Discovery of a novel miconazole analogue as a dual apo-IDO1 inhibitor and ABCB1 modulator for cancer immunotherapy and chemosensitizing


Chen P., Chang Y., Ho Y., Tseng K., Lin K., SARI S., ...Daha Fazla

European Journal of Pharmaceutical Sciences, cilt.224, 2026 (SCI-Expanded, Scopus)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 224
  • Basım Tarihi: 2026
  • Doi Numarası: 10.1016/j.ejps.2026.107605
  • Dergi Adı: European Journal of Pharmaceutical Sciences
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Chemical Abstracts Core, EMBASE, MEDLINE, Directory of Open Access Journals, Academic Search Ultimate (EBSCO)
  • Anahtar Kelimeler: ABCB1, Azole, IDO1, Kynurenine, Multidrug resistance
  • Hacettepe Üniversitesi Adresli: Evet

Özet

Indoleamine 2,3-dioxygenase 1 (IDO1) facilitates tumoral immune evasion via the kynurenine (Kyn) pathway, while ABCB1-mediated efflux drives multidrug resistance. Previously, miconazoles were reported as potent IDO1 inhibitors and some azole antifungals inhibit efflux pumps. Herein, we report a miconazole analogue, 1g, which inhibits both mechanisms. An in-house library of miconazole analogues, incorporating oxime ether derivatives with imidazole and pyrazole rings, was screened against Kyn production in IDO1-expressing SK-OV-3 and HeLa cells, yielding the hit pyrazole derivative 1g (IC50(Kyn) = ∼5.8 µM). In vitro LDH assay showed minimal cytotoxicity for 1g and it was well tolerated by in vivo zebrafish model at 2 × IC50(Kyn-SK-OV-3) concentrations. Molecular modelling and biochemical assays indicated apo-form preference for 1g, which suppressed Kyn production without affecting IDO1 protein levels or inducing apoptosis. In indirect co-cultured models, 1g reversed Kyn-mediated immunosuppression, significantly restoring pro-IL1B and TNF levels in LPS-induced THP-1 macrophages. Furthermore, 1g restored Jurkat T cell proliferation, aggregate formation, and PDCD1 expression independent of direct 1g exposure, confirming a Kyn-dependent mechanism. Finally, 1g inhibited ABCB1 function in a dose-dependent manner and enhanced the sensitivity of ABCB1-expressing cells to paclitaxel, demonstrating its efficacy as a multidrug resistance (MDR) reversal agent. Our findings characterised 1g as a promising low-micromolar dual inhibitor of apo-IDO1 and ABCB1 with minimal cytotoxicity. It simultaneously disrupts the immunosuppressive Kyn axis and modulates ABCB1-mediated efflux, which provides a robust pharmacological basis for further development of next-generation combinatorial therapies.