvaged and consumed — not a xenobiotic cleared by a single pathway. The one controlled human IV study explicitly did not establish an elimination half-life.

P21 (P021, Ac-DGGL(A)G-NH2) is a CNTF-derived tetrapeptide with a C-terminal adamantylated glycine, developed in Khalid Iqbal's lab at the NYS Institute for Basic Research. It is not Cerebrolysin-derived; the association comes from EVER Neuro Pharma's involvement in its stability characterisation. No in-vivo pharmacokinetic study exists in any species and there are no human trials, so no elimination half-life has ever been measured. The 'over 3 hours' figure repeated across vendor pages (with drifted variants of '2-4 hours' and '4-6 hours') is an ex-vivo plasma-stability incubation reported alongside artificial gastric/intestinal fluid stability in Kazim et al. 2014 (Neurobiol Dis 71:110-130) - a degradation endpoint, not a clearance rate. We render 'Not established' rather than launder it.

Pegylation extends MGF systemic stability from minutes to a longer window, but no elimination half-life has been measured. The widely-repeated "days" figure traces to no study and is not published here as a measured value.

Pinealon is the EDR tripeptide (Glu-Asp-Arg), a Khavinson short-peptide brain bioregulator. No established human elimination half-life; short peptides of this class are cleared quickly but no dedicated PK figure is published.

Not applicable. SNAP-8 is a topical cosmetic ingredient and was never developed as a systemic drug, so no half-life exists or would be meaningful. Published data covers percutaneous penetration only.

This one is genuinely surprising. Elamipretide has an FDA label (Forzinity, 2025) and that label does not state an elimination half-life. What it does give: Tmax 0.5-1 h, absolute subcutaneous bioavailability approximately 92%, near-complete urinary recovery by 48 h. The widely repeated "~4 h" appears nowhere in it.

Thymalin is a polypeptide fraction extracted from thymus tissue (Khavinson bioregulator tradition), not a single defined sequence, so no single elimination half-life applies or has been established.