Thymosin-α1 - Immune restoring therapy to improve sepsis outcomes

Description of the potential effects of Thymosin-α1 based on the literature. (This is not a product description, disclaimer at the bottom of the page)

Sepsis is a severe, often fatal condition caused by an uncontrolled and harmful reaction of the body's immune system to an infection [1]. This reaction leads to organ damage and remains the leading cause of death in intensive care units worldwide, despite advances in antibiotics, supportive treatment and early detection. Importantly, one of the main reasons for the low survival rate for sepsis is the profound and rapidly changing disruption of the immune system. Patients typically begin with an intense and damaging inflammatory response, followed by a phase of immunosuppression [1]. This later phase, sometimes called immunoparalysis, is characterized by weaker antigen presentation, loss of key immune cells such as lymphocytes, and poor cytokine signaling. As a result, patients become more susceptible to secondary infections, experience delayed organ healing and are at risk of increased late mortality.

Thymosin-α1 (Tα1) is a naturally occurring peptide consisting of 28 amino acids, known for its immune system enhancing and modulating effects. Specifically, it promotes T-cell development and activation, enhances dendritic cell function, increases the expression of human leukocyte antigen DR (HLA-DR) on monocytes, and helps rebalance cytokine signals. Because of these actions, Tα1 has gained attention as a potential agent to help restore immune function in sepsis. Over the past two decades, randomized controlled trials and meta-analyses have evaluated its role as an adjunct treatment to standard care for sepsis patients, either alone or in combination with other immune supportive therapies such as ulinastatin or blood purification therapies.

A growing body of clinical evidence suggests that short, intensive cycles of Tα1 treatment, often starting with two doses per day of subcutaneous injections, can improve immune system recovery, shorten the duration of organ failure and reduce short-term mortality without raising new safety issues. In addition, the combination of Tα1 with the serine protease inhibitor ulinastatin showed the most consistent survival benefits and stronger reductions in harmful inflammatory molecules such as tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6). These immune-targeted strategies are also associated with better severity scores, faster weaning from mechanical ventilation and, in some cases, shorter intensive care unit stays, although the impact on overall hospital resource utilization remains inconclusive.

The following section provides an overview of the major clinical trials and pooled analyses on Tα1 in sepsis. It summarizes the results of large multicenter studies such as Wu et al. (2013), combination treatment with ulinastatin as described by Li et al. (2009), Han et al. (2015) and Feng et al. (2016), meta-analyses of Tα1 alone by Gu et al. (2025), Li et al. (2015) and Liu et al. (2016), and more recent strategies combining Tα1 with advanced supportive interventions such as blood purification described by Zhou et al. (2009) and Bai et al. (2022). All of these studies provide an evidence base for considering Tα1 as an immune-restoring supplement in modern sepsis treatment.

Clinical results of thymosin-α1 use in sepsis (human studies)

Adding thymosin-α1 (Tα1) to standard sepsis treatment may help restore immune function and reduce deaths in the short term without causing additional safety concerns. Wu et al (2013) conducted a large multicenter randomized trial involving 361 patients with severe sepsis in the intensive care unit. Patients received an ETASS regimen, Tα1 at a dose of 1.6 mg subcutaneously twice daily for 5 days, followed by once daily for another 2 days, in addition to standard care. After 28 days, mortality dropped from 35.0% in the control group to 26.0% in the group receiving Tα1 (log-rank p = 0.049; relative risk [RR] 0.74, 95% CI 0.54-1.02). Moreover, immune reconstitution was stronger: monocyte HLA-DR (a marker of immune activation) increased by +3.9% on day 3 (p = 0.037) and +5.8% on day 7 (p = 0.017). In addition, organ failure scores (SOFA) improved, and there were no drug-related serious adverse events. This 7-dose treatment rapidly reversed sepsis-induced immunosuppression and showed a survival benefit [2].

Combining Tα1 with another immune-boosting drug may further improve treatment outcomes. Li et al (2009) randomly assigned 56 patients with severe sepsis to a group receiving ulinastatin in combination with Tα1 or placebo along with standard care. Interestingly, survival after 28 days was higher in the group receiving the drug combination (78% vs. 60%). Patients receiving Tα1 and ulinastatin also had faster improvement in APACHE II scores, faster normalization of white blood cell and lymphocyte counts, better coagulation function and lower levels of inflammatory cytokines. These findings suggest that combining Tα1 with another immune-boosting drug may accelerate recovery and improve survival [3]. In addition, pooled data support a survival benefit, especially when Tα1 is combined with ulinastatin. In a meta-analysis of six randomized controlled trials (n = 915), Han et al. (2015) found that the addition of Tα1 and ulinastatin reduced mortality at 28 days (RR 0.67, 95% CI 0.57-0.80) and mortality at 90 days (RR 0.75, 95% CI 0.61-0.93). In addition, inflammatory markers dropped sharply: TNF-α decreased by an average of 73.86 ng/l, and IL-6 dropped by 55.04 ng/l. Patients also spent about 2.3 fewer days on mechanical ventilation (weighted mean difference -2.26). Safety remained at an acceptable level in the study. Although dosing varied, most programs used short, intensive treatments similar to ETASS. These results indicate fewer deaths, less inflammation and faster restoration of ventilatory support with the combination of Tα1 and ulinastatin [4].

When used alone, Tα1 also shows potential, although the benefit may depend on patient selection and study design. Gu et al (2025) analyzed 11 randomized trials (967 patients receiving Tα1; 960 control patients) that tested Tα1 monotherapy. Overall, mortality at 28 days decreased (odds ratio [OR] 0.73, 95% CI 0.59-0.90; p = 0.003). However, the benefit was weaker in high-quality (OR 0.82) or multicenter studies (OR 0.86). Subgroup analysis suggested better outcomes in patients with cancer (moderate certainty) and possible benefit in patients with diabetes or heart disease (low certainty). Sequential analysis of the studies showed that larger-scale trials are needed to confirm these results. Overall, Tα1 monotherapy may reduce the number of early deaths in sepsis, but its effectiveness likely depends on the selection of appropriate patients and the timing of treatment initiation, when immunosuppression is most severe [5].

Moreover, the addition of thymosin-α1 (Tα1) to ulinastatin (UTI) provides the most reliable survival benefit in patients with severe sepsis, although other ICU outcomes are less consistent. Feng et al (2016) pooled the results of randomized trials conducted through September 2015 and found that UTI combined with Tα1 (often referred to as the UCT regimen) reduced mortality at 28 days from about one-third to one-fifth (RR 0.67; 95% CI 0.57-0.80; n = 915) and reduced mortality at 90 days (RR 0.75; 95% CI 0.61-0.93; n = 547). The quality of evidence regarding these outcomes was rated as moderate. In contrast, UTI alone showed no clear benefit at 28 days (RR 0.60; 95% CI 0.30-1.20; n = 182; low quality). Tα1 alone reduced mortality at 28 days (RR 0.72; 95% CI 0.55-0.93; n = 494; low quality), but did not reduce deaths at 90 days (RR 0.84; 95% CI 0.54-1.31; n = 91; very low quality). Based on these results, the combination of UCT provided the clearest and most reproducible increase in survival [6].

In addition, Tα1 itself is also associated with lower mortality rates, although the studies supporting this are smaller and less rigorous. Li et al (2015) analyzed 12 controlled studies involving 1,480 patients with sepsis. In these studies, despite different doses and regimens of Tα1 administration, mortality dropped by about one-third (RR 0.68; 95% CI 0.59-0.78; p < 0.00001). Many studies have used short induction cycles similar to the ETASS regimen (1.6 mg subcutaneously once or twice a day for several days, followed by gradual dose reduction). However, the authors caution that most of the included studies were conducted at a single center and were of moderate quality. Nonetheless, the consistent direction of benefit supports the use of Tα1 as an adjunct to standard sepsis therapy, pending large, high-quality multicenter trials [7]. Tα1 also appears to help restore immune function while improving survival, although its impact on ICU resources varies by dosing regimen. Liu et al (2016) reviewed 19 randomized trials and focused on 10 studies (n = 530) on mortality. Mortality rates were lower when Tα1 was used (RR 0.59; 95% CI 0.45-0.77; p = 0.0001). Administration of the drug once a day and twice a day produced similar survival benefits. Interestingly, once-daily administration of Tα1 resulted in a greater decrease in APACHE II scores (SMD -0.80), while twice-daily administration had no such effect. Neither regimen significantly shortened intensive care unit stay, mechanical ventilation time or the incidence of multiple organ failure. In terms of mechanism of action, Tα1 increased monocyte HLA-DR expression (SMD 1.23), enhanced CD3⁺ and CD4⁺ T cells, reduced levels of inflammatory cytokines such as IL-6 and TNF-α, and increased levels of the anti-inflammatory IL-10. Although the included studies were generally of low quality, the pattern of immune restoration is consistent with the observed improvement in survival [8].

Another study showed that combining Tα1 with ulinastatin can improve both survival and immune reconstitution, while showing some benefit in intensive care unit use. Wang et al (2016) combined the results of six randomized trials (n = 944). Patients who received UTI in combination with Tα1 had better 28-day survival (odds ratio [OR] 2.01; 95% CI 1.53-2.64), a mean APACHE II decrease of -4.72 points, and needed about two days less mechanical ventilation. The length of stay in the intensive care unit was biased toward shorter, but did not reach clear statistical significance. In addition, immunologic studies showed an increase in CD4⁺ T cells of about 5%, while changes in CD8⁺ cells were less consistent. Safety was good in all studies. These results confirm that UCT is an immune booster that improves short-term survival and immune balance in severe sepsis [9]. Tα1 may help restore the immune system and accelerate clinical stabilization in sepsis, although early studies did not show a clear survival benefit. Yu et al (2009) systematically reviewed five randomized controlled trials (n = 198). Most of the studies used short cycles of subcutaneous injections of Tα1 (usually 1.6 mg once or twice a day for a few days, then reduced in frequency). In all studies, Tα1 improved immunity: the number of CD4⁺ T cells increased by an average of 6.24 cells/μl, and the CD4⁺/CD8⁺ ratio increased by 0.14. Disease severity scores decreased (APACHE II decreased by -3.82 points). In addition, patients needed about 4.2 fewer days of mechanical ventilation and spent about 4.9 fewer days in the intensive care unit. However, overall mortality was not significantly lower compared to the control group. Overall, early studies showed better immune system recovery and faster clinical improvement, but larger studies were needed to prove a survival benefit [10].

Adding thymosin-α1 to the anti-inflammatory drug ulinastatin (UTI) appears to improve survival and reduce harmful inflammation in patients with sepsis. Liu et al (2017) conducted a meta-analysis of eight randomized controlled trials involving 1112 patients. Importantly, the treatment regimens typically included administration of Tα1 at a dose of about 1.6 mg subcutaneously several times a week, in addition to standard care and UTIs, although the exact dosage varied across the studies. The analysis showed that the combination of these drugs reduced mortality at 28 days by about 36%, mortality at 60 days by about 35% and mortality at 90 days by about 31% compared with standard therapy. In addition, patients' clinical status improved: APACHE II scores dropped faster, and patients were able to be disconnected from ventilators sooner. Markers of inflammation in the blood also improved, with levels of interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) falling, while levels of the anti-inflammatory cytokine IL-10 remained largely unchanged. However, the effects on length of stay in the intensive care unit and use of z-drugs were heterogeneous and varied widely across studies. Importantly, safety remained at an acceptable level and no new serious side effects were reported. Overall, these results suggest that the addition of Tα1 to UTIs may provide significant improvements in sepsis survival and immunity, although larger, high-quality studies are still needed to confirm these results [11]. 

In cases of drug-resistant intra-abdominal sepsis, the combination of Tα1 and UTIs with antibiotics led to a significant increase in survival and better immune balance. Zhang et al (2008) randomly assigned 120 patients with carbapenem-resistant infections to a group receiving carbapenems in combination with Tα1+UTI or carbapenems in combination with placebo. Tα1 was administered at standard clinical doses (approximately 1.6 mg subcutaneously at intervals) along with UTIs. The combination of these drugs improved many outcomes: APACHE II and multiple organ failure scores decreased, and Glasgow Coma Scale scores improved. Immune balance changed favorably with an increase in CD4⁺ and CD8⁺ T-cell counts and improved cytokine profiles (lower levels of TNF-α, IL-1β, IL-6, IL-8; higher levels of IL-4, IL-10). Survival was significantly improved: +17.8% at day 28, +25.9% at day 60 and +27.4% at day 90 compared to placebo. These results show that Tα1 in combination with UTI can restore immune function and survival even in high-risk, antibiotic-resistant sepsis [12]. In addition, the addition of Tα1 to blood purification (BP) for septic shock can accelerate stabilization and extend life expectancy. Bai et al (2022) randomly assigned 86 ICU patients with septic shock to a group receiving BP alone or BP in combination with Tα1 (1.6 mg subcutaneously three times a week). Both groups had similar disease severity and a similar response to emergency care. The Tα1+BP group recovered faster: shock duration and ICU stay were shorter, and overall clinical response rates were higher. Immunologic markers improved more strongly (increases in CD3⁺ and CD4⁺ T cells), along with better control of inflammatory cytokines and cardiac stress markers. One-year overall survival was similar, but life expectancy was prolonged by Tα1. Treatment was well tolerated and no new safety issues emerged. These results suggest that Tα1 is a useful addition to the modern treatment of septic shock, helping patients stabilize and restore immune function [13].

Combining thymosin-α1 (Tα1) with extracorporeal blood purification can restore immune balance, reduce the length of stay in the intensive care unit and reduce mortality in cases of severe sepsis. Zhou et al (2009) conducted a four-arm randomized controlled trial involving 91 intensive care unit patients. Participants were assigned to groups: continuous blood purification (CBP), Tα1 alone, CBP plus Tα1, or standard care under the Surviving Sepsis Campaign (SSC). Tα1 was administered at a dose of 1.6 mg subcutaneously once daily for seven days. On day 8, patients treated with Tα1 alone showed higher CD3⁺ T-cell counts compared to those receiving standard care. Continuous blood purification, used alone or in combination with Tα1, decreased key inflammatory markers such as IL-6, TNF-α and the IL-6/IL-10 ratio, while increasing the expression of HLA-DR and T-cell subsets. Importantly, the CBP plus Tα1 group showed faster improvement, with a stronger reduction in TNF-α levels and faster increases in CD3⁺ and CD4⁺ cells by day 4. Clinically, both CBP and combination therapy reduced the duration of ventilator use and intensive care unit stay. The combination approach also reduced mortality at 28 and 90 days compared to standard care for patients with sepsis. Overall, Tα1 helps rebuild immune defenses, while CBP removes inflammatory mediators; used together, they promote faster recovery and better survival [14].

Short cycles of intensive thymosin-α1 (Tα1) therapy can rapidly improve immune function and reduce deaths from septic shock. Chen (2007) conducted a randomized trial involving 42 intensive care unit patients, assigning them to a group receiving Tα1 at a dose of 1.6 mg subcutaneously twice daily for a week plus standard antibiotics or antibiotics alone. On days 3-7, patients receiving Tα1 showed higher numbers of CD3⁺, CD4⁺ and natural killer (NK) cells, as well as improved CD4⁺/CD8⁺ ratios (all p < 0.01). In addition, Tα1 reduced the duration of fever, intensive care unit stay and mechanical ventilation time, while lowering the total cost of care (all p < 0.01). Most importantly, mortality at 28 days was significantly lower in the Tα1 group compared to the group receiving antibiotics alone. These findings support the use of short-term, intensive dosing of Tα1 in the early phase of septic shock to restore immune balance and improve survival [15]. In addition, both Tα1 and continuous blood purification help restore immune function and promote organ regeneration in severe sepsis, but their effects are faster and more potent when used together. Li et al (2009) conducted a four-arm randomized controlled trial involving 91 intensive care unit patients, comparing standard Surviving Sepsis Campaign (SSC) care, continuous blood purification (CBP; CRRT or MARS daily for three days), Tα1 at a dose of 1.6 mg subcutaneously daily for seven days, or a combination of CBP and Tα1. All treatment groups had shorter intensive care unit stays, fewer days of mechanical ventilation and lower mortality at 28 days compared with SSC alone. Tα1 increased HLA-DR expression and the number of CD3⁺, CD4⁺ and CD8⁺ T cells by day 7. CBP improved APACHE II and Marshall organ function scores as early as day 3. Importantly, the group receiving the combination of CBP and Tα1 showed the earliest and greatest increase in CD3⁺ T-cell count by day 3 and showed the strongest overall clinical recovery. Based on the results, it can be concluded that the combination of Tα1 with CBP accelerates immune normalization and leads to better outcomes than either therapy alone [16].

The combination of thymosin-α1 with ulinastatin supports faster recovery, stronger immune balance and better survival in cases of severe sepsis. Chen et al (2009) conducted a multicenter pilot randomized controlled trial involving 114 patients who were assigned to receive standard care in combination with ulinastatin (UTI) and Tα1 or placebo. Combination therapy led to faster improvements in organ function, as demonstrated by a more rapid reduction in multiple organ failure and APACHE II scores. Immune improvement was also stronger: the CD4⁺/CD8⁺ ratio normalized more quickly, while pro-inflammatory markers TNF-α and IL-6 decreased, and anti-inflammatory cytokines IL-4 and IL-10 remained stable. Clinically, patients with em in the group receiving combination therapy had a shorter stay in the intensive care unit, spent fewer days on ventilators and required less antibiotic and dopamine support. Survival improved at each time point, with an increase of 17.3% at 28 days, 28.9% at 60 days and 31.4% at 90 days compared to placebo. Overall, targeting both excess inflammation with UTIs and immunosuppression with Tα1 promotes faster recovery, better immune reconstitution, and higher short- and intermediate-term survival rates for severe sepsis [18]. Similarly, thymosin-α1 with ulinastatin enhances immune reconstitution, reduces inflammation and improves survival rates in sepsis patients. Su et al (2009) conducted a randomized controlled trial involving 242 patients assigned to standard care under the Surviving Sepsis Campaign (SSC) or SSC plus ulinastatin (UTI; 200 kU intravenously twice daily for four days, followed by 100 kU daily for six days) and Tα1 (1.6 mg subcutaneously twice daily for four days, followed by once daily for six days). The combination therapy increased the expression of HLA-DR monocytes and changed the CD4⁺ T-cell profile toward a more active, infection-fighting profile, as shown by a higher CD4⁺IFN-γ⁺/CD4⁺IL-4⁺ ratio. Inflammatory markers such as IL-6 and IL-10 decreased, disease severity scores (APACHE II) improved, and multiple organ dysfunction syndrome (MODS) decreased from 47% to 21%. Ventilator use also decreased (6.1 ± 2.5 vs. 8.2 ± 3.5 days). Intensive care unit stay and duration of infection remained similar in both groups. Most importantly, mortality at 28 days decreased from 33% for standard care to 20% for combination treatment. Overall, these results show that the combination of Tα1 with ulinastatin provides stronger immune support and greater survival benefit than standard treatment for sepsis [17].

Dose of thymosin-α1 in sepsis

In sepsis studies, thymosin-α1 (Tα1) dosing is very consistent, with most studies using 1.6 mg per injection and adjusting the schedule according to the severity of the disease and additional treatments.
A common approach is a 7-day treatment in which the drug is initially administered twice a day and then once a day, gradually reducing the dose. One large study conducted in an intensive care unit administered 1.6 mg subcutaneously (SC) twice daily for 5 days, followed by once daily for 2 days. In another study of septic shock, 1.6 mg SC was used twice daily for a full week along with antibiotics.

Two studies with four arms compared Tα1 alone, continuous blood purification (CBP), a combination of the two, or standard care. In both, the selected Tα1 regimen was 1.6 mg SC once daily for 7 days, while CBP included CRRT or MARS daily for 3 days.

The dual immunotherapy strategy combined Tα1 at a dose of 1.6 mg subcutaneously twice daily for 4 days, then once daily for 6 days (10 days total) with ulinastatin at a dose of 200 kU intravenously twice daily for 4 days, then 100 kU daily for 6 days. In another multicenter study, Tα1 was added to ulinastatin, but the dosage was not specified; centers generally followed similar dosing regimens from 7 to 10 days, ranging from twice a day to once a day.

More recent protocols have used 1.6 mg subcutaneously three times a week when Tα1 was combined with blood purification methods. Meta-analyses show that most sepsis studies use a dose of 1.6 mg once or twice a day for about 7-10 days. Some treatment regimens start with induction twice a day for a few days and then reduce the dose to once a day, while others use a dose of once a day for a week or twice a day for a full week in severe cases.

Concomitant interventions are often used:

• Ulinastatin often at a dose of 200 kU intravenously twice a day for 4 days, followed by 100 kU once a day for 6 days.
• Continuous blood purification (CRRT or MARS) usually performed daily for three sessions.

In practice, the most reliable regimen is to administer 1.6 mg subcutaneously twice a day for several days, followed by once a day for about a week to 10 days, with dose adjustments when combined with ulinastatin treatment or blood purification. This regimen is consistent with most clinical programs for the administration of Tα1 in severe sepsis and septic shock.

Disclaimer

This article was written for educational purposes and is intended to raise awareness of the substance under discussion. It is important to note that the article is about the substance in general - it is not a description of a specific product (chemical reagent). We do not suggest the use of chemical reagents on humans - this is prohibited by law, for a product to be used for treatment it must be registered as a drug. The information contained in the text is based on available scientific research and is not intended to serve as medical advice or promote self-medication. The reader should consult any health and treatment decisions with a qualified health professional.

References

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