Target intelligence / Profile preview

NADH:ubiquinone oxidoreductase subunit A7 (NDUFA7)

Target
NDUFA7
Molecular classification
Enzyme subunit (respiratory complex), Mitochondrial protein, Other (Accessory protein of Complex I)
01

Overview

NADH:ubiquinone oxidoreductase subunit A7 (NDUFA7) is an accessory, non-catalytic subunit of mitochondrial complex I (NADH:ubiquinone oxidoreductase), the first and largest enzyme of the respiratory electron transport chain[1][6][7]. Located on the inner mitochondrial membrane, complex I drives electron transfer from NADH to ubiquinone, powering ATP production by creating a proton gradient. NDUFA7 is a small hydrophobic protein (12.5 kDa, 113 amino acids) that contributes structurally to the integrity and stability of the multiprotein complex but is not involved directly in electron transfer or catalysis[1][2][3]. Mutations or dysfunction of NDUFA7 and other complex I subunits can compromise mitochondrial respiration, resulting in a range of inherited or acquired disorders, including several types of anemia, neurodegenerative conditions, metabolic diseases, and various cancers[1][2]. While NDUFA7 is not typically considered a direct therapeutic target, its role is crucial for proper mitochondrial function and cellular energy homeostasis.

Other names
NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subunit 7CI-B14.5aB14.5aComplex I-B14.5aNADH-ubiquinone oxidoreductase subunit B14.5acomplex I B14.5a subunitNDUFA7
02

Mechanism of action

Not targeted directly by drugs; complex I inhibitors act by blocking electron transport or ubiquinone reduction in the entire complex

03

Biological functions

Mitochondrial electron transportATP synthesis (via oxidative phosphorylation)Electron transfer from NADH to ubiquinoneStructural stabilization of complex I
04

Disease associations

Mitochondrial disordersDiamond-Blackfan anemiaLeukoencephalopathy with ovarian failureType 1 and type 2 diabetes mellitusSchizophreniaBreast cancerBipolar disorderUrinary bladder carcinomaProstate cancer
05

Safety considerations

Not drug-targeted directly; general complex I inhibition may lead to mitochondrial dysfunction, energy failure, or increased reactive oxygen species.
06

Interacting drugs

None known specific to NDUFA7; complex I inhibitors (e.g., rotenone, piericidin A) target the complex as a whole, not individual subunits
07

Biomarkers

None specific to NDUFA7 currently described; changes in complex I activity (including that involving NDUFA7) may serve as indirect mitochondrial dysfunction biomarkers in certain diseases

Beyond the preview

Go deeper on NADH:ubiquinone oxidoreductase subunit A7 (NDUFA7).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on NADH:ubiquinone oxidoreductase subunit A7 (NDUFA7).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call