The in vivo immunomodulatory and synergistic anti-tumor activity of thymosin α1-thymopentin fusion peptide and its binding to TLR2.
Li. Juan J; Cheng. Yanna Y; Zhang. Xinke X; Zheng. Lei L; Han. Zhen Z; Li. Pingli P; Xiao. Yuliang Y; Zhang. Qian Q; Wang. Fengshan F
Key Findings
- Tα1‑TP5 (305 µg/kg) reduced immunosuppression caused by hydrocortisone in mice.
- When combined with cyclophosphamide, Tα1‑TP5 improved tumor growth inhibition compared to the chemo drug alone.
- Tα1‑TP5 binds to Toll‑like receptor 2 with a KD of 6.84 µM, a stronger affinity than thymosin‑α1 alone.
Practical Outcomes
- The study suggests the fusion peptide could boost immune function and enhance chemotherapy effects, but it’s still an early‑stage animal experiment. For biohackers, there’s no ready‑to‑use protocol, dosage, or safety data for humans, so the immediate actionable value is limited. Keep an eye on future research if you’re interested in novel immune‑modulating agents.
Summary
A new combined peptide made from thymosin‑α1 and thymopentin (called Tα1‑TP5) helped mice recover from drug‑induced immune suppression and worked better with a chemotherapy drug to slow tumor growth. It also sticks to a immune sensor called TLR2 more strongly than thymosin‑α1 alone.
Abstract
In the present study, the immunomodulatory and synergistic anti-tumor activity of thymosin α1-thymopentin fusion peptide (Tα1-TP5) was investigated in vivo. In addition, the potential receptor of Tα1-TP5 was investigated by surface plasmon resonance (SPR) binding studies. It was found that Tα1-TP5 (305 μg/kg) alleviated immunosuppression induced by hydrocortisone (HC). Tα1-TP5 (305 μg/kg) combined with cyclophosphamide (CY) had a better tumor growth inhibitory effect than CY alone. Furthermore, Tα1-TP5 had a higher affinity (KD=6.84 μmol/L) to toll-like receptor 2 (TLR2) than Tα1 (K(D)=35.4 μmol/L), but its affinity was not significantly different from that of TP5. The results of our present work indicate that Tα1-TP5 can possibly be developed as a new immunomodulatory agent.
Study Information
pubmed
2013
2013-05-14T00:00:00.000Z
10.1016/j.canlet.2013.05.006
34
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