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 start with an intense and damaging inflammatory response, followed by a phase of immunosuppression [1]. This later phase, sometimes referred to as immunoparalysis, is characterised by weaker antigen presentation, loss of key immune cells such as lymphocytes and poor cytokine signalling. 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. In particular, 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 to 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, randomised controlled trials and meta-analyses have evaluated its role as an adjunct treatment to standard sepsis care, 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 by subcutaneous injection, can improve immune system recovery, shorten the duration of organ failure and reduce short-term mortality without causing new safety issues. In addition, the combination of Tα1 with the serine protease inhibitor ulinastatin showed the most consistent survival benefit and a stronger reduction in harmful inflammatory molecules such as tumour 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 ICU stays, although the impact on overall hospital resource utilisation remains inconclusive.

The following section provides an overview of the main clinical trials and pooled analyses on Tα1 in sepsis. It summarises the results of large multicentre studies such as Wu et al. (2013), the ulinastatin combination treatment 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 outcomes of thymosin-α1 in sepsis (human studies)

Adding thymosin-α1 (Tα1) to the standard treatment of sepsis may help to restore immune function and reduce deaths in the short term without causing additional safety concerns. Wu et al (2013) conducted a large multicentre randomised trial involving 361 patients with severe sepsis presenting in the intensive care unit. Patients received an ETASS regimen, Tα1 at a dose of 1.6 mg subcutaneously twice daily for five days, followed by once daily for a further two days, in addition to standard care. After 28 days, mortality decreased 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). Furthermore, 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 no drug-related serious adverse events were reported. This 7-dose treatment rapidly reversed sepsis-induced immunosuppression and showed a survival benefit [2].

Combining Tα1 with another immune supportive drug may further improve treatment outcomes. Li et al (2009) randomly allocated 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 normalisation of white blood cell and lymphocyte counts, better coagulation function and lower levels of inflammatory cytokines. These results suggest that combining Tα1 with another immune-enhancing drug may accelerate recovery and improve survival [3]. In addition, pooled data support a survival benefit, particularly when Tα1 is combined with ulinastatin. In a meta-analysis of six randomised 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 decreased sharply: TNF-α decreased by an average of 73.86 ng/l and IL-6 decreased by 55.04 ng/l. Patients also spent approximately 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 programmes used short, intensive treatments similar to ETASS. These results indicate fewer deaths, less inflammation and faster restoration of respiratory 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) analysed 11 randomised 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 multicentre 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 studies are needed to confirm these results. Overall, Tα1 monotherapy may reduce the number of early deaths in sepsis, but its effectiveness is likely to depend on the selection of appropriate patients and the timing of treatment initiation, when immunosuppression is most severe [5].

Furthermore, 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 randomised trials conducted up to September 2015 and found that UTI combined with Tα1 (often referred to as the UCT regimen) reduced mortality at 28 days from approximately 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 for these outcomes was assessed 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 was found to provide the clearest and most reproducible increase in survival [6].

Furthermore, Tα1 itself is also associated with lower mortality rates, although the studies supporting this are smaller and less rigorous. Li et al (2015) analysed 12 controlled trials involving 1,480 patients with sepsis. In these studies, despite different doses and regimens of Tα1 administration, mortality decreased by approximately one-third (RR 0.68; 95% CI 0.59-0.78; p < 0.00001). A number of studies have used short induction cycles similar to the ETASS regimen (1.6 mg subcutaneously once or twice daily for several days, followed by gradual dose reduction). However, the authors caution that most of the included studies were conducted at a single centre and were of moderate quality. Nevertheless, the consistent direction of benefit supports the use of Tα1 as an adjunct to standard sepsis therapy, pending large, high-quality multi-centre trials [7]. Tα1 also appears to help restore immune function while improving survival, although its impact on ICU resources varies according to dosing regimen. Liu et al (2016) reviewed 19 randomised trials and focused on 10 studies (n = 530) on mortality. Mortality rates were lower with Tα1 use (RR 0.59; 95% CI 0.45-0.77; p = 0.0001). Administration of the drug once daily and twice daily provided similar survival benefits. Interestingly, once-daily administration of Tα1 resulted in a greater decrease in APACHE II scores (SMD -0.80), whereas twice-daily administration had no such effect. Neither regimen significantly reduced intensive care unit stay, mechanical ventilation time or the incidence of multiple organ failure. In terms of mechanism of action, Tα1 increased HLA-DR expression of monocytes (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 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 the combination of 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 randomised 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 approximately two days less mechanical ventilation. The length of stay in the intensive care unit was biased to be shorter, but did not reach clear statistical significance. In addition, immunological studies showed an increase in CD4⁺ T-cells of approximately 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 stabilisation in sepsis, although early studies did not show a clear survival benefit. Yu et al (2009) systematically reviewed five randomised controlled trials (n = 198). Most of the studies used short cycles of subcutaneous injections of Tα1 (usually 1.6 mg once or twice daily for a few days and then reduced in frequency). In all studies, Tα1 improved immunity: the CD4⁺ T-cell count 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].

The addition of 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 randomised controlled trials involving 1112 patients. Importantly, treatment regimens typically included the administration of Tα1 at a dose of approximately 1.6 mg subcutaneously several times a week, in addition to standard care and UTIs, although the exact dosage varied between studies. Analysis showed that the combination of these drugs reduced mortality at 28 days by approximately 36%, mortality at 60 days by approximately 35% and mortality at 90 days by approximately 31% compared with standard therapy. In addition, the clinical status of the patients improved: APACHE II scores fell 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 tumour necrosis factor α (TNF-α) falling, while levels of the anti-inflammatory cytokine IL-10 remained largely unchanged. However, the effect on ICU length of stay and z-drug use was heterogeneous and varied considerably between 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]. 

For 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 allocated 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) together 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 favourably with increases 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 with 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) in septic shock can accelerate stabilisation and prolong life expectancy. Bai et al (2022) randomly assigned 86 ICU patients with septic shock to a group receiving BP alone or BP combined 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: duration of shock and ICU stay were shorter and overall clinical response rates were higher. Immunological markers improved more strongly (increases in CD3⁺ and CD4⁺ T-cell counts), 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 to stabilise 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 randomised controlled trial involving 91 intensive care unit patients. Participants were allocated to groups: continuous blood purification (CBP), Tα1 alone, CBP plus Tα1 or standard care in 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 patients 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 HLA-DR and T-cell subgroup expression. Importantly, the CBP plus Tα1 group showed more rapid improvement, with stronger reductions 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 defences, 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 randomised trial involving 42 ICU patients, assigning them to a group receiving Tα1 at a dose of 1.6 mg subcutaneously twice daily for one 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 an improvement in the CD4⁺/CD8⁺ ratio (all p < 0.01). In addition, Tα1 reduced the duration of fever, intensive care unit stay and mechanical ventilation time, while reducing 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 results 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 randomised controlled trial involving 91 ICU 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 a shorter intensive care unit stay, 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 largest increase in CD3⁺ T-cell counts by day 3 and showed the strongest overall clinical recovery. Based on the results, the combination of Tα1 with CBP accelerates immune normalisation 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 severe sepsis. Chen et al (2009) conducted a multicentre pilot randomised controlled trial involving 114 patients who were allocated standard care in combination with ulinastatin (UTI) and Tα1 or placebo. Combination therapy led to a more rapid improvement in organ function, as shown by a more rapid reduction in multi-organ failure and APACHE II scores. Immune improvement was also stronger: the CD4⁺/CD8⁺ ratio normalised more rapidly, 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 increases of 17.3% at 28 days, 28.9% at 60 days and 31.4% at 90 days compared with placebo. Overall, targeting both over-inflammation with UTI 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 of sepsis patients. Su et al (2009) conducted a randomised controlled trial involving 242 people assigned to standard care in 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). Combination therapy increased HLA-DR expression of monocytes and changed the CD4⁺ T-cell profile towards a more active, infection-fighting profile, as shown by higher CD4⁺IFN-γ⁺/CD4⁺IL-4⁺ ratios. 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, the dosage of thymosin-α1 (Tα1) 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. In one large study conducted in an intensive care unit, 1.6 mg was administered 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 these 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 followed by once daily for 6 days (10 days total) with ulinastatin at a dose of 200 kU intravenously twice daily for 4 days followed by 100 kU daily for 6 days. In another multicentre study, Tα1 was added to ulinastatin, but dosing was not specified; centres generally followed similar dosing regimens from 7 to 10 days, ranging from twice daily to once daily.

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 whole week in severe cases.

Often concomitant interventions are used:

• Ulinastatin often at a dose of 200 kU intravenously twice daily for 4 days, followed by 100 kU once daily 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 daily for a few days and then once daily 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 programmes for the administration of Tα1 in severe sepsis and septic shock.

Disclaimer

This article has been 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 are not suggesting 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 medicine. The information contained in the text is based on available scientific research and is not intended as medical advice or to promote self-medication. The reader should consult with a qualified health professional for all health and treatment decisions.

References

1. Gyawali, B., Ramakrishna, K. and Dhamoon, A. S. (2019). Sepsis: evolution of definition, pathophysiology and management. SAGE open medicine, 7, 2050312119835043. https://doi.org/10.1177/2050312119835043 https://pmc.ncbi.nlm.nih.gov/articles/PMC6429642/ 
2. Wu, J., Zhou, L., Liu, J., Ma, G., Kou, Q., He, Z., Chen, J., Ou-Yang, B., Chen, M., Li, Y., Wu, X., Gu, B., Chen, L., Zou, Z., Qiang, X., Chen, Y., Lin, A., Zhang, G. and Guan, X. (2013). Efficacy of thymosin alfa 1 in severe sepsis (ETASS): a multicentre, single-blind, randomised, controlled trial. Critical Care, 17(1), R8. https://doi.org/10.1186/cc11932 https://pubmed.ncbi.nlm.nih.gov/23327199/
3. Li, Y., Chen, H., Li, X., Zhou, W., He, M., Chiriva-Internati, M., Wachtel, M. S. and Frezza, E. E. (2009). Novel immunomodulatory therapy in severe sepsis: ulinastatin in combination with thymosin α1. Journal of Intensive Care Medicine, 24(1), 47-53. https://doi.org/10.1177/0885066608326970https://pubmed.ncbi.nlm.nih.gov/19033321/ 
4. Han, D., Shang, W., Wang, G., Sun, L., Zhang, Y., Wen, H. and Xu, L. (2015). Immunomodulatory strategy based on ulinastatin and thymosin α1 in the treatment of sepsis: a meta-analysis. International Immunopharmacology, 29(2), 377-382. https://doi.org/10.1016/j.intimp.2015.10.026 https://pubmed.ncbi.nlm.nih.gov/26522590/
5. Gu, B., Zhou, Y., Nie, Y., Wang, L., Liang, L., Liao, Z., Wen, J., Guan, X., Chen, M., Wu, J. and Pei, F. (2025). Efficacy of thymosin α1 in the treatment of sepsis: a systematic review and meta-analysis of randomised controlled trials. Frontiers in Cellular and Infection Microbiology, 15, 1673959. https://doi.org/10.3389/fcimb.2025.1673959https://pubmed.ncbi.nlm.nih.gov/40969554/ 
6. Feng, Z., Shi, Q., Fan, Y., Wang, Q. and Yin, W. (2016). Ulinastatin and/or thymosin α1 in severe sepsis: a systematic review and meta-analysis. Journal of Trauma and Acute Care Surgery, 80(2), 335–340. https://doi.org/10.1097/TA.0000000000000909 https://pubmed.ncbi.nlm.nih.gov/26517783/
7. Li, C., Bo, L., Liu, Q. and Jin, F. (2015). Thymosin alpha1-based immunomodulatory therapy for the treatment of sepsis: a systematic review and meta-analysis. International Journal of Infectious Diseases, 33, 90-96. https://doi.org/10.1016/j.ijid.2014.12.032 https://pubmed.ncbi.nlm.nih.gov/25532482/
8. Liu, F., Wang, H. M., Wang, T., Zhang, Y. M. and Zhu, X. (2016). Efficacy of thymosin α1 as an immunomodulatory treatment for sepsis: a systematic review of randomized controlled trials. BMC Infectious Diseases, 16(1), 488. https://doi.org/10.1186/s12879-016-1823-5. PMID: 27633969; PMCID: PMC5025565 https://pubmed.ncbi.nlm.nih.gov/27633969/
9. Wang, F. Y., Fang, B., Qiang, X. H., Yu, T. O., Zhong, J. R., Cao, J. and Zhou, L. X. (2016). Efficacy and immunomodulatory effects of ulinastatin and thymosin α1 in sepsis: a systematic review and meta-analysis. BioMed Research International, 2016, 9508493. https://doi.org/10.1155/2016/9508493. PMID: 27340674; PMCID: PMC4906180 https://pubmed.ncbi.nlm.nih.gov/27340674/
10. Yu, Y., Tian, J. H., Yang, K. H. and Zhang, P. (2009). [Evaluation of the efficacy of thymosin alpha1 in the treatment of sepsis: a systematic review]. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue, 21(1), 21-24. PMID: 19141185. https://pubmed.ncbi.nlm.nih.gov/19141185/
11. Liu, D., Yu, Z., Yin, J., Chen, Y., Zhang, H., Xin, F., Fu, H. and Wan, B. (2017). Effect of ulinastatin combined with thymosin alpha1 on sepsis: a systematic review and meta-analysis of Chinese and Indian patients. Journal of Critical Care, 39, 259-266. https://doi.org/10.1016/j.jcrc.2016.12.013. PMID: 28069319. https://pubmed.ncbi.nlm.nih.gov/28069319/
12. Zhang, Y., Chen, H., Li, Y., Zheng, S., Chen, Y., Li, L., Zhou, L., Xie, H. and Praseedom, R. K. (2008). Immunomodulatory strategy based on thymosin alpha1 and ulinastatin for sepsis due to intra-abdominal infection caused by carbapenem-resistant bacteria. Journal of Infectious Diseases, 198(5), 723-730. https://doi.org/10.1086/590500. PMID: 18613793 https://pubmed.ncbi.nlm.nih.gov/18613793/
13. Bai, L., Qiu, X., Ding, X., Bai, X., Huang, W., Yang, L. and Shi, X. (2022). The value of combining thymosin α1 with blood purification to enhance the rescue efficacy of patients in shock. Alternative Therapies in Health and Medicine, 28(7), 146-152. PMID: 35951068. https://pubmed.ncbi.nlm.nih.gov/35951068/
14. Zhou, L. X., Tan, J. J., Li, Y. N., Luo, H. T., Shao, Y. H., Qiang, X. H., Yu, T. O., Ma, M. Y., Mao, K. J. and Fang, B. (2009). Immune and inflammatory disorders in severe sepsis and the effects of bi-immunomodulatory therapy: a prospective, randomized, controlled clinical trial. Zhonghua Yi Xue Za Zhi, 89(15), 1028-1033. PMID: 19595251. https://pubmed.ncbi.nlm.nih.gov/19595251/
15. Chen, J. (2007). [Effects of thymosin alpha-1 on cellular immune function in patients with septic shock]. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue, 19(3), 153-155. PMID: 17376268. https://pubmed.ncbi.nlm.nih.gov/17376268/
16. Li, Y., Zhou, L., Qiang, X., Yu, T., Mao, K., Feng, B., Wen, W., Zou, Y., Li, W. and Li, C. (2009). Effects of continuous blood purification and thymosin alpha1 on cellular immunity in patients with severe sepsis: a prospective, randomised, controlled clinical trial. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue, 21(3), 139-142. PMID: 19278581. https://pubmed.ncbi.nlm.nih.gov/19278581/
17. Su, L., Meng, F., Tang, Y., Wen, Q., Liu, Y., Tang, L., Duan, P. and Luo, R. (2009). Clinical effects of ulinastatin and thymosin alpha1 on immune modulation in patients with sepsis. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue, 21(3), 147-150. PMID: 19278583. https://pubmed.ncbi.nlm.nih.gov/19278583/
18. Chen, H., He, M. and Li, Y. (2009). Treatment of patients with severe sepsis with ulinastatin and thymosin alpha1: a prospective, randomized, controlled pilot study. Chin Med J (Engl), 122(8), 883-888. doi:10.3760/cma.j.issn.0366-6999.2009.08.012. PMID: 19493408 https://pubmed.ncbi.nlm.nih.gov/19493408/