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Thymosin Alpha-1 Clinical Evidence Review

Thymosin alpha-1 (Ta1) is one of the most clinically tested peptides in existence. More than 11,000 subjects have been enrolled in over 30 clinical trials. Post-marketing surveillance covers more than 600,000 treated patients.

Thymosin alpha-1 (Ta1) is one of the most clinically tested peptides in existence. More than 11,000 subjects have been enrolled in over 30 clinical trials. Post-marketing surveillance covers more than 600,000 treated patients. Its synthetic form, thymalfasin (brand name Zadaxin), has been approved in more than 35 countries for treating hepatitis B and C and as an immune-modulating therapy.

And yet, the clinical evidence tells a complicated story.

Some conditions show clear benefit. Others show mixed or null results from large, well-designed trials. Understanding where Thymosin Alpha-1 actually works — and where it falls short — requires looking at the specific studies, their designs, and what the data actually shows rather than relying on summary claims.

This article reviews the clinical evidence across the major conditions where Ta1 has been tested: viral hepatitis, cancer, sepsis, COVID-19, and immune deficiency syndromes.


Table of Contents


What Thymosin Alpha-1 Is and How It Works

Thymosin alpha-1 is a 28-amino acid peptide originally isolated from the thymus gland — the organ behind your breastbone that trains immune cells during childhood and gradually shrinks with age. The peptide was first identified by Allan Goldstein at George Washington University in the 1970s as part of "thymosin fraction 5," a mix of immunologically active peptides extracted from bovine thymus tissue [1].

The synthetic version, thymalfasin, is chemically identical to the natural human peptide. It's typically administered as a subcutaneous injection at 1.6 mg doses.

Mechanism of Action

Ta1 works through several interconnected immune pathways:

Toll-like receptor activation. Ta1 binds to multiple toll-like receptors (TLR2, TLR3, TLR4, TLR7, TLR9) on immune cells. This activates downstream signaling through NF-kappa-B and IRF3 pathways, stimulating immune cell proliferation and activation [2].

Dendritic cell maturation. Ta1 promotes functional maturation of dendritic cells — the "professional antigen-presenting cells" that prime your adaptive immune system. It does this by signaling through the MyD88-dependent pathway and the p38 MAPK/JNK pathway, triggering IL-12 production and driving Th1 immune responses [3].

T cell differentiation and maturation. This is the most established mechanism. Ta1 promotes maturation of CD34+ stem cells into CD3+4+ T cells and increases CD4+, CD8+, and CD3+ cell populations. It stimulates production of Th1 cytokines like interferon-gamma and interleukin-2 [1].

NK cell activation. Ta1 activates natural killer cells and boosts their cytotoxic function against infected or abnormal cells [1].

Macrophage polarization. Recent research found that Ta1 can push tumor-associated macrophages from the immunosuppressive M2 type to the pro-inflammatory M1 type, potentially reversing tumor-driven immune suppression [4].

Immune TargetTa1 Effect
Toll-like receptorsActivates TLR2, 3, 4, 7, 9
Dendritic cellsMaturation, IL-12 production
CD4+ T cellsIncreased count and function
CD8+ T cellsIncreased count and cytotoxicity
NK cellsActivation, increased killing
MacrophagesM2 to M1 polarization
CytokinesIncreases IFN-gamma, IL-2

For a broader look at immune-supporting peptides, see our guide on the best peptides for immune support.


Hepatitis B: The Strongest Clinical Evidence

Chronic hepatitis B affects an estimated 296 million people worldwide. Ta1 has been tested in multiple randomized controlled trials for this condition, producing some of the strongest clinical data in its research history.

The Phase III Multicenter Trial (Mutchnick et al., 1999)

This was the gold-standard trial — multicenter, double-blind, placebo-controlled. Ninety-seven patients with HBV DNA-positive and HBeAg-positive chronic hepatitis B received either Ta1 or placebo [5].

Results:

  • Sustained HBV DNA loss with negative HBeAg: 25% (Ta1) vs. 13% (placebo) — not statistically significant (P < 0.11)
  • Complete virological response: 14% (Ta1) vs. 4% (placebo) (P = 0.084)

The trial technically failed to reach statistical significance, though the trends favored Ta1. The relatively small sample size (n=97) may have been insufficient to detect a real but modest effect.

The Chang Gung Memorial Hospital Trial (Chien et al., 1998)

This randomized controlled trial enrolled 98 chronic hepatitis B patients into three groups: 26-week Ta1 treatment, 52-week Ta1 treatment, and untreated controls. Follow-up continued for 18 months [6].

Results:

GroupComplete Virological Response (18 months)
26-week Ta140.6%
52-week Ta126.5%
Untreated controls9.4%

Two notable findings emerged. First, the 26-week course outperformed the 52-week course, which was unexpected. Second, virological response continued to accumulate gradually after treatment ended — a pattern distinct from most antiviral therapies. Blinded liver biopsy assessment showed significant improvement in lobular necroinflammation. No significant side effects were observed.

Head-to-Head Against Interferon Alpha

Multiple trials compared Ta1 directly against interferon-alpha, the standard of care. In a study by You et al., 62 chronic hepatitis B patients were randomized to either Ta1 (1.6 mg twice weekly) or IFN-alpha for six months [7].

Results:

  • Ta1 gradually induced more sustained ALT normalization and HBV DNA/HBeAg loss
  • Ta1 was substantially better tolerated (only injection site discomfort vs. flu-like symptoms, fatigue, headache, and leucopenia with interferon)
  • Response rate with Ta1: 48.3% — effective but "less than ideal"

A meta-analysis of these head-to-head trials confirmed that Ta1 was as effective as interferon-alpha for HBeAg-negative chronic hepatitis B, with far fewer side effects [8].

This open-label RCT enrolled 120 patients with HBV-related acute-on-chronic liver failure (ACLF) — a much more severe condition — from 2017 to 2019 [9].

Results:

OutcomeTa1 GroupStandard Therapy
90-day transplant-free survival75.0%53.4% (P = 0.030)
New infections32.1%58.6% (P = 0.005)
Hepatic encephalopathy8.9%24.1% (P = 0.029)
Mortality from severe infection8.9%24.1% (P = 0.029)

This was perhaps the most striking hepatitis B result for Ta1, showing a 22-percentage-point improvement in transplant-free survival for patients with the most severe form of the disease.


Cancer: Adjuvant Immunotherapy Evidence

Ta1 has been studied as a cancer treatment adjunct — not as a standalone therapy, but as an immune system booster given alongside chemotherapy, radiation, or newer immunotherapies. The FDA granted orphan drug designation for thymalfasin in malignant melanoma and hepatocellular carcinoma.

Hepatocellular Carcinoma (HCC)

Because HCC develops primarily in patients with chronic hepatitis B and C — conditions where Ta1 has known activity — the peptide has a natural application here.

Several pilot studies showed that adding Ta1 to treatment after liver tumor resection significantly prolonged overall survival and time to tumor recurrence. In advanced HCC, combining Ta1 with the kinase inhibitor sorafenib increased median survival time and improved immune parameters [10].

More recent research (2024-2025) has examined Ta1 combined with modern immunotherapy:

  • A retrospective study found that Ta1 combined with lenvatinib plus sintilimab was effective and safe in unresectable HCC [10]
  • A prospective study of 273 patients at Tongji Hospital examined Ta1 plus anti-PD-1 antibodies after hepatectomy, comparing recurrence-free survival and overall survival against anti-PD-1 alone [10]

The theory: Ta1 may amplify the effects of checkpoint inhibitors by improving dendritic cell function and T cell activation — essentially priming the immune system to respond better to PD-1/PD-L1 blockade.

Melanoma

Clinical investigation of Ta1 in melanoma spans multiple decades:

Phase II trials tested Ta1 with dacarbazine (with or without interferon-alpha) for stage 4 melanoma. Danielli et al. (2018) studied Ta1 combined with immune checkpoint antibodies in metastatic melanoma, reporting no adverse effects and follow-up exceeding 4 years [11].

A retrospective analysis by Danielli et al. compared melanoma patients who received Ta1 before CTLA-4 inhibitor treatment versus those who did not. Patients primed with Ta1 showed improved response to CTLA-4 inhibitors — suggesting Ta1 may function as an immune primer that makes subsequent immunotherapy more effective [11].

Preclinical work supports this: in B16 melanoma mouse models, Ta1 increased T cell responses and showed antitumor activity against both experimental and spontaneous metastasis [11].

The Broader Cancer Picture

A 2019 review in Frontiers in Oncology noted three possible mechanisms for Ta1's cancer activity [4]:

  1. Direct effect on tumor cells — including macrophage polarization from M2 to M1
  2. Immune priming — preparing the immune system to respond better to chemo- and immunotherapy
  3. Immune maintenance — sustaining long-term immunological protection against recurrence

While these mechanisms are plausible and supported by pilot data, large-scale randomized trials proving survival benefits in cancer remain limited. Most evidence comes from retrospective analyses and small prospective studies.


Sepsis: The TESTS Trial and What It Showed

Sepsis — the body's overwhelming immune response to infection — was considered a strong candidate for Ta1 therapy. Earlier small-scale trials and a large single-blinded RCT from China showed promising results. Then came the definitive trial.

The TESTS Trial (BMJ, January 2025)

The TESTS trial (The Efficacy and Safety of Thymosin alpha-1 for Sepsis) was a multicenter, double-blinded, placebo-controlled phase 3 trial conducted at 22 centers in China from 2016 to 2020 [12].

Design:

  • 1,106 adults aged 18-85 with sepsis (Sepsis-3 criteria)
  • Randomized 1:1 to Ta1 or placebo
  • Subcutaneous injection every 12 hours for seven days
  • Primary outcome: 28-day all-cause mortality

Results:

OutcomeTa1 Group (n=536)Placebo Group (n=553)P-value
28-day mortality23.4%24.1%0.93
Hazard ratio0.99 (95% CI: 0.77-1.27)

No significant difference in any outcome. Ta1 did not reduce mortality in the overall sepsis population.

But the Subgroup Data Was Interesting

Prespecified subgroup analyses revealed potential differential effects [12]:

SubgroupHazard Ratio95% CI
Age < 60 years1.671.04 - 2.67 (worse)
Age >= 60 years0.810.61 - 1.09 (trend toward benefit)
With diabetes0.580.35 - 0.99 (significant benefit)
Without diabetes1.160.87 - 1.53

P-value for interaction (age): 0.01

The pattern suggested that Ta1 might actually harm younger sepsis patients while potentially benefiting older patients and those with diabetes. This is biologically plausible — older and diabetic patients tend to have weaker baseline immune function, which Ta1 could help restore, while younger patients with sepsis may already have excessive immune activation that Ta1 could worsen.

2025 Meta-Analysis

A systematic review in Frontiers in Cellular and Infection Microbiology pooled data from 11 RCTs [13]:

  • 28-day mortality: 24.1% (Ta1) vs. 26.8% (control) — HR 0.88 (95% CI: 0.72-1.08), not statistically significant
  • Subgroup benefits confirmed: Septic patients with cancer (HR 0.59), diabetes (HR 0.64), and coronary heart disease (HR 0.56) showed significant improvement
  • But: Trial sequential analysis showed the evidence remains inconclusive, and results from multi-center, high-quality studies did not match the pooled findings

What This Means

The sepsis evidence points toward a potentially important lesson for peptide therapeutics: broad, unselected patient populations may not benefit, but specific subgroups — particularly older or immunocompromised patients — might. The field appears to be moving toward personalized immunomodulation rather than one-size-fits-all approaches.


COVID-19: Conflicting Results

Ta1 was widely used during the COVID-19 pandemic, particularly in China. The resulting clinical data is a case study in why observational studies can mislead.

The Positive Study: Liu et al. (2020)

An early retrospective study of 76 severe COVID-19 cases in Wuhan found that Ta1 treatment significantly reduced mortality: 11.1% vs. 30.0% (P = 0.044). The proposed mechanism was restoration of lymphocyte counts and reversal of T cell exhaustion [14].

This study generated significant enthusiasm for Ta1 as a COVID-19 treatment.

The Negative Studies

Subsequent, larger studies told a different story:

Multicenter cohort study (Frontiers in Immunology, 2021): Across five hospitals in Hubei province, all crude outcomes — mortality, intubation rate, ARDS incidence, ICU length of stay — were significantly worse in the Ta1 group. After adjusting for disease severity, Ta1 was associated with a higher non-recovery rate (OR 1.5, 95% CI 1.1-2.1, P = 0.028). However, when SOFA scores were included in the adjustment model, the association became non-significant — suggesting sicker patients were more likely to receive Ta1 [15].

Multicenter study of critically ill patients (Sun et al., 2021): Among 771 patients, 28-day mortality appeared lower in the Ta1 group (41.3% vs. 60.6%, P < 0.001). But after propensity score matching to account for baseline differences, mortality was nearly identical: 51.0% vs. 52.9%, no significant difference [16].

Systematic Review and Meta-Analysis (2022)

A pooled analysis of 9 studies encompassing 5,352 patients found that Ta1 had no statistically significant effect on mortality: RR 1.03 (95% CI: 0.60-1.75, P = 0.92, I-squared = 90%) [17].

The extremely high I-squared value (90%) reflects massive heterogeneity across studies — the results were wildly inconsistent.

Lessons from the COVID-19 Data

StudyNFindingKey Issue
Liu et al. (2020)76Mortality reducedSmall sample, retrospective
Multicenter cohort (2021)2,282Worse outcomes (raw)Confounding by indication
Sun et al. (2021)771No benefit after matchingPropensity score matching
Meta-analysis (2022)5,352No effectI-squared = 90%

The COVID-19 data illustrates a common problem in observational research: confounding by indication. Sicker patients received Ta1, so it appeared the drug caused worse outcomes when in reality the drug was being given to patients who were already doing worse. Once researchers controlled for disease severity, the apparent harm vanished — but so did any benefit.


Other Clinical Applications

DiGeorge Syndrome

Ta1 received FDA orphan drug designation for DiGeorge syndrome, a genetic condition involving thymic hypoplasia and resulting immune deficiency. This is perhaps the most biologically logical application of a thymic peptide — replacing what the body cannot produce [1].

Vaccine Boosting

In immunocompromised populations — including elderly patients and those on immunosuppressive therapy — Ta1 has been studied as a vaccine adjuvant to improve antibody responses. The rationale: if Ta1 boosts T cell function, it should improve vaccine-generated immunity in people whose immune systems respond poorly [1].

Autoimmune Conditions

Ta1's ability to promote regulatory T cells (Tregs) alongside Th1 responses suggests potential in autoimmune conditions. The peptide appears to balance inflammation rather than simply amplifying it. For more on this topic, see our guide on the best peptides for autoimmune conditions.

Severe Acute Pancreatitis

A 2025 meta-analysis examined Ta1 in severe acute pancreatitis and found insufficient evidence to support a beneficial therapeutic effect, though individual studies showed some improvements in infection rates and inflammatory markers [18].


Safety Profile Across All Trials

If there is one area where the clinical evidence is unambiguous, it's safety. Across all conditions studied, Ta1 has an exceptionally clean safety record.

Key safety data points:

  • Over 11,000 subjects in clinical trials with no significant harm reported [19]
  • Post-marketing surveillance of 600,000+ treated patients confirms excellent tolerability [19]
  • Most common adverse effect: local irritation, redness, or discomfort at injection site
  • Rare side effects in combination with interferon-2b: fever, fatigue, muscle aches, nausea, neutropenia (attributable to interferon rather than Ta1)
  • No evidence of immune overstimulation or autoimmune reactions

This safety profile is notable because many immune-modulating drugs carry significant risks. Interferon-alpha, the comparator in hepatitis trials, causes flu-like symptoms, fatigue, depression, and blood count changes. Checkpoint inhibitors used in cancer can trigger serious autoimmune reactions. Ta1 does neither.


Regulatory Status and Access

Ta1's regulatory history is complex:

  • Approved in 35+ countries for hepatitis B/C treatment and immune support
  • FDA orphan drug designation for melanoma, hepatitis B, DiGeorge syndrome, and hepatocellular carcinoma
  • FDA restriction (2023): Included in a list of peptides restricted from commercial compounding pharmacies in the United States
  • Still available in many countries outside the US, and remains a subject of active clinical research

The FDA restriction was part of a broader action affecting multiple peptides and was controversial within the medical community, given Ta1's established safety record and the volume of clinical data supporting its use [19].


Clinical Evidence Summary Table

ConditionEvidence LevelKey FindingLargest Trial
Chronic Hepatitis BModerate-StrongEffective; delayed sustained response; better tolerated than IFNn=98 (Chien)
HBV Acute-on-Chronic Liver FailureModerate75% vs. 53% transplant-free survivaln=120
Hepatocellular CarcinomaModerateImproves survival as adjuvant therapyMultiple pilot studies
MelanomaLow-ModerateMay prime response to checkpoint inhibitorsPhase II trials
Sepsis (unselected)Strong (null)No mortality benefit (TESTS trial)n=1,106
Sepsis (elderly/diabetic)ModeratePossible subgroup benefitSubgroup of n=1,106
COVID-19Weak (conflicting)No clear benefit after confounding controlMeta: n=5,352
DiGeorge SyndromeLow (orphan)Biologically logical; limited dataSmall studies
SafetyStrongExcellent across all populations600,000+ patients

FAQ

What conditions has thymosin alpha-1 been tested for in clinical trials?

Ta1 has been tested in clinical trials for chronic hepatitis B, hepatitis C, HIV, hepatocellular carcinoma, melanoma, non-small cell lung cancer, sepsis, COVID-19, DiGeorge syndrome, severe acute pancreatitis, and as a vaccine adjuvant in immunocompromised patients. The strongest clinical evidence supports its use in chronic hepatitis B.

Does thymosin alpha-1 work for sepsis?

The largest and best-designed trial to date — the TESTS trial with 1,106 patients — found no mortality benefit for unselected sepsis patients. However, subgroup analyses suggest potential benefits for older patients (age 60+) and those with diabetes. The field is shifting toward studying Ta1 in specific immunocompromised subpopulations rather than all sepsis patients.

Is thymosin alpha-1 safe?

Yes, by the standards of immune-modulating drugs. Over 11,000 clinical trial subjects and 600,000+ post-marketing patients have been monitored, with no significant adverse effects. The most common side effect is injection site discomfort. Ta1 is substantially better tolerated than interferon-alpha, the other major immune therapy it has been compared against.

How does thymosin alpha-1 compare to other immune-modulating peptides?

Ta1 is distinct from peptides like LL-37, which is primarily antimicrobial, or BPC-157, which focuses on tissue healing. Ta1's primary action is immune system modulation — particularly T cell maturation, dendritic cell activation, and NK cell function. For a comparison of immune-supporting peptides, see our best peptides for immune support guide.

Why was thymosin alpha-1 restricted by the FDA?

In 2023, the FDA included Ta1 in a list of peptides restricted from commercial compounding pharmacies in the United States. This was part of a broader regulatory action and remains controversial given Ta1's clinical safety record and approval in 35+ countries. The peptide is still available in many countries and continues to be studied in clinical trials.

Can thymosin alpha-1 be combined with cancer immunotherapy?

Early evidence suggests Ta1 may improve responses to immune checkpoint inhibitors (anti-PD-1 and anti-CTLA-4 antibodies). Retrospective data in melanoma showed improved outcomes when Ta1 was given before CTLA-4 inhibitor therapy. Prospective studies combining Ta1 with anti-PD-1 antibodies in hepatocellular carcinoma are ongoing. This combination approach is based on Ta1's ability to mature dendritic cells and prime T cell responses.

What is the typical dosing for thymosin alpha-1?

In clinical trials, the standard dose is 1.6 mg administered subcutaneously. For hepatitis B, dosing is typically twice weekly for 26 weeks. For sepsis trials, dosing was every 12 hours for seven days. For cancer adjuvant therapy, various schedules have been used alongside chemotherapy or immunotherapy regimens.


The Bottom Line

Thymosin alpha-1 has one of the largest clinical evidence bases of any peptide therapeutic — and that evidence paints a nuanced picture.

The hepatitis B data is the most convincing. Multiple trials show that Ta1 produces delayed but sustained virological responses, improves liver histology, and matches interferon-alpha effectiveness with far fewer side effects. The ACLF trial showing a 22-point improvement in transplant-free survival is particularly compelling.

In cancer, Ta1 shows the most promise not as a standalone treatment but as an immune primer — a therapy that makes other treatments (particularly checkpoint inhibitors) work better. The melanoma and HCC data supports this concept, though large randomized trials are still needed.

The sepsis and COVID-19 data is where honest evaluation matters most. Despite biological plausibility and encouraging early studies, the best-designed trials showed no benefit in unselected populations. The subgroup signals — potential benefit in elderly and diabetic sepsis patients — are worth pursuing but haven't been confirmed in dedicated trials.

What runs through all of this is a consistent pattern: Ta1 seems to work best in people whose immune systems are already compromised. Chronic viral hepatitis, age-related immune decline, cancer-related immunosuppression, diabetes — these are the contexts where restoring immune function with a thymic peptide makes biological sense and where clinical outcomes trend positive.

The safety data is unambiguous. Across 600,000+ treated patients and decades of use, Ta1 has maintained an excellent safety profile. Whatever debates exist about efficacy in specific conditions, tolerability is not in question.

For more on how thymosin alpha-1 fits into the broader immune peptide picture, see our Thymosin Alpha-1 research overview and our peptide stacking guide.


References

  1. Costantini, C., et al. (2020). Thymosin alpha 1: A comprehensive review of the literature. World Journal of Virology, 9(5), 67-78. PMC7747025

  2. Li, C., et al. (2023). Thymosin alpha-1 and its role in viral infectious diseases: The mechanism and clinical application. Molecules, 28(8), 3539.

  3. Romani, L., et al. (2004). Thymosin alpha 1 activates dendritic cells for antifungal Th1 resistance through toll-like receptor signaling. Blood, 103(11), 4232-4239.

  4. Stecca, B., et al. (2019). A reappraisal of thymosin alpha1 in cancer therapy. Frontiers in Oncology, 9, 873. PMC6742685

  5. Mutchnick, M.G., et al. (1999). Thymosin alpha1 treatment of chronic hepatitis B: Results of a phase III multicentre, randomized, double-blind and placebo-controlled study. Journal of Viral Hepatitis, 6(5), 397-403.

  6. Chien, R.N., et al. (1998). Efficacy of thymosin alpha1 in patients with chronic hepatitis B: A randomized, controlled trial. Hepatology, 27(5), 1383-1387.

  7. You, J., et al. (2006). Efficacy of thymosin alpha-1 and interferon alpha in treatment of chronic viral hepatitis B: A randomized controlled study. World Journal of Gastroenterology, 12(41), 6715-6721.

  8. Yang, Y.F., et al. Comparison of the efficacy of thymosin alpha-1 and interferon alpha in the treatment of chronic hepatitis B: A meta-analysis. DARE Quality-assessed Reviews.

  9. Shen, C., et al. (2022). Safety and efficacy of thymosin alpha-1 in the treatment of hepatitis B virus-related acute-on-chronic liver failure: A randomized controlled trial. Hepatology International, 16, 775-788.

  10. Multiple sources: Nature Scientific Reports (2025), ASCO Journal of Clinical Oncology (2024). Thymosin alpha-1 combination studies in hepatocellular carcinoma.

  11. Danielli, R., et al. (2018). Thymosin alpha-1 therapy with immune checkpoint antibodies in metastatic melanoma. Multiple publications reviewed in Frontiers in Oncology, 2019.

  12. Wu, J., et al. (2025). The efficacy and safety of thymosin alpha-1 for sepsis (TESTS): Multicentre, double blinded, randomised, placebo controlled, phase 3 trial. BMJ, 388, e080561. PMC11780596

  13. Frontiers in Cellular and Infection Microbiology (2025). Efficacy of thymosin alpha-1 for sepsis: A systematic review and meta-analysis of randomized controlled trials.

  14. Liu, Y., et al. (2020). Thymosin alpha 1 reduces the mortality of severe coronavirus disease 2019 by restoration of lymphocytopenia and reversion of exhausted T cells. Clinical Infectious Diseases, 71(16), 2150-2157.

  15. Sun, Q., et al. (2021). Efficacy of thymosin alpha 1 in the treatment of COVID-19: A multicenter cohort study. Frontiers in Immunology, 12, 673693. PMC8366398

  16. Wu, M., et al. (2021). The effect of thymosin alpha-1 on mortality of critical COVID-19 patients: A multicenter retrospective study. International Immunopharmacology, 90, 107143.

  17. Tao, S., et al. (2022). Thymosin alpha1 use in adult COVID-19 patients: A systematic review and meta-analysis on clinical outcomes. International Immunopharmacology, 113, 109400. PMC9754924

  18. Frontiers in Immunology (2025). Thymosin alpha 1 alleviates inflammation and prevents infection in patients with severe acute pancreatitis through immune regulation: A systematic review and meta-analysis.

  19. Dinetz, A., et al. (2024). Comprehensive review of the safety and efficacy of thymosin alpha 1 in human clinical trials. Alternative Therapies in Health and Medicine.