ACAD8

Chr 11AR

acyl-CoA dehydrogenase family member 8

Also known as: ACAD-8, ARC42, IBDH

The protein is isobutyryl-CoA dehydrogenase, a mitochondrial enzyme that catalyzes the conversion of 2-methylpropanoyl-CoA to (2E)-2-methylpropenoyl-CoA in the valine catabolic pathway. Mutations cause isobutyryl-CoA dehydrogenase deficiency, inherited in an autosomal recessive pattern. The gene shows low constraint against loss-of-function variants (LOEUF 1.27), consistent with the recessive inheritance pattern where heterozygous carriers are typically unaffected.

Summary from RefSeq, OMIM, UniProt
Research Assistant →

Primary Disease Associations & Inheritance

Isobutyryl-CoA dehydrogenase deficiencyMIM #611283
AR
0
Active trials
8
Pubs (1 yr)
145
P/LP submissions
12%
P/LP missense
1.27
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryACAD8
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Gene-Disease Validity (ClinGen)
isobutyryl-CoA dehydrogenase deficiency · ARDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
127 unique Pathogenic / Likely Pathogenic· 152 VUS of 419 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.27LOEUF
pLI 0.000
Z-score 0.51
OE 0.89 (0.641.27)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.22Z-score
OE missense 0.96 (0.861.07)
221 obs / 230.5 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.89 (0.641.27)
00.351.4
Missense OE0.96 (0.861.07)
00.61.4
Synonymous OE1.26
01.21.6
LoF obs/exp: 22 / 24.7Missense obs/exp: 221 / 230.5Syn Z: -1.95
DN
0.7033th %ile
GOF
0.6931th %ile
LOF
0.3649th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and gain-of-function). Both the Badonyi & Marsh prediction and the broader genomic evidence point to dominant-negative as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median
GOFprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

419 submitted variants in ClinVar

Classification Summary

Pathogenic103
Likely Pathogenic24
VUS152
Likely Benign63
Benign41
Conflicting23
103
Pathogenic
24
Likely Pathogenic
152
VUS
63
Likely Benign
41
Benign
23
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
8
5
89
1
103
Likely Pathogenic
5
10
9
0
24
VUS
2
109
34
7
152
Likely Benign
0
7
29
27
63
Benign
0
1
39
1
41
Conflicting
23
Total1513220036406

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

ACAD8 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
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