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Protein / target

Medium-chain specific acyl-CoA dehydrogenase, mitochondrial

Encoded byACADMP11310Homo sapiensSwiss-Prot
UniProt: P11310Ensembl: ENSG00000117054HGNC: HGNC:89NCBI Gene: 34
Small-molecule tractable
Druggability
Structure with Ligand
1
Research papers

Protein at a glance

Biological role

Medium-chain fatty acyl-CoA dehydrogenase

Strongest disease association

Genetic Diseases, Inborn

Via encoding gene ACADM · Genetic evidence · score 0.84

Research activity

Emerging research

1 papers · latest 1999

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Medium-chain specific acyl-CoA dehydrogenase is one of the acyl-CoA dehydrogenases that catalyze the first step of mitochondrial fatty acid beta-oxidation (FAO), breaking down fatty acids into acetyl-CoA and allowing the production of energy from fats.

View complete UniProt function annotation

Medium-chain specific acyl-CoA dehydrogenase is one of the acyl-CoA dehydrogenases that catalyze the first step of mitochondrial fatty acid beta-oxidation (FAO), breaking down fatty acids into acetyl-CoA and allowing the production of energy from fats (PubMed:1970566, PubMed:21237683, PubMed:2251268, PubMed:8823175). The first step of FAO consists in the proR-proR stereospecific alpha, beta-dehydrogenation of fatty acyl-CoA thioesters using the electron transfer flavoprotein (ETF) as their physiologic electron acceptor, resulting in the formation of trans-2-enoyl-CoA ((2E)-enoyl-CoA) (PubMed:2251268). ETF is the electron acceptor that transfers electrons to the main mitochondrial respiratory chain via ETF-ubiquinone oxidoreductase (ETF dehydrogenase) (PubMed:15159392, PubMed:25416781). Among the different mitochondrial acyl-CoA dehydrogenases, medium-chain specific acyl-CoA dehydrogenase has preference for fatty acyl-CoAs with saturated 6 to 12 carbons long primary chains, making it but can also catalyze longer chains such as C14 and C16 (PubMed:1970566, PubMed:21237683, PubMed:2251268, PubMed:8823175)

Subcellular location

Mitochondrion matrix
Domains and Gene Ontology detail (18)

Gene Ontology

  • Caxon
  • Ccytoplasm
  • Cmitochondrial matrix
  • Cmitochondrial membrane
  • Cmitochondrion
  • Cnucleus
  • Facyl-CoA dehydrogenase activity
  • Fflavin adenine dinucleotide binding
  • Fidentical protein binding
  • Fmedium-chain fatty acyl-CoA dehydrogenase activity
  • Pcarnitine biosynthetic process
  • Pcarnitine metabolic process, CoA-linked

421 aa · 47 kDa · 2 isoforms

Biological roles

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Lipid & lipoprotein metabolismUniProt · GO
View supporting evidence

Lipid & lipoprotein metabolism

  • ·Medium-chain specific acyl-CoA dehydrogenase is one of the acyl-CoA dehydrogenases that…
  • ·fatty acid beta-oxidation
  • ·fatty acid beta-oxidation using acyl-CoA dehydrogenase
  • ·medium-chain fatty acid catabolic process

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene ACADM

Gene-level evidence surfaced through the gene ACADM that encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Genetic Diseases, Inborn
0.85Well supported

Genetic evidence dominant · Open Targets 0.52

Skin Diseases
0.47Limited support

Genetic evidence dominant · Open Targets 0.29

Heart Diseases
0.42Limited support

Genetic evidence dominant · Open Targets 0.25

View evidence synthesis (3)
Genetic Diseases, InbornWell supported
0.85
agreement 0.71–0.98
Genetic99%Literature1%

Open Targets aggregate 0.52 · 2 independent evidence families

Skin DiseasesLimited support
0.47
agreement 0.35–0.59
Genetic100%

Open Targets aggregate 0.29 · 1 independent evidence family

Heart DiseasesLimited support
0.42
agreement 0.28–0.56
Genetic99%Literature1%

Open Targets aggregate 0.25 · 2 independent evidence families

The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations
Genetic Diseases, Inborn0.52
Skin Diseases0.29
Heart Diseases0.25

Tractability

Small molecules — Emerging

Feasibility evidence (structure with ligand and high-quality pocket) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

Feasibility evidence (database ubiquitination and half-life data) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (4)
SM · Structure with LigandSM · High-Quality PocketPR · Database UbiquitinationPR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 1999

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

Peroxisome proliferator-activated receptor alpha mediates the adaptive response to fasting.1,252 cites

Kersten S · The Journal of clinical investigation · 1999

Recent

Peroxisome proliferator-activated receptor alpha mediates the adaptive response to fasting.

Kersten S · The Journal of clinical investigation · 1999

Europe PMC papers linked directly to this protein.