Thymosin alpha 1 for use in treatment of cystic fibrosis
View Patent ↗The present invention concerns Thymosin alpha 1 (Tα1) for use in treatment of cystic fibrosis as a CFTR corrector, CFTR potentiator and anti-inflammatory agent.
1. A method of down-regulating inflammatory cytokines or regulating Th cell balance attributed to cystic fibrosis (CF) in a CF patient, comprising administering to the patient in need thereof a pharmaceutical composition comprising Thymosin alpha 1, wherein the method (i) down-regulates an inflammatory cytokine selected from the group consisting of IL-1α and IL-1β or (ii) promotes the Th1/Treg tolerogenic axis and restrains the inflammatory Th17/Th2 axis.
2. The method of claim 1 , further comprising administering to the patient at least one agent selected from the group consisting of antibiotic, antifungal, cystic fibrosis transmembrane conductance regulator (CFTR) corrector, CFTR potentiator, and anti-inflammatory agent.
3. The method of claim 2 , wherein the antibiotic agent is selected from the group consisting of tobramycin, ciprofloxacin, and colistin.
4. The method of claim 2 , wherein the antifungal agent is selected from the group consisting of itraconazole and amphotericin B.
5. The method of claim 2 , wherein the CFTR corrector or potentiator agent is selected from the group consisting of ivacaftor and lumacaftor.
6. The method of claim 2 , wherein the anti-inflammatory agent is ibuprofen.
7. The method of claim 2 , wherein Thymosin alpha 1 and the at least one agent are administered to the patient together, separately, or sequentially.
8. The method of claim 1 , wherein the pharmaceutical composition comprises one or more excipients and/or coadjuvants.
9. The method of claim 1 , wherein the patient has a CFTR mutation ΔF508.
10. The method of claim 1 , wherein the method down-regulates the inflammatory cytokines IL-1β and IL-1α.
11. The method of claim 10 , wherein the method promotes the Th1/Treg tolerogenic axis and restrains the inflammatory Th17/Th2 axis.
12. The method of claim 1 , wherein the method promotes the Th1/Treg tolerogenic axis and restrains the inflammatory Th17/Th2 axis.