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Thymosin alpha-1

Also identified as TA-1, Tα1, Thymalfasin

Thymic peptide

Sequence: 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
3108.3
Molecular formula
C129H215N33O55
Published studies reviewed
5

FOR RESEARCH USE ONLY. NOT FOR HUMAN OR VETERINARY USE. NOT FOR HUMAN CONSUMPTION.

Compounds described on this site are supplied solely for laboratory research. They are not offered for human or veterinary use or for clinical use, and they are not intended to diagnose, mitigate, cure or prevent any disease.

Thymosin alpha-1 (thymalfasin in its synthetic form) is a 28-residue peptide, acetylated at the N-terminus and identical to residues 2 to 29 of human prothymosin alpha; it is a different molecule from thymosin beta-4 and TB-500. Five publications are reviewed: a dendritic-cell signalling study in cells and mice, a pharmacokinetic study in healthy volunteers, and three randomised placebo-controlled trials. Each of those trials reported no statistically significant difference on its primary outcome, and studies pairing the peptide with another agent are excluded.

At a glance

Also identified as
TA-1, Tα1, Thymalfasin
Class
Thymic peptide
Target or mechanism
Toll-like receptor / MyD88 signalling in dendritic cells
Evidence types represented
in vitro, animal, human
Published studies reviewed
5
Regulatory and registry records
4
Last reviewed
2026-09-21

Overview

Thymosin alpha-1 is a 28-residue peptide, acetylated at its N-terminus, identical to residues 2 to 29 of human prothymosin alpha. Thymalfasin is its synthetic form.

⚠️ It is a different molecule from thymosin beta-4 and from TB-500, despite the shared family name. Nothing recorded for either of those applies here.

The publications on this page are one laboratory and mouse study of signalling in dendritic cells, one pharmacokinetic study in healthy volunteers, and three randomised, placebo-controlled trials — in sepsis, in acute necrotising pancreatitis and in chronic hepatitis B.

Each of the three trials reported no statistically significant difference from placebo on its primary outcome. That is the result, and it is printed here as the result. Much of the wider literature gave thymosin alpha-1 together with another agent; those studies are of a combination and are not recorded on this page.

Mechanism under investigation

Thymosin alpha-1
  • Toll-like receptor / MyD88 signalling in dendritic cells

One publication recorded here reports that thymosin alpha-1 induced maturation and interleukin-12 production in dendritic cells through the MyD88-dependent pathway, involving Toll-like receptors, and activated T-helper 1 antifungal immunity in mice. It does not identify a single receptor the peptide binds. The human trials measured clinical outcomes, not mechanism.

Scope of the published work

Areas investigated
  • Dendritic-cell signalling
  • Pharmacokinetics
  • Mortality in sepsis
  • Infected pancreatic necrosis
  • Hepatitis B virological response
Models used
  • Dendritic-cell cultures
  • Mouse transplant model
  • Crossover study in healthy volunteers
  • Randomised human studies

Every human figure on this page was recorded in a controlled study, under supervision, using material prepared for that study, in a population selected by its entry criteria. It is not the research material PepGenex supplies and no result here transfers to it.

Limitations

Evidence represented on this page: in vitro, animal and human. The page reviews 5 published studies, and each figure is reported for the study that published it; results are not pooled across studies.

Common questions

What is Thymosin alpha-1?

Thymosin alpha-1 is a 28-residue peptide, acetylated at its N-terminus, identical to residues 2 to 29 of human prothymosin alpha.

How does Thymosin alpha-1 work, according to the published research?

One publication recorded here reports that thymosin alpha-1 induced maturation and interleukin-12 production in dendritic cells through the MyD88-dependent pathway, involving Toll-like receptors, and activated T-helper 1 antifungal immunity in mice. It does not identify a single receptor the peptide binds. The human trials measured clinical outcomes, not mechanism.

What has published research on Thymosin alpha-1 found, and what are its limits?

This page records 5 publications, reporting laboratory (in vitro) work in 1, animal work in 1, human work in 4. Each is listed with its identifier under References.

Human studies represented: Ke et al., 2022, PMID 35713670; Rost et al., 1999, PMID 10027483; Wu et al., 2025, PMID 39814420; Mutchnick et al., 1999, PMID 10607256.

Evidence represented on this page: in vitro, animal and human.

The page reviews 5 published studies, and each figure is reported for the study that published it; results are not pooled across studies.

Every human figure on this page was recorded in a controlled study, under supervision, using material prepared for that study, in a population selected by its entry criteria. It is not the research material PepGenex supplies and no result here transfers to it.

Is Thymosin alpha-1 approved by the U.S. FDA?

This page cites no FDA approval record for Thymosin alpha-1; PepGenex Science states a U.S. regulatory status only where a sourced record exists.

PepGenex research materials are not FDA approved and are not for human or veterinary use.

What risks have published studies of Thymosin alpha-1 reported?

The human studies recorded on this page include no adverse-event findings among the records published here. That is not evidence that Thymosin alpha-1 carries no risk.

Published research

Grouped by the kind of study. Select one to narrow what is shown below.

Preclinical (animal)(1)

Laboratory (in vitro)Preclinical (animal)

Thymosin alpha 1 activates dendritic cells for antifungal Th1 resistance through toll-like receptor signaling.

Romani L, Bistoni F, Gaziano R, et al., Blood, 2004;103(11):4232-4239

published

  • Reports that thymosin alpha-1 induced functional maturation and interleukin-12 production in dendritic cells exposed to the fungus Aspergillus fumigatus, through the p38 MAP kinase / NF-κB pathway, signalling via the MyD88-dependent pathway and involving distinct Toll-like receptors.
  • In mice that had received haematopoietic transplants, the synthetic peptide activated T-helper 1-dependent antifungal immunity, accelerated myeloid cell recovery and protected against aspergillosis.
Context

The signalling work was done in cell culture and in mice, in a fungal-infection model. It describes a pathway, not a receptor the peptide is shown to bind, and none of the human trials on this page measured it.

View publication →

Human study (phase not stated)(2)

Human study (phase not stated)n = 508

Ke et al., 2022 (title withheld on this site; see the publication record)

Ke L, Zhou J, Mao W, et al.; Chinese Acute Pancreatitis Clinical Trials Group (CAPCTG), Intensive Care Medicine, 2022;48(7):899-909

published

Multicentre, double-blind, randomised, placebo-controlled trial. Participants received thymosin alpha-1 or matching saline placebo over 14 days. The primary outcome was infected pancreatic necrosis during the index admission. 508 were randomised, 254 to each group; 479 (94.3%) required intensive care.

Infected pancreatic necrosis (primary outcome)
Randomised, controlled · Index admission · Adults with predicted severe acute necrotising pancreatitis (APACHE II score of 8 or more, CT severity score of 5 or more), admitted within 7 days of symptom onset
ArmReported
thymosin alpha-140 of 254 (15.7%)
placebo46 of 254 (18.1%)
  • Difference −2.4 percentage points (95% CI −7.4 to 5.1; p = 0.48), and similar across four predefined subgroups. Other major complications did not differ: new-onset organ failure 10.6% vs 15%, bleeding 6.3% vs 3.5%, gastrointestinal fistula 2% vs 2.4%. The authors conclude the peptide did not reduce the incidence of infected necrosis.
View publication →
Human study (phase not stated)n = 9

Rost et al., 1999 (title withheld on this site; see the publication record)

Rost KL, Wierich W, Masayuki F, et al., International Journal of Clinical Pharmacology and Therapeutics, 1999;37(1):51-57

published

Randomised, three-way crossover comparison of three formulations of thymosin alpha-1 — Zadaxin, Timosina and a Hoffmann-La Roche preparation — in nine healthy Caucasian volunteers, with single-dose and multiple-dose pharmacokinetics.

  • Endogenous serum concentrations were below the assay's limit of quantification in most participants. The peptide was well absorbed, reaching peak concentration at 1 to 2 hours with every formulation; peak concentrations of 30 to 80 µg/L and exposure (AUC) of 95 to 267 µg·h/L did not differ between single and multiple doses, consistent with an elimination half-life of under 3 hours. The apparent volume of distribution, 30 to 40 L, suggests distribution within the extracellular volume. Exposure was similar for Zadaxin and the Roche preparation and higher for Timosina.
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Human phase 3(2)

Human phase 3n = 1106

The efficacy and safety of thymosin α1 for sepsis (TESTS): multicentre, double blinded, randomised, placebo controlled, phase 3 trial.

Wu J, Pei F, Zhou L, et al.; TESTS study collaborator group, BMJ, 2025;388:e082583

published; corrected (BMJ 2025;389:r1098)

Multicentre, double-blind, placebo-controlled phase 3 trial at 22 centres in China, September 2016 to December 2020. Participants were randomised 1:1, stratified by age and centre, to thymosin alpha-1 or placebo for seven days, unless stopped earlier by discharge from intensive care, death or withdrawal of consent. The primary outcome was 28-day all-cause mortality.

1,106 adults were randomised (552 to thymosin alpha-1, 554 to placebo); 1,089 formed the modified intention-to-treat set (542 and 547).

All-cause mortality (primary outcome)
Randomised, controlled · Day 28 · Adults aged 18 to 85 with sepsis (sepsis-3 criteria) · Analysis set: Modified intention-to-treat
ArmReported
thymosin alpha-1127 of 542 (23.4%)
placebo132 of 547 (24.1%)
  • Hazard ratio for 28-day mortality, thymosin alpha-1 versus placebo: 0.97 (95% CI 0.76 to 1.24; P = 0.82, log-rank), as corrected after publication. No secondary or safety outcome differed statistically significantly between the groups. The authors conclude there is no clear evidence that thymosin alpha-1 decreases 28-day all-cause mortality in adults with sepsis.
  • In prespecified subgroup analyses, the authors report a potential differential effect by age — hazard ratio 1.67 (1.04 to 2.67) under 60 years and 0.81 (0.61 to 1.09) at 60 or over; P for interaction = 0.01 — and by diabetes — 0.58 (0.35 to 0.99) with diabetes and 1.16 (0.87 to 1.53) without; P for interaction = 0.04.
What this study establishes

Three randomised, placebo-controlled trials in three unrelated conditions, and none separated from placebo on its primary outcome. The largest, TESTS, enrolled 1,106 adults and found 28-day mortality of 23.4% against 24.1%. A null result from an adequately sized trial is a finding, not an absence of one.

Limitations

The subgroup figures point in both directions — a hazard ratio above 1 under age 60, below 1 with diabetes — and the authors describe them as a potential differential effect. Subgroup analyses of a trial that was null overall generate questions; they do not answer them, and neither direction is established by this study.

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Human phase 3n = 97

Mutchnick et al., 1999 (title withheld on this site; see the publication record)

Mutchnick MG, Lindsay KL, Schiff ER, et al., Journal of Viral Hepatitis, 1999;6(5):397-403

published

Phase 3, multicentre, randomised, double-blind, placebo-controlled study. 49 participants received thymosin alpha-1 and 48 received placebo for 6 months, followed by 6 months of observation. The groups were comparable at entry for age, sex, histological grade, aminotransferase and HBV DNA levels.

  • A delayed response (HBV DNA negativity reached after the 12-month study period) was seen in 5 (10%) of the thymosin alpha-1 group and 4 (8%) of the placebo group. In total, 12 (25%) and 6 (13%) showed a sustained loss of HBV DNA with negative HBeAg during or after the study period (P < 0.11, as printed). The authors state that these results do not confirm the efficacy reported in earlier studies.
View publication →

Registered clinical trials

A ClinicalTrials.gov search returned 47 interventional records naming Thymosin alpha-1 as an intervention on 2026-09-24. The 4 listed here were selected to show how the registered research is organised, by phase.

Each entry shows registry fields only, as ClinicalTrials.gov listed them when fetched. None of them reports a result here. Published findings are under Published research, each with its publication.

Phase 1/2

NCT00580450

Official title
Phase I/II Clinical Trial on Thymosin Alfa 1 of Allogeneic Hematopoietic Transplantation
Sponsor
University Of Perugia
Phase
Phase 1/2
Design
Randomized, parallel assignment, open label
Enrollment
9 (estimated)
Status
Unknown
Start
2007-12
Primary completion
2007-12
Study completion
2010-12 (estimated)
Last update posted
2007-12-24
Last verified
2026-09-24

Phase 2

NCT01031966

Brief title
A Pilot Study to Evaluate ZADAXIN's® (Thymalfasin) Ability to Enhance Immune Response to the H1N1sw Influenza Vaccine
Sponsor
sigma-tau i.f.r. S.p.A.
Phase
Phase 2
Design
Randomized, parallel assignment, open label
Enrollment
120 (actual)
Status
Completed
Start
2009-11
Primary completion
2010-05
Study completion
2010-07
Last update posted
2012-03-29
Last verified
2026-09-24

Phase 3

NCT01178996

Brief title
Thymosin Alpha-1 in Combination With Peg-Interferon Alfa- 2a and Ribavirin for the Therapy of Chronic Hepatitis C Nonresponsive to the Combination of IFN and Ribavirin.
Sponsor
sigma-tau i.f.r. S.p.A.
Phase
Phase 3
Design
Randomized, parallel assignment, double-blind
Enrollment
552 (actual)
Status
Completed
Start
2004-12
Primary completion
2008-05
Study completion
2009-07
Last update posted
2010-08-10
Last verified
2026-09-24

Phase 4

NCT02473406 (TRACE)

Official title
Thymosin Alpha 1 in the Prevention of Pancreatic Infection Following Acute Necrotizing Pancreatitis
Sponsor
Weiqin Li
Phase
Phase 4
Design
Randomized, parallel assignment, quadruple-blind
Enrollment
508 (actual)
Status
Completed
Start
2018-03-27
Primary completion
2020-12-24
Study completion
2021-03-24
Last update posted
2021-04-05
Last verified
2026-09-24

References

Published studies reviewed (5)

  1. Thymosin alpha 1 activates dendritic cells for antifungal Th1 resistance through toll-like receptor signaling. — Romani L, Bistoni F, Gaziano R, et al., Blood, 2004;103(11):4232-4239
    DOI 10.1182/blood-2003-11-4036 · PMID 14982877
  2. Rost et al., 1999 (title withheld on this site; see the publication record) — Rost KL, Wierich W, Masayuki F, et al., International Journal of Clinical Pharmacology and Therapeutics, 1999;37(1):51-57
    PMID 10027483
  3. The efficacy and safety of thymosin α1 for sepsis (TESTS): multicentre, double blinded, randomised, placebo controlled, phase 3 trial. — Wu J, Pei F, Zhou L, et al.; TESTS study collaborator group, BMJ, 2025;388:e082583
    DOI 10.1136/bmj-2024-082583 · PMID 39814420 · PMC11780596 · NCT02867267
  4. Ke et al., 2022 (title withheld on this site; see the publication record) — Ke L, Zhou J, Mao W, et al.; Chinese Acute Pancreatitis Clinical Trials Group (CAPCTG), Intensive Care Medicine, 2022;48(7):899-909
    DOI 10.1007/s00134-022-06745-7 · PMID 35713670 · PMC9205279
  5. Mutchnick et al., 1999 (title withheld on this site; see the publication record) — Mutchnick MG, Lindsay KL, Schiff ER, et al., Journal of Viral Hepatitis, 1999;6(5):397-403
    DOI 10.1046/j.1365-2893.1999.00181.x · PMID 10607256

Regulatory and registry records (4)

  1. ClinicalTrials.gov, NCT00580450
    Registry record, phase 1/2. Registry fields only. Retrieved 2026-09-24.
  2. ClinicalTrials.gov, NCT01031966
    Registry record, phase 2. Registry fields only. Retrieved 2026-09-24.
  3. ClinicalTrials.gov, NCT01178996
    Registry record, phase 3. Registry fields only. Retrieved 2026-09-24.
  4. ClinicalTrials.gov, NCT02473406 (TRACE)
    Registry record, phase 4. Registry fields only. Retrieved 2026-09-24.

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