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Updated: Jan 17, 2026

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes
Published on: March 12, 2013
Inhibition of the oncogenic channel Kv10.1 by the antipsychotic drug penfluridol
Paulina León-Sánchez1, Andrea Lizeth Cedillo-Hernández1, María Luisa Durán-Pastén1
1Laboratorio Nacional de Canalopatías, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, México City, México.
Abstract:
Drug repurposing is an increasingly recognized strategy in pharmaceutical development that focuses on identifying new therapeutic uses for already approved drugs, as an alternative to the time-consuming and costly process of developing new molecular entities. This approach has gained traction in oncology, especially in exploring the anticancer potential of non-oncologic agents. In recent years, the antipsychotic drug penfluridol (PNFL) has been identified as having antitumoral properties; however, the underlying mechanisms remain poorly understood. We hypothesized that PNFL may exert its effects by inhibiting the oncogenic potassium channel Kv10.1. Our results demonstrate that PNFL inhibits Kv10.1 activity and reduces cell migration in HEK-Kv10.1 cells. These findings suggest a novel mechanism that may contribute to the drug's antitumoral effects.
Insights
The antipsychotic drug penfluridol (PNFL) shows anticancer potential by inhibiting the Kv10.1 potassium channel. This discovery offers a new mechanism for PNFL
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Drug repurposing accelerates pharmaceutical development by finding new uses for existing drugs.
- Oncology increasingly explores non-cancer drugs for anticancer potential.
- The antipsychotic penfluridol (PNFL) exhibits antitumoral properties, but its mechanism is unclear.
Purpose of the Study:
- To investigate the mechanism behind penfluridol's (PNFL) antitumoral effects.
- To test the hypothesis that PNFL inhibits the oncogenic potassium channel Kv10.1.
Main Methods:
- Electrophysiological recordings to assess Kv10.1 channel activity.
- Cell migration assays using HEK-Kv10.1 cells.
Main Results:
- Penfluridol (PNFL) was confirmed to inhibit Kv10.1 channel activity.
- PNFL significantly reduced cell migration in HEK-Kv10.1 cells.
Conclusions:
- PNFL's inhibition of Kv10.1 represents a novel mechanism for its antitumoral effects.
- This finding supports drug repurposing strategies in oncology.
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