Skin-cancer drug tirbanibulin blocks chikungunya virus entry and works by mouth in mice
- A screen of an approved-drug library for chikungunya virus inhibitors identified tirbanibulin, a microtubule and Src kinase inhibitor, with broad cell-culture activity and favorable selectivity in neuronal and liver cell lines.
- It acts after virus attachment by interfering with clathrin-mediated uptake and possibly fusion, and binding studies indicated direct, tight engagement of the viral E1/E2 glycoprotein complex.
- Given orally in mice, it improved survival and lowered brain viral burden in a lethal neuroinfection model and reduced joint swelling and inflammation in an arthritis model.
💡 Points Based on the abstract
Repurposing is attractive, but a microtubule/Src inhibitor clearing a virus is a red flag for host cytotoxicity masquerading as antiviral activity; "direct E1/E2 binding" needs orthogonal proof. The real question is whether oral exposure in mice exceeds the EC50 at tolerable doses, and whether a topical-dose safety profile survives systemic, repeated dosing.