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Free U.S. shipping on orders over $150Thymosin alpha 1 (Tα1 or TA1) is a 28-amino acid peptide naturally present and isolated from the thymus. It holds an integral role in regulating inflammation, restoring immunity, and enhancing immune tolerance [1].
These functions are crucial for defenses against viral, bacterial, and fungal infections, as well as for inhibiting autoimmunity and tumorigenesis.
Tα1 stimulates the innate, adaptive, and humoral immune responses, acting as agonists of toll-like receptors (TLRs) 9 and 2 in specialized antigen-presenting cells, such as myeloid and dendritic cells [1].
Moreover, Tα1 can increase the levels of cytokines: IL-2, IL-10, IL-12, and interferon (IFN) α and γ [1]. These actions are fundamental for fighting viral, bacterial, and fungal infections.
On the other hand, Tα1 down-regulates IL-1β and tumor necrosis factor-α, reducing the inflammatory response that may be responsible for autoimmunity and cytokine storms [1].
Tα1-induced immunosuppression can prevent cytokine storm, a catastrophic event seen in some infectious diseases or sepsis.
Finally, Tα1 promotes T-cell maturation into CD4+/CD8+ T cells and activates natural killer cells, giving it a crucial role in anti-cancer immunity [1].
Tα1 has been rigorously tested and has a track record of safety.
Since its discovery in the early 1980s, it has been used in various clinical settings as adjuvant treatment, and it has been approved for treating hepatitis B and C in some countries [1].
Besides hepatitis B and C, Tα1 has been proven to be a beneficial treatment for patients with HIV, serving as a safe adjuvant to antiretroviral therapy [1].
In addition, it has shown positive effects in immunocompromised patients following bone marrow transplant or in lowering mortality in patients with sepsis [1, 2]. Tα1 also improves immunogenicity of the influenza vaccine [1].
Additionally, Tα1 helps regulate immunity and reduce inflammation in patients with autoimmune diseases such as rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus, likely through its anti-inflammatory activity [3].
Tα1 has been used as an adjuvant therapy in many infectious diseases, including chronic hepatitis B and C, HIV, pseudomonas [4], and mold pneumonia in immunocompromised patients [4].
As an adjuvant in HIV antiretroviral therapy, it helps in increasing CD4+ cell count, stimulates the function of CD4+ cells, and decreases viral load [1].
In addition, Tα1 significantly increases levels of sjTREC in patients with advanced HIV disease, in contrast with the dramatic decline of sjTREC levels as the disease progresses and naive T cells are depleted.
An important feature of Tα1 is that it also has an immunomodulatory role that can mitigate sepsis and cytokine storms. A single-blind randomized control trial conducted in six tertiary hospitals in China demonstrated 9% lower mortality in the Tα1-treated group compared to the control group of patients with sepsis [2].
The anti-tumor effect of Tα1 was studied both in cancer cell lines and in vivo. It has been studied as a single immunotherapeutic agent or combined with chemotherapy, radiotherapy, or surgery.
Tα1 inhibits cell proliferation, induces apoptosis, as well as promotes immunosurveillance by increasing the expression of major histocompatibility complex (MHC) I and tumor antigens [3].
In 2015, Guo et al. concluded that Tα1 can decrease proliferation and induce apoptosis in human cancer cell lines such as human leukemia, non-small cell lung cancer, melanoma, and other cancers [1].
Tα1 has shown promising results in patients with malignancies. Tα1 tripled the response rate to dacarbazine in stage IV melanoma patients, compared to dacarbazine alone.
It also has proven beneficial effects in head, neck, and hepatocellular carcinoma as well as lung and breast cancer, possibly acting as an immune checkpoint inhibitor [1, 3].
Autoimmune diseases like rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus are characterized by a dysregulated immune system.
Tα1 levels are not only dramatically lower in patients with psoriatic arthritis when compared with healthy individuals but also when compared with patients with systemic lupus or rheumatoid arthritis [5].
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). Thymosin Alpha 1 is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
Thymosin Alpha-1, also called thymalfasin, is described as a peptide hormone produced by the thymus gland. It is described as having immunomodulatory properties, and one description also attributes anti-inflammatory and antioxidant properties to it. It is described as a thymus-derived immunomodulatory peptide that has been investigated as an adjunctive therapy in cancer care.
A review describes Thymosin alpha-1 as helping restore immune function by stimulating T-cell differentiation, enhancing thymic output, and modulating dendritic cell and macrophage activity. Another source describes thymosin alpha 1 (Tα1) as replenishing the T cell pool via thymic rejuvenation, and this description was given as the rationale for combining it with interleukin-15 in hepatocellular carcinoma research. Thymosin alpha 1 is also described as having an immune-balancing role that is recognized in contexts of immune dysregulation.
In in vitro studies, Thymosin Alpha-1 (Tα-1) bound to tumor apoptotic bodies and interacted with apoptotic body-borne microRNAs, including miR-146a-5p, after the apoptotic bodies were taken up into the endolysosomal compartment of dendritic cells. In these in vitro studies, Tα-1 protected miR-146a-5p from lysosomal RNase A-mediated degradation, which allowed miR-146a-5p to activate Toll-like receptor 7 (TLR7) and license dendritic cell maturation.
In animal studies of hepatocellular carcinoma (HCC), combined IL-15 and Thymosin Alpha-1 (Tα1) therapy was concluded to reverse CD8+ T cell senescence and enhance antitumor immunity. The researchers attributed these effects to suppression of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. In the same animal work, the combination attenuated chronically overactivated PI3K/AKT signaling in hepatic CD8+ T cells, as shown by transcriptomic and protein-level analyses.
In a human clinical trial, patients with HBeAG-positive chronic hepatitis B received thymalfasin plus entecavir, while the control group received entecavir alone. Compared with the control group, patients receiving thymalfasin plus entecavir had lower total bilirubin and ALT levels and more satisfactory improvement in immune function-related indicators. These patients also had lower levels of HA, LN and IVC than the control group, and the differences between the two groups were statistically significant (P<0.05).
In a human clinical trial, Thymosin Alpha-1 significantly reduced the overall incidence of extrapancreatic infections in patients with severe acute pancreatitis (RR=0.56, 95%CI [0.40, 0.78], P=0.0005). The reduction was especially marked for blood infections (RR=0.60, 95%CI [0.38, 0.94], P=0.03) and abdominal infections (RR=0.38, 95%CI [0.19, 0.78], P<0.0001), while the reduction in lung infections was not statistically significant. A human review of these patients concluded that Thymosin Alpha-1 may exert anti-inflammatory and extrapancreatic infection-preventive effects and may improve their condition or prognosis.
The only report in these facts is a single case in a patient with nasopharyngeal carcinoma. That patient received sintilimab, a PD-1 inhibitor, in combination with thymosin alpha-1 (Tα1) and developed multisystem immune-related adverse events. The patient presented with high fever, rash, interstitial pulmonary edema, and multiple organ failure. The case describes severe multisystem immune-related toxicity during the combination treatment, but it did not establish that thymosin alpha-1 specifically caused these effects.
A review of human studies of Thymosin Alpha-1 in cancer patients reported several favorable clinical, immune-related, or treatment-tolerance signals. The review noted that heterogeneity among these studies limited how comparable they were. In an observational study of patients, median progression-free survival and overall survival were significantly longer in the chemotherapy-containing thymalfasin groups than in the group receiving an immune checkpoint inhibitor plus thymalfasin. In a clinical trial in patients, the authors concluded that thymalfasin may help preserve and coordinate systemic antitumor immunity without excessive toxicity, and they stated that this hypothesis warrants larger randomized trials.
A review describes the clinical use of selected peptides, including thymosin alpha-1, as largely investigational in the context of thyroid disease. That review examined thymosin alpha-1 as one of several selected peptides for thyroid relevance, alongside thymosin beta-4, BPC-157, and growth hormone secretagogues.
A review reports that preclinical and clinical studies show Thymosin alpha-1 can improve vaccine response in the elderly and mitigate immunosenescence, the age-related decline of the immune system. The review does not specify which of these findings came from preclinical work and which from clinical work, or from which species.
In a multicenter randomized controlled trial in humans, thymosin alpha 1 (Tα1) is being evaluated as a supplement added to standard care to prevent organ dysfunction after repair of acute type A aortic dissection. The trial's primary endpoint is the difference in mean postoperative Sequential Organ Failure Assessment (SOFA) scores between groups, measured daily from postoperative day 7. Tα1 is intended to act by targeting post-operative immune system imbalance, with the aim of reducing systemic inflammatory response syndrome (SIRS)-mediated organ injury.
In the formulation described in this in vitro study, ethanol was one of the ingredients selected, with its role described as reducing viscosity and stabilizing the peptide drug Tα1.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.