Also known as: thymalfasin · Zadaxin · Tα1 · TA1
| Parameter | Value | Source |
|---|---|---|
| Elimination Half-Life (SC) | ~2 hours | Goldstein AL, Garaci E. PMID 17934061 |
| Tmax (SC) | ~30–60 min | Human PK data, PMID 17934061 |
| Route(s) of Administration | Subcutaneous injection | — |
| Plasma Protein Binding | No published data | — |
| Time to Steady State | ~10 h with repeat dosing (5× t½) | Calculated |
| Full Clearance (5 half-lives) | ~10 hours | Calculated from PMID 17934061 t½ |
| Standard Dosing Frequency | 1.6 mg SC twice weekly (in approved markets) | Zadaxin prescribing information |
| Data Quality | Human PK Study — Goldstein AL, Garaci E. Ann N Y Acad Sci. 2007. PMID 17934061 | |
Thymosin Alpha-1 (thymalfasin) has a plasma elimination half-life of approximately 2 hours after subcutaneous injection, based on human pharmacokinetic data.[1] The peptide is a 28 amino acid sequence (molecular weight ~3,108 Da) originally isolated from thymic tissue by Allan Goldstein's laboratory. It is cleared primarily by proteolytic degradation with no single organ dominating clearance — consistent with the rapid decay observed after SC injection.
This ~2-hour half-life places Thymosin Alpha-1 among immunomodulatory peptides with rapid plasma clearance but sustained downstream biological effects — a pharmacokinetic–pharmacodynamic dissociation central to understanding its dosing rationale.
Published human PK data characterizes the plasma concentration-time profile after SC injection of the 1.6 mg dose used in approved indications. The concentration-time curve follows a two-compartment model with a distribution phase followed by terminal elimination. The ~2-hour half-life is derived from the slope of the log-linear decay of the terminal elimination phase.[1]
Thymosin Alpha-1's ~2-hour plasma half-life describes circulation clearance only. Immunological effects — enhanced T-cell maturation, increased CD4+ lymphocyte counts, upregulated interleukin-2 and interferon-gamma production, and augmented NK cell cytotoxicity — operate through gene expression changes and cell differentiation programs that take days to weeks to manifest and persist well beyond plasma clearance.[1][2] Plasma t½ governs dosing interval; it does not predict effect duration.
After the last subcutaneous dose, plasma Thymosin Alpha-1 reaches pharmacologically negligible levels (~3% of Cmax) within approximately 10 hours — five half-lives of the ~2-hour t½.
| Half-Lives Elapsed | Time After Last Dose | % Remaining in Plasma | Clinical Note |
|---|---|---|---|
| 1 | ~2 hours | 50% | Peak immune-signaling window |
| 2 | ~4 hours | 25% | Receptor signaling still active |
| 3 | ~6 hours | 12.5% | Rapid plasma decline; immune cascades ongoing |
| 4 | ~8 hours | 6.25% | Near-complete plasma clearance |
| 5 (clinical clearance threshold) | ~10 hours | ~3% | Pharmacologically negligible plasma level |
Biological effect duration is much longer than plasma half-life. T-cell maturation programs initiated by Thymosin Alpha-1's interaction with dendritic cells and thymocytes can persist for days to weeks, which is why twice-weekly dosing is clinically effective despite the 2-hour plasma t½.[1]
The approved clinical dose of 1.6 mg SC twice weekly reflects immunological biology, not PK trough maintenance. Thymosin Alpha-1 binds to Toll-like receptor 9 (TLR9) on plasmacytoid dendritic cells and promotes T-helper cell differentiation cascades. Once these cascades are initiated, they proceed independently of plasma drug concentration. The twice-weekly schedule provides sufficient receptor engagement while allowing immune response intervals between doses.[1][2]
Because plasma clearance occurs within ~10 hours, a missed dose does not affect steady-state levels in the conventional pharmacokinetic sense — there is no meaningful inter-dose accumulation with the twice-weekly schedule. Missing a single dose delays the next immune-signaling stimulus by 3–4 days rather than creating a PK trough problem.
| Compound | Half-Life | Mechanism | Dosing Frequency | Approval Status |
|---|---|---|---|---|
| Thymosin Alpha-1 (Zadaxin) | ~2 hours (SC) | TLR9 / T-cell maturation | 1.6 mg SC twice weekly | Not FDA-approved; Zadaxin approved 35+ countries |
| TB-500 (thymosin β4 analogue) | ~30–60 min (SC, estimated) | Actin sequestration / VEGF | 2–5 mg SC weekly | Not FDA-approved |
| BPC-157 | <30 min (SC) | Angiogenesis / VEGF / NO signaling | 250–500 µg SC daily | Not FDA-approved |
| Route | Half-Life | Bioavailability | Tmax | Notes |
|---|---|---|---|---|
| Subcutaneous | ~2 hours | High (exact % not published) | ~30–60 min | Standard route in all clinical studies |
| Intravenous | Shorter (no published human comparison) | 100% | Immediate | Reference route; not used clinically |
| Intramuscular | No published data | No published data | No published data | Not a studied or approved route |
| Oral | Not viable | <1% estimated | — | Proteolytic GI degradation; oral route not viable |
Thymosin Alpha-1 is not included in standard WADA or workplace drug screening panels. The peptide has no psychoactive or abuse potential that would trigger inclusion in standard panels.
Specialized LC-MS/MS can detect peptides in the 3,000 Da molecular weight class in biological samples. No published forensic detection window study characterizing the urinary detection window for Thymosin Alpha-1 specifically has been identified in PubMed-indexed literature. Given the ~2-hour plasma half-life and proteolytic clearance, detectable levels in urine without specialized validated assays would be expected to be limited to a narrow post-dose window of a few hours.
Thymosin Alpha-1 is a 28 amino acid peptide with an N-terminal acetyl group (Ac-Ser-Asp-Ala-Ala-Val-Asp-Thr-Ser-Ser-Glu-Ile-Thr-Thr-Lys-Asp-Leu-Lys-Glu-Lys-Lys-Glu-Val-Val-Glu-Glu-Ala-Glu-Asn), molecular weight ~3,108 Da.[1] Its small size makes it susceptible to renal filtration and plasma protease degradation. Unlike larger biologics, it lacks albumin binding, FcRn recycling, or PEGylation that would extend half-life.
The N-terminal acetylation provides partial protection against aminopeptidase cleavage, contributing modestly to the 2-hour stability relative to the seconds-to-minutes range of unmodified peptides. The compound is cleared primarily by distributed proteolytic degradation across multiple tissues — no single organ dominates clearance.[2]
The absence of structural modifications to extend t½ is intentional: the immunological mechanism does not require sustained plasma exposure. Thymosin Alpha-1 acts as a signal initiator rather than a continuous agonist, making the 2-hour t½ mechanistically appropriate for the twice-weekly dosing paradigm used clinically.
Log Thymosin Alpha-1 doses, track injection timing, and monitor your protocol against the ~2-hour plasma half-life curve. On-device, no account required.
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