Thymosin Alpha-1

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Synthetic thymic hormone — the most-researched peptide for immune modulation, T-cell recovery, and vaccine response.

A 28-residue acetylated peptide originally isolated from thymic tissue, characterised in the primary literature as a TLR-9 modulator with published effects on T-cell maturation markers in preclinical models. For laboratory characterisation only.

Thymosin alpha-1 is a 28-amino-acid thymic peptide that modulates immunity primarily through TLR-2 and TLR-9 agonism, promoting T-cell maturation, reversing T-cell exhaustion, activating NK cells, and balancing pro/anti-inflammatory responses. Approved in 35+ countries for viral hepatitis and cancer immunotherapy adjunct.

Thymosin alpha-1 is a 28-amino-acid thymic peptide that modulates immunity primarily through TLR-2 and TLR-9 agonism, promoting T-cell maturation, reversing T-cell exhaustion, activating NK cells, and balancing pro/anti-inflammatory responses. Approved in 35+ countries for viral hepatitis and cancer immunotherapy adjunct. It has a molecular formula C129H215N33O55, mass 3108.29 Da. Its published amino-acid sequence is Ac-SDAAVDTSSEITTKDLKEKKEVVEEAEN. Common synonyms in the literature include Tα1, TA1, and Thymalfasin.

Investigation of Thymosin Alpha-1 to date is clinical-investigational, with the majority of citations concentrated in animal models and in-vitro assays rather than randomized controlled human trials. Published work referencing Thymosin Alpha-1 spans Hepatitis B/C treatment: Tα1 is approved in numerous countries as adjunct therapy for chronic viral hepatitis. Clinical studies show improved sustained virological response rates when combined with standard antiviral therapies, enhanced T-cell responses to viral antigens, and improved clearance of hepatitis B e-antigen, Cancer immunotherapy adjunct: Research and approved use in some countries examines Tα1 as an immunoadjuvant alongside chemotherapy. Studies report enhanced immune recovery, reduced chemotherapy-induced immunosuppression, and improved quality of life measures in cancer patients, and COVID-19 research: During the pandemic, studies examined Tα1's ability to modulate cytokine dysregulation in severe COVID-19. Ex vivo treatment of COVID-19 patient blood cells reduced IL-6, TNF-α, and IL-1β expression while maintaining IL-10, suggesting potential for cytokine storm mitigation. Proposed mechanisms in the literature include TLR2/TLR9 signaling: engages Toll-like receptors on dendritic cells, activating NF-κB and JNK/p38/AP1 pathways and Dendritic cell activation: stimulates myeloid and plasmacytoid DCs to initiate adaptive immune responses. None of this material describes therapeutic outcomes in humans, and No vendor listed here provides dosing guidance for Thymosin Alpha-1 outside laboratory research.

For the full mechanistic profile, published references, and constraint notes on Thymosin Alpha-1, see the Thymosin Alpha-1 research page. All references cited on that page are peer-reviewed primary literature.

Binding and functional-assay data for Thymosin Alpha-1, from peer-reviewed in-vitro pharmacology publications. Values are receptor activity parameters — not clinical outcomes.

Study designs referencing this compound in the published literature. Descriptions cover framework only — phase, participant count, duration, and citation — not outcomes. Click a card to review the source directly.