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Last update 08 May 2025

FDXR

Last update 08 May 2025

Basic Info

Synonyms

ADR, Adrenodoxin reductase, ADXR

+ [5]

Introduction

Serves as the first electron transfer protein in all the mitochondrial P450 systems including cholesterol side chain cleavage in all steroidogenic tissues, steroid 11-beta hydroxylation in the adrenal cortex, 25-OH-vitamin D3-24 hydroxylation in the kidney, and sterol C-27 hydroxylation in the liver.

Drugs associated with FDXR

ADR + CAR19 iNK (Fate Therapeutics)

Target

CD19 x FDXR

Mechanism

CD19 inhibitors [+1]

Active Org.

Fate Therapeutics, Inc.

Originator Org.

Fate Therapeutics, Inc.

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with FDXR

100 Translational Medicine associated with FDXR

0 Patents (Medical) associated with FDXR

4,069

Literatures (Medical) associated with FDXR

01 Aug 2025·Bioelectrochemistry

Ferredoxin NADP+ reductase for NADPH and NADH regeneration in a flow bioelectrochemical reactor

Article

Author: Etienne, Mathieu ; Housseini, Wassim El ; Lapicque, François ; Lojou, Elisabeth ; Rouhier, Nicolas ; Walcarius, Alain

Ferredoxin-NADP⁺ reductase (FNR) is an efficient and selective biocatalyst to continuously regenerate the NADPH cofactor consumed in biomolecular synthesis for the chemical and pharmaceutical sectors. In this work, FNR from Chlamydomonas reinhardtii was applied to electrochemical regeneration of the nicotinamide cofactors, by combining this enzymatic catalyst in a flow reactor with the oxidation of hydrogen, a clean source of electrons and protons. FNR was immobilized on the surface of oxidized multi-walled carbon nanotubes, which allowed maintaining its activity for over six days under high flow rate. Surprisingly, this modified FNR electrode was effective not only in regenerating NADPH but also NADH. The cofactor regeneration was then applied to the NADH-dependent production of lactate from pyruvate, using L-lactate dehydrogenase (LDH) in the presence of low NAD⁺ concentration (10 µM). Both FNR and LDH enzymes were immobilized in the bioelectrochemical system that achieved a remarkable total turnover number (TTN) of 10⁴ for the nicotinamide cofactor and a faradaic efficiency higher than 80 %.

01 Jul 2025·European Journal of Pharmacology

Tetrandrine and adriamycin reverse multidrug resistance by regulating NLRP3/Caspase-1/GSDMD signaling in human breast cancer cells

Article

Author: Liu, Yuhan ; Hou, Yanxiu ; Xin, Guosong ; Li, Hairu

PURPOSEThis study examined the effects and underlying mechanisms of tetrandrine (TET) combined with adriamycin (ADR) in reversing multidrug resistance (MDR) in breast cancer cells.METHODSCell viability, proliferation, and drug resistance were assessed via the MTT assay. Small interfering RNA (siRNA) transfection was used to knock down GSDMD expression in MCF-7/ADR cells. Pyroptosis induction by the combined TET and ADR treatment was evaluated through morphological observations, cytotoxicity assays, and flow cytometry. The expression levels of mRNA and proteins were analyzed using qRT-PCR and western blotting, respectively.RESULTSAt non-cytotoxic concentrations, the combined treatment of TET and ADR significantly inhibited the growth of MCF-7/ADR cells, demonstrating a synergistic effect in reversing MDR. This combination effectively reduced MDR protein expression in MCF-7/ADR cells via GSDMD modulation, which diminished efflux activity and promoted ADR accumulation. The increased accumulation of ADR subsequently activated the NLRP3/Caspase-1/GSDMD signaling pathway, leading to elevated LDH release and enhanced pyroptosis rates.CONCLUSIONThe combined use of TET and ADR not only suppresses MCF-7/ADR cell growth but also reverses MDR by targeting the NLRP3/Caspase-1/GSDMD pyroptosis pathway. These findings propose a promising therapeutic strategy for combatting MDR in breast cancer and highlight the potential for further clinical application of this combination therapy.

01 Jul 2025·European Journal of Pharmacology

TRPM4 channels contribute to Adriamycin chemoresistance in breast cancer cells

Article

Author: Zhong, Wu ; Lan, Kun ; Wang, Mengyuan ; Yang, Xinyue ; Yan, Li ; Chen, Xingjuan ; Cao, Ruiyuan ; Guo, Juan ; Liu, Fang ; Yang, Shangze

Chemoresistance presents a critical challenge in breast cancer treatment. Here, we report that transient receptor potential melastatin 4 (TRPM4) plays a role in modulating doxorubicin (ADR) resistance in breast cancer cells. TRPM4 expression was significantly upregulated at both the mRNA and protein levels in MCF-7/ADR cells, a human breast cancer cell line resistant to the chemotherapy drug ADR. Pharmacological inhibition or knockdown of TRPM4 restored ADR sensitivity, while its overexpression in non-resistant MCF-7 cells diminished drug response, confirming the regulatory role of TRPM4 in resistance mechanisms. Western blot analyses confirmed that elevated TRPM4 expression drives P-glycoprotein (P-gp) upregulation in both MCF-7/ADR and KBv200 cells (KB vinblastine 200 resistant cell line), as well as in Huh7 (human hepatocellular carcinoma cell line) and HCT116 (human colorectal cancer cell line). In addition, we demonstrate that TRPM4 inhibition suppresses the level of NF-κB, a pivotal transcription factor regulating P-gp expression. Furthermore, we found that TRPM4-mediated cellular swelling, rather than membrane depolarization, is the primary driver of P-gp overexpression. Drug-resistant MCF-7/ADR cells exhibited significantly larger cell sizes compared to non-resistant MCF-7 cells, and this effect was reversed following TRPM4 inhibition. The swelling was induced by hypotonic stress rather than changes in membrane potential, further confirming the role of TRPM4 in P-gp regulation through volume changes. Analysis of the TCGA (The Cancer Genome Atlas) database revealed that elevated TRPM4 expression correlates with reduced patient survival, suggesting that TRPM4 plays a role in both drug resistance and tumor progression. Our findings provide new insights into the role of TRPM4 in resistance mechanisms and propose that targeting TRPM4 could represent an innovative therapeutic strategy to overcome chemoresistance and enhance drug efficacy in breast cancer.

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FDXR

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