How does MSD CRP measurement compare to high-sensitivity CRP (hsCRP) assays?

MSD measures CRP across the full dynamic range ( 100 µg/mL) in a single measurement. hsCRP assays are optimized for the low range used in cardiovascular risk stratification. ECL avoids dilution reanalysis when values exceed hsCRP linear range.

Why does the Vascular Injury Panel need 1:1,000 dilution?

CRP and SAA circulate at µg/mL — 1,000-100,000× higher than typical cytokines. 1:1,000 dilution brings them into linear range while preserving ICAM-1 and VCAM-1 measurement at endogenous ng/mL levels.

Can I run the Vascular Injury Panel alongside cytokine or angiogenesis panels?

Yes. All MSD panels run on the same instrument from the same 25 µL per panel. A single 100 µL plasma aliquot can support Vascular Injury + Angiogenesis + Proinflammatory + Metabolic panels.

What is the difference between ICAM-1 and VCAM-1?

ICAM-1 binds all leukocytes and reflects general endothelial activation. VCAM-1 is selective for monocytes and lymphocytes — in atherogenesis, VCAM-1 expression precedes morphological lesion formation.

What sample types are compatible with the Vascular Injury Panel?

Serum and EDTA plasma are both validated. Maintain consistent matrix within a study. For samples with CRP >100 µg/mL, additional dilution can be applied.

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MSD Vascular Injury Panel — CRP, ICAM-1, VCAM-1 & SAA Assay

MSD V-PLEX · U-PLEX

Endothelial Activation · Acute Phase Response · Vascular Inflammation

MSD Vascular Injury Panel — CRP, ICAM-1, VCAM-1 & SAA Assay

Quantify endothelial activation (ICAM-1, VCAM-1), acute-phase response (CRP, SAA), and coagulation (Factor VII) using electrochemiluminescence — a single 25 µL sample replaces four separate ELISA measurements while providing 4–5 log dynamic range that CRP ELISA cannot match without serial dilution.

CRP and SAA span 3+ orders of magnitude from healthy baseline (<1 µg/mL) to acute inflammation (>100 µg/mL). In conventional ELISA, this means running every sample at minimum two dilutions with dilution linearity verification. MSD's ECL detection measures the full range in a single 25 µL well — validated against established clinical methods in a 574-participant cross-study (PLoS ONE, 2013). ICAM-1 and VCAM-1 are shed from activated endothelium into circulation, where their soluble forms reflect the total body endothelial activation burden. The 5-Plex adds Factor VII, connecting endothelial status to the extrinsic coagulation cascade — relevant for metabolic syndrome and diabetes research where vascular activation and hypercoagulability co-exist. Each biomarker is measured on its own spatially separated electrode spot within one well, eliminating the cross-assay variability that comes from running these markers across separate ELISA plates, separate dilutions, and separate analytical runs.

Inquire About Vascular Injury Panels View Panel Configurations

Vascular Injury Biomarker Panel — Endothelial Activation & Systemic Inflammation

Vascular health depends on the balance between endothelial barrier integrity and systemic inflammatory tone. The endothelium is not a passive conduit — it is a metabolically active organ that regulates leukocyte trafficking, vascular tone, coagulation, and nutrient exchange. Endothelial activation is an early event in atherosclerosis, diabetes, hypertension, and drug-induced vascular injury. ICAM-1 and VCAM-1 are adhesion molecules stored in endothelial Weibel-Palade bodies and rapidly surface-expressed upon cytokine stimulation (TNF-α, IL-1β). Their extracellular domains are proteolytically shed into circulation, where soluble levels reflect the aggregate endothelial activation state across the entire vascular bed. CRP and SAA are hepatocyte-derived acute-phase reactants induced by IL-6 — but they capture different aspects of the inflammatory response: CRP is the stable, widely standardized cardiovascular risk marker; SAA is more dynamically responsive (up to 1,000-fold induction), rapidly associates with HDL, and displaces ApoA-I, converting HDL from anti-inflammatory to pro-inflammatory. Factor VII bridges to coagulation — activated endothelium expresses tissue factor that initiates the extrinsic cascade, and Factor VII is the first enzyme in that pathway. Measuring all five in one well captures the endothelial-inflammatory-coagulation axis that no single marker can represent.

Why Multiplex Matters Here
CRP spans 3+ logs — ECL captures it in one run: CRP circulates at <1 µg/mL in low-risk individuals and exceeds 100 µg/mL during acute inflammation. Conventional hsCRP ELISA has a narrow linear range requiring 1:100–1:1,000 dilution with serial linearity checks. MSD's 4–5 log dynamic range measures all concentrations in a single 25 µL well, eliminating the most common source of CRP reanalysis.
ICAM-1 and VCAM-1 measure different leukocyte recruitment: ICAM-1 binds CD11a/CD18 (LFA-1) on all leukocytes — it is a broad endothelial activation marker. VCAM-1 binds VLA-4 (α4β1), expressed only on monocytes, lymphocytes, and eosinophils — it is selective for mononuclear cell recruitment. Measuring both distinguishes broad endothelial activation (ICAM-1) from monocyte-specific recruitment (VCAM-1), which is the initiating step in atherogenesis.
SAA vs CRP — different biology, same panel: CRP is stable and standardized; SAA is more dynamically responsive, directly interacts with HDL, and may better capture acute inflammatory changes. Studies comparing both in the same multiplex panel show they provide complementary rather than redundant information in cardiovascular and metabolic research.
Cross-validated against clinical methods: The MSD 4-plex (CRP-SAA-ICAM-1-VCAM-1) was validated against established ELISA/immunoturbidimetric methods in 574 participants, with intra-class correlation coefficients of 0.996 (CRP), 0.895 (ICAM-1), and 0.858 (VCAM-1) after Deming regression (PLoS ONE, 2013).

Vascular Injury Panel Configurations

Panel Type	Plex	Biomarkers	Format	Best For
Vascular Injury Panel 2	4	CRP, ICAM-1, SAA, VCAM-1	V-PLEX	Core endothelial activation + systemic inflammation; 1:200 dilution
Vascular Injury Combo 1	5	CRP, Factor VII, ICAM-1, SAA, VCAM-1	U-PLEX	Adds Factor VII for coagulation; 1:2 dilution for higher sensitivity
Vascular Injury U-PLEX Custom	2–10	Select from vascular injury catalog: add E-Selectin, P-Selectin, Thrombomodulin, MCP-1, IL-8, or other endothelial markers as needed	U-PLEX	Extended vascular panel beyond the standard 4/5-plex; add exploratory markers
54/71-Plex (with Vascular Injury)	54–71	CRP, SAA, ICAM-1, VCAM-1 + VEGF-A, PlGF, Tie-2, FGF basic, Eotaxin, IP-10, MCP-1, MDC, TARC, 40+ cytokines	V-PLEX	Vascular injury + angiogenic + cytokine profiling from one 25 µL sample

The V-PLEX format requires a 1:200 dilution to accommodate CRP µg/mL concentrations alongside ng/mL ICAM-1/VCAM-1. The U-PLEX format offers improved sensitivity (pg/mL range) at a lower 1:2 dilution and adds Factor VII for coagulation context. Both panels measure all analytes from a single 25 µL sample aliquot. For research use only.

Vascular Injury Biomarkers — CRP, SAA, ICAM-1 & VCAM-1 Assay

CRP — Acute-Phase Inflammation Marker

C-reactive protein is the most extensively studied systemic inflammation biomarker. Its concentration spans from <1 µg/mL to >100 µg/mL. Conventional hsCRP ELISA tops out at ~10 µg/mL — every sample above that requires dilution and re-run. MSD ECL detects the full range in a single measurement. LOD: 0.04 µg/mL. No hook effect to 5,000 µg/mL.

SAA — HDL-Associated Acute-Phase Protein

Serum Amyloid A becomes the predominant HDL protein during acute-phase response, displacing ApoA-I and redirecting HDL to pro-inflammatory functions. Up to 1,000-fold induction. Elevation correlates with HDL dysfunction in metabolic syndrome and cardiovascular disease. LOD: 0.03 µg/mL.

ICAM-1 — Pan-Leukocyte Adhesion Marker

Intercellular Adhesion Molecule-1 (CD54) shed from activated endothelium reflects the total body endothelial activation burden. Binds LFA-1 on all leukocytes — a broad, non-selective endothelial stress marker. Elevated in atherosclerosis, hypertension, and diabetes research. LOD: 0.002 µg/mL.

VCAM-1 — Monocyte-Selective Adhesion Marker

VCAM-1 (CD106) binds VLA-4 expressed on monocytes and lymphocytes, but not neutrophils — more specific for monocyte-mediated inflammation. VCAM-1 is among the earliest endothelial changes in atherogenesis. ICAM-1 alone = broad activation; ICAM-1 + VCAM-1 = monocyte recruitment signal. LOD: 0.02 µg/mL.

Wide-Range CRP Detection — ECL vs Conventional ELISA

The Problem: ELISA Cannot Span the CRP Range

CRP is the most commonly requested biomarker in vascular research — yet it is among the most analytically challenging to measure across the full biological range.

hsCRP ELISA: Linear range ~0.1–10 µg/mL. Any sample >10 µg/mL (common in acute CV events, post-surgical, infection) requires 1:100–1:500 dilution and reanalysis. Studies report 15–30% of cardiovascular research samples require dilution re-runs.
ECL (MSD): Linear range 0.04–100 µg/mL. No dilution re-runs for the full biological range. A single measurement covers everyone from low-risk cohort participants to acute myocardial infarction patients.
Cross-validated: In 574 participants (PLoS ONE, 2013), MSD ECL showed intra-class correlation of 0.996 with clinical CRP methods after Deming regression — demonstrating that the wider range does not compromise accuracy.

Vascular Injury Panel Specifications

TechnologyMSD V-PLEX · U-PLEX

CRP Range0.04–100 µg/mL (no hook to 5,000)

SAA Range0.03–1,000 µg/mL

ICAM-1 Range0.002–100 µg/mL

VCAM-1 Range0.02–100 µg/mL

Sample Volume25 µL per well

V-PLEX Dilution1:200

U-PLEX Dilution1:2 (higher sensitivity)

Plate Format96-well MULTI-SPOT 4-spot

Read Time~70 seconds

Validated MatricesSerum, EDTA Plasma

Cross-ValidationICCs: CRP 0.996, ICAM-1 0.895, VCAM-1 0.858

Service Details

Service Package

Item	Full Service	Notes
Sample Processing	Included	1:200 dilution with documented dilution factor
Standards	8-point per analyte	Wide-range CRP calibrators covering 0.04–100 µg/mL
QC Samples	3-level, duplicate	Low, medium, high across CRP range
Report	Excel + PDF	Concentrations, QC, dilution info, temporal plots

For Research Use Only. Not for diagnostic procedures.

How to Get Started

Select Configuration

4-Plex (endothelial + inflammation) or 5-Plex (adds Factor VII for coagulation context).

Collect & Ship

Serum or EDTA plasma. Standardize AM collection (CRP has diurnal variation). Ship on dry ice.

Receive Data

Endothelial activation + inflammatory marker data with QC and dilution documentation.

What You Receive

Quantitative vascular injury report — CRP, SAA, ICAM-1, VCAM-1 (± Factor VII) concentrations with per-analyte QC metrics, standard curve R², and LOD/LLOQ (Excel + PDF)
Raw ECL data — per-spot signal values, plate maps, and standard curve plots for each of the 4–5 analytes
CRP range documentation — dilution factor, linearity verification, no hook confirmation for samples >100 µg/mL
Longitudinal tracking — serial CRP/SAA trends with fold-change from baseline, ICAM-1/VCAM-1 time-course plots
Methods summary — panel composition, dilution protocol, QC criteria, and published validation reference (PLoS ONE, 2013)

Why Choose MSD for Vascular Injury Markers

Four markers from one 25 µL sample — vs. 400 µL for ELISA: CRP, SAA, ICAM-1, and VCAM-1 measured simultaneously. Equivalent ELISA coverage requires 4 separate assays, 4 separate dilutions, and 400+ µL.
CRP across the full biological range — no re-runs: Single ECL measurement covers <1 µg/mL to >100 µg/mL. ELISA requires 1:100–1:500 dilution re-runs for the same range, with documented dilution linearity failures in 5–15% of samples.
ICAM-1 vs VCAM-1 differential: Measuring both in one well distinguishes broad endothelial activation (ICAM-1) from monocyte-selective recruitment (VCAM-1) — providing mechanistic insight, not just a single activation score.
Cross-validated against established methods: 574-participant study confirmed MSD ECL vs clinical CRP/ELISA methods with ICCs of 0.996 (CRP), 0.895 (sICAM-1), and 0.858 (sVCAM-1).
Coagulation add-on (5-Plex): Factor VII links endothelial activation to the extrinsic coagulation cascade — relevant for metabolic syndrome, diabetes, and COVID-19-associated coagulopathy research where vascular activation and thrombotic risk co-exist.

Supporting Publications

van Bussel, B.C.T. et al. (2013) PLoS ONE. 8(3):e58576. "Multiple Inflammatory Biomarker Detection in a Prospective Cohort Study: A Cross-Validation between Well-Established Single-Biomarker Techniques and an Electrochemiluminescence-Based Multi-Array Platform." DOI: 10.1371/journal.pone.0058576 · PMID: 23554903 — 574-participant cross-validation of MSD 4-plex vs clinical CRP/ELISA methods; ICCs of 0.996 (CRP), 0.895 (sICAM-1), 0.858 (sVCAM-1).
Ridker, P.M. et al. (2017) NEJM. 377(12):1119-1131. "Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease." DOI: 10.1056/NEJMoa1707914 · PMID: 28845751 — CANTOS trial demonstrating CRP-guided anti-inflammatory therapy in CV disease.
Libby, P. et al. (2021) Circulation Research. 128(12):1819-1833. "Inflammation and cardiovascular disease." PMID: 34085822 — Comprehensive review of ICAM-1, VCAM-1, and CRP in CV research.
Gustafson, B. et al. (2007) Diabetologia. 50(11):2340-2348. "Inflammation and endothelial activation in obesity and insulin resistance." PMID: 17823774 — MSD multiplex measurement of CRP, ICAM-1, and VCAM-1 in metabolic disease.

Vascular Injury Panel FAQ

How does MSD's wide-range CRP compare to hsCRP — are results interchangeable?

The 574-participant cross-validation study (van Bussel et al., PLoS ONE, 2013) directly addressed this question. After Deming regression to align calibration between methods, the intra-class correlation between MSD ECL and clinical CRP methods was 0.996 — indicating near-perfect agreement across the measured range. The key difference is that MSD measures CRP from <1 µg/mL to >100 µg/mL in a single well, while hsCRP ELISA requires 1:100–1:500 dilution for samples exceeding its ~10 µg/mL linear range. For research studies where CRP may span this full range — cardiovascular cohorts including acute events, post-surgical samples, metabolic syndrome — MSD avoids the reanalysis rate that ELISA imposes. All services are for research use only.

Why measure both ICAM-1 and VCAM-1 — aren't they redundant?

They are complementary, not redundant. ICAM-1 binds LFA-1 on all leukocyte subtypes, making it a broad endothelial activation marker. VCAM-1 binds VLA-4, expressed selectively on monocytes, lymphocytes, and eosinophils but not neutrophils — making it more specific for monocyte-mediated inflammation, which is the initiating step in atherogenesis. In research contexts, elevated ICAM-1 + VCAM-1 suggests active monocyte recruitment beyond general endothelial activation. Several studies have shown that the combination provides better cardiovascular risk discrimination than either marker alone. Measuring both in the same well eliminates cross-assay variability as a confound when comparing their relative elevations. For research use only.

What does Factor VII add to the vascular injury assessment?

Factor VII is the initiating enzyme of the extrinsic coagulation cascade — it binds tissue factor exposed at sites of endothelial injury and activates Factor X, leading to thrombin generation. Including Factor VII in the 5-Plex bridges endothelial activation status to coagulation potential. This is particularly relevant in metabolic syndrome and diabetes research, where activated endothelium and hypercoagulability co-exist. Elevated Factor VII in these populations correlates with cardiovascular risk independently of CRP. For research use only.

What sample handling affects CRP and SAA measurements?

CRP exhibits diurnal variation with a morning peak — standardize collection time across study visits. CRP is stable in serum/plasma for 7 days at 4°C and at least 12 months at −80°C. SAA is similarly stable but more sensitive to repeated freeze-thaw than CRP — single-use aliquots recommended. Hemolyzed samples do not interfere with ECL readout but may indicate collection technique issues. For research use only.

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