Fragment-Derived Nicotinic Acid Analogues Inhibit hCA III and Downregulate CA3 Expression in HepG2 Cells
affecting mitochondrial membrane potential. Taken together, these findings identify tractable nicotinic acid-derived fragment hits and associated cellular phenotypes that warrant further mechanistic investigation. These fragment-like hits provide a practical starting point for studying the redox-linked biology of hCA III.
Authors
- Ali M. Qaisi
- Adan Madadha
- Areej Abuhammad (ORCID: https://orcid.org/0000-0003-4978-5059)
- Kapil Gupta (ORCID: https://orcid.org/0000-0002-2115-3503)
- Nidaa A. Ababneh (ORCID: https://orcid.org/0000-0002-2155-3013)
- Yusuf Al‐Hiari
- Edith Sim (ORCID: https://orcid.org/0000-0002-1441-4322)
- Imre Berger (ORCID: https://orcid.org/0000-0001-7518-9045)
- Mohammad A. Ismail (ORCID: https://orcid.org/0000-0001-5039-8764)
- Tamara Sabri
- Dareen T. Yazjeen
- Rya A. Ali
- Rama J. Alghanem
Institutions
- University of Jordan (JO)
- At Bristol (GB)
- University of Bristol (GB)
- University of Oxford (GB)
- Max Planck-Bristol Centre for Minimal Biology (GB)
Publication Details
- Journal
- Biomolecules
- Published
- 2026-04-17
- DOI
- https://doi.org/10.3390/biom16040599
- Primary Topic
- Enzyme function and inhibition
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- University of Jordan
- Deanship of Scientific Research, University of Jordan