Complement C5b-9 (MAC)
complexC5b-9 amplifies endothelial injury and inflammatory cell recruitment through complement-driven lysis and activation.
Pathway placement
Cascade stepPlaque inflammation
Confidencehigh
RationaleComplement membrane-attack complex; direct inflammation marker elevated in AMI.
Also acts inEndothelial activation/erosion
Druggability
Not assessed (no mapped human gene target).
Type I vs Type II discrimination
ScoresType-II-associated
R — rupture / Type-I—
C — confounder / Type-II67
A — assay feasibility58
E — evidence strength8
T1DI (composite)1
Specificity differential (R−C)-52
Confounder panel (Type-II drivers)
1sepsis / systemic inflammationmag 2
2anemia / acute blood lossn/a
3hypovolemia / dehydrationn/a
4tachyarrhythmian/a
5hypoxemia / respiratory failuren/a
6hypertensive emergencyn/a
7high-demand / peri-operative stressn/a
Coverage: 1/7 confounders with evidence
Tier: deep-scored (abstract-extracted) · 2 supporting references. See the discrimination table for all markers.
Assay & specimen
Class-level default (no specific cleared assay)— generic method inferred from analyte class; confirm against a specific product insert before use.
Specimen
Plasma (citrate for coagulation complexes)
Collection tube
Sodium citrate 3.2% (light blue-top) · K2/K3-EDTA (lavender-top)
Method / principle
Sandwich ELISA against neo-complex epitope
Reagent / substrate
Antibody pair recognizing the assembled complex
Platform
ELISA plate
Turnaround · availability
Research / send-out · Research/specialized
Literature evidence(2)
- DSCAML1+ extracellular vesicles revealed by single-vesicle proteomics as a novel biomarker and therapeutic target in myocardial infarction.Journal of nanobiotechnology · 2026 · PMID 41872860 · doi
- Multiplex quantitative imaging of human myocardial infarction by mass spectrometry-immunohistochemistry.International journal of legal medicine · 2018 · PMID 29556718 · doi