SOURCES
Every Citation, In One Place
The full reference list behind every numbered claim on this site, spanning all four compounds.
How to use this list
Every bracketed number on this site — [1], [2], and so on — points to an entry below. Entries are drawn from peer-reviewed journals, clinical trial reports, and other published literature; where available, a DOI or PubMed link is provided so a reader can go straight to the primary source rather than taking this site's word for it.
- Aronne LJ, et al. (SURMOUNT-5 Investigators). Tirzepatide as Compared with Semaglutide for the Treatment of Obesity. N Engl J Med. 2025. ↗
- Perkovic V, et al. (FLOW Trial Committees and Investigators). Effects of Semaglutide on Chronic Kidney Disease in Patients with Type 2 Diabetes. N Engl J Med. 2024. ↗
- Lincoff AM, et al. (SELECT Trial Investigators). Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes. N Engl J Med. 2023. ↗
- Wilding JPH, et al. (STEP 1 Study Group). Once-Weekly Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2021. ↗
- Smits MM, Van Raalte DH. Safety of Semaglutide. Front Endocrinol (Lausanne). 2021. ↗
- Wu J, Pei F, Zhou L, et al. The efficacy and safety of thymosin alpha1 for sepsis (TESTS): multicentre, double blinded, randomised, placebo controlled, phase 3 trial. BMJ. 2025. ↗
- Dominari A, Hathaway Iii D, Pandav K, et al. Thymosin alpha 1: A comprehensive review of the literature. World J Virol. 2020. ↗
- Liu Y, Pan Y, Hu Z, et al. Thymosin Alpha 1 Reduces the Mortality of Severe Coronavirus Disease 2019 by Restoration of Lymphocytopenia and Reversion of Exhausted T Cells. Clin Infect Dis. 2020. ↗
- Costantini C, Bellet MM, Pariano M, et al. A Reappraisal of Thymosin Alpha1 in Cancer Therapy. Front Oncol. 2019. ↗
- Wu J, Zhou L, Liu J, et al. The efficacy of thymosin alpha 1 for severe sepsis (ETASS): a multicenter, single-blind, randomized and controlled trial. Crit Care. 2013. ↗
- Romani L, Bistoni F, Montagnoli C, et al. Thymosin alpha1 activates dendritic cell tryptophan catabolism and establishes a regulatory environment for balance of inflammation and tolerance. Blood. 2006. ↗
- Goldstein AL, Low TL, McAdoo M, et al. Thymosin alpha1: isolation and sequence analysis of an immunologically active thymic polypeptide. Proc Natl Acad Sci U S A. 1977. ↗
- Lee E, Burgess K. Safety of Intravenous Infusion of BPC157 in Humans: A Pilot Study. Altern Ther Health Med. 2025. ↗
- McGuire FP, et al. Regeneration or Risk? A Narrative Review of BPC-157 for Musculoskeletal Healing. Curr Rev Musculoskelet Med. 2025. ↗
- He L, et al. Pharmacokinetics, distribution, metabolism, and excretion of body-protective compound 157, a potential drug for treating various wounds, in rats and dogs. Front Pharmacol. 2022;13:1026182. ↗
- Hsieh MJ, et al. Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation. J Mol Med (Berl). 2017;95:323-333. ↗
- Xue XC, et al. Protective effects of pentadecapeptide BPC 157 on gastric ulcer in rats. World J Gastroenterol. 2004;10:1032-1037. ↗
- Kumagai H, Kim SJ, Miller B, et al. MOTS-c modulates skeletal muscle function by directly binding and activating CK2. iScience. 2024;27(11):111212. ↗
- Bolignano D, Greco M, Presta P, Duni A, et al. The Mitochondrial-Derived Peptide MOTS-c May Refine Mortality and Cardiovascular Risk Prediction in Chronic Hemodialysis Patients: A Multicenter Cohort Study. Blood Purification. 2024;53(10):824-837. ↗
- Wan W, Zhang L, Lin Y, Rao X, Wang X, Hua F, Ying J. Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging. Journal of Translational Medicine. 2023;21(1):36. ↗
- Reynolds JC, Lai RW, Woodhead JST, Joly JH, Mitchell CJ, Cameron-Smith D, Lu R, Cohen P, Graham NA, Benayoun BA, Merry TL, Lee C. MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nature Communications. 2021;12(1):470. ↗
- Kim KH, Son JM, Benayoun BA, Lee C. The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress. Cell Metabolism. 2018;28(3):516-524.e7. ↗