Target intelligence / Profile preview

Ferredoxin--NADP(+) reductase (human mitochondrial) (FDXR)

Target
FDXR
Molecular classification
Enzyme, Oxidoreductase, Mitochondrial protein
01

Overview

**Ferredoxin--NADP(+) reductase (FDXR)** is a mitochondrial flavoprotein enzyme that catalyzes electron transfer from NADPH to mitochondrial ferredoxins, primarily FDX1 and FDX2[1][3][5]. This provides the reducing power necessary for mitochondrial cytochrome P450 enzymes involved in steroid hormone biosynthesis, heme production, and iron–sulfur (Fe-S) cluster assembly[1][3][5]. FDXR is also a transcriptional target of the p53 family and participates in cellular stress responses and apoptosis regulation[5]. Loss-of-function mutations in FDXR cause rare mitochondrial disorders, including sensorineural hearing loss and optic atrophy, due to disturbed Fe-S cluster biogenesis and iron metabolism[1][5].

Other names
Adrenodoxin reductase, NADPH:adrenodoxin oxidoreductase, mitochondrialADXRARADRANOAFerredoxin reductaseFerredoxin--NADP(+) reductaseadrenodoxin-NADP(+) reductaseMMDS9Bepididymis secretory sperm binding protein[4][5]
02

Mechanism of action

Drugs modulating this enzyme would be expected to alter mitochondrial steroidogenesis, iron–sulfur cluster assembly, or cause mitochondrial dysfunction via disrupted electron transport; Mechanisms would include inhibition or activation of electron transfer from NADPH to ferredoxin isoforms, thereby impacting downstream pathways[1][3][5]

03

Biological functions

Electron transferSteroid biosynthesisIron–sulfur cluster biogenesisCellular metabolismCellular stress responseApoptosis regulation[1][3][5]
04

Disease associations

Mitochondriopathies/mitochondrial diseaseNeurosensory deficits (e.g., optic atrophy, hearing loss)Tumor suppression/cancerDisorders of steroid hormone biosynthesisIron metabolism disorders[1][5]
05

Safety considerations

Dysfunction or inhibition can disrupt mitochondrial homeostasis, leading to impaired energy metabolism, iron overload, neurosensory deficits, and steroid disturbancesSystemic inhibition likely causes significant toxicity[1][5]
06

Interacting drugs

None directly documented for primary clinical use

1 more in the full profile.

07

Biomarkers

FDXR expression or mutation status may serve as a biomarker in mitochondrial disease (sensorineural hearing loss, optic atrophy)May also be relevant for mitochondrial stress response or p53 pathway activity in oncology research[1][5]

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