In mice, giving the peptide thymosin‑alpha‑1 helped protect the bone‑marrow from damage caused by the chemotherapy drug 5‑fluorouracil. It did this by boosting factors that support blood‑cell growth and by helping immature T‑cells mature into functional immune cells. The protective effect vanished when T‑cells were blocked, showing the peptide works through the immune system.

Thymosin alpha 1 was shown to prevent the 5-fluorouracil(5-FU)-induced bone marrow toxicity in BDF1 mice, as determined by the cellularity, haemopoietic stem cells (CFU-s) and granulocyte-macrophage colony forming unit (GM-CFU). Furthermore, thymosin alpha 1 increased the levels of colony stimulating factor (CSF) in sera or in culture media of spleen cells derived from 5-FU-treated mice. The treatment of spleen cells with anti-Thy 1,2 antibody plus complement abolished completely the CSF production. The in vivo treatment of donor mice with anti-Thy 1,2 antibody following 5-FU abolished completely the capability of their bone marrow cells to save lethally irradiated recipients. Thymosin alpha 1 treatment prevented the damage by such combined treatment. The present study indicates that thymosin alpha 1 exerts its protective effect against the 5-FU-induced bone marrow toxicity, at least partially, through its effect on the maturation of immature T cells to functional T cells which produce various kinds of lymphokines including CSF.