Assay Report
Methods · Standard Curves · QC · Results
Quantify cardiac troponins (cTnT, cTnI), heart-type fatty acid-binding protein (FABP3), cardiac myosin light chain (Myl3), and skeletal muscle injury markers (CK, TIMP-1) using electrochemiluminescence — multiplex panels for myocardial injury and drug-induced cardiotoxicity research in rat preclinical models.
Drug-induced cardiotoxicity remains a leading cause of drug candidate attrition — from anthracycline cardiomyopathy to kinase inhibitor-induced cardiac dysfunction. Traditional preclinical cardiac safety assessment relies on histopathology and echocardiography, which detect established structural damage. Cardiac troponins provide earlier, quantitative molecular evidence of cardiomyocyte injury — released into circulation within hours of damage. Our cardiovascular panel combines cTnT, cTnI, FABP3, and Myl3 in a single multiplex measurement from 25 µL of plasma, with complementary skeletal muscle injury markers to distinguish cardiac from skeletal muscle toxicity.
| Panel | Plex | Analytes | Application |
|---|---|---|---|
| Rat Cardiac Injury Panel | 5 | FABP3, cTnT, cTnI (fast-twitch), cTnI (cardiac), Myl3 | Cardiotoxicity screening; repeat-dose toxicology |
| Rat Muscle Injury 2-Plex | 2 | CK, TIMP-1 | Skeletal muscle toxicity screening |
| Rat Muscle Injury 5-Plex | 5 | FABP3, cTnT, cTnI (fast-twitch), cTnI (cardiac), Myl3 | Combined cardiac + muscle assessment with isoform discrimination |
The cTnI fast-twitch isoform identifies skeletal muscle damage, while cTnI cardiac and cTnT are cardiomyocyte-specific — enabling tissue-of-origin discrimination from a single measurement. All services are for research use only.
Anthracyclines, HER2 inhibitors, tyrosine kinase inhibitors can cause cardiac injury. Serial troponin monitoring during preclinical repeat-dose toxicology detects cardiomyocyte injury before functional changes on echocardiography.
FABP3 rises within 1–3 hours — earlier than troponins. Combined with troponins and Myl3, provides temporal resolution of the ischemic injury timeline.
CK is the established myocyte damage marker. Combined with the cardiac panel, skeletal muscle markers enable comprehensive striated muscle safety assessment — distinguishing cardiac-specific from generalized myotoxicity.
| Item | Full Service | Notes |
|---|---|---|
| Sample Processing | Included | EDTA plasma processing protocol |
| Standard Curves | Per-analyte calibrators | Isoform-specific standards |
| QC Samples | Multi-level, duplicate | Low, medium, high |
| Data Report | With temporal plots | Cardiac vs. skeletal isoform summary |
For Research Use Only. Not for diagnostic procedures.
Choose cardiac-only or combined cardiac + muscle panels based on expected toxicity profile.
EDTA plasma, processed within 30 min at 4°C, frozen at −80°C. Ship on dry ice.
Receive quantitative troponin, FABP3, Myl3, and muscle injury data with temporal plots.
| Feature | MSD Cardiac/Muscle Panels | Clinical Chemistry (CK-MB) | Histopathology |
|---|---|---|---|
| Cardiac-Specific Detection | cTnI (cardiac isoform) + cTnT — cardiomyocyte-exclusive | CK-MB — also present in skeletal muscle | Gold standard — direct lesion visualization |
| Temporal Resolution | Serial — within-animal from 25 µL | Serial — functional but less specific | Terminal only — single endpoint |
| Muscle vs. Cardiac Discrimination | Cardiac cTnI + fast-twitch sTnI in same well | Cannot distinguish cardiac from skeletal | Can distinguish by tissue |
| Early Detection | FABP3: 1–3h; cTnI/cTnT: 3–6h | CK-MB: 4–6h | Variable — depends on lesion maturity |
| Animal Reduction (3Rs) | Yes — within-animal serial sampling | Yes — serial chemistry | No — terminal sacrifice groups |
Herman, E.H. et al. (2011) Toxicologic Pathology. 39(4):653-663. "Baseline serum cardiac troponin I concentrations in Sprague-Dawley, SHR, Wistar, WKY, and Fisher rats." DOI: 10.1177/0192623311406931 · PMID: 21521875
O'Brien, P.J. et al. (2006) Laboratory Animals. 40(2):153-171. "Cardiac troponin I is a sensitive, specific biomarker of cardiac injury in laboratory animals." PMID: 16513236
Reagan, W.J. et al. (2013) Toxicologic Pathology. 41(8):1146-1158. "Comparison of cardiac troponin I and T as indicators of doxorubicin-induced cardiotoxicity." DOI: 10.1177/0192623313482056 · PMID: 23531791
Herman, E.H. et al. (2011) Toxicologic Pathology. 39(7):1091-1106. "A multifaceted evaluation of imatinib-induced cardiotoxicity in the rat." DOI: 10.1177/0192623311419524 · PMID: 21937741
While both are cardiac-specific isoforms, cTnI is released exclusively from necrotic cardiomyocytes, while cTnT can also be released from viable cardiomyocytes under stress. Combined with FABP3 and Myl3, the four-marker panel provides temporal resolution from early membrane changes through established structural injury. For research use only.
The cardiac and muscle injury panels are configured for rat preclinical models. For human cardiovascular research, endothelial and vascular markers are available in Vascular Injury panel. Human-specific cardiac troponin assays may be available via U-PLEX custom configuration. For research use only.
Unlike colorimetric ELISA, electrochemiluminescence detection is unaffected by sample color. We recommend noting hemolysis grade on the manifest and processing samples promptly. We flag hemolyzed samples during QC review and report hemolysis grade alongside quantitative data. For research use only.
Yes. Liver injury (ARG1 + GST-α, 25 µL), kidney injury (KIM-1 + NGAL, 25 µL), and cardiac panels (cTnI + cTnT + FABP3, 25 µL) all run on the same instrument. A single 75 µL aliquot supports comprehensive multi-organ safety at each timepoint. For research use only.
CK-MB lacks specificity — it constitutes 1-3% of total CK in skeletal muscle, producing false-positive cardiac injury signals during skeletal muscle damage. MSD panels use cardiac-specific cTnI isoform for unambiguous cardiac origin discrimination, with FABP3 detecting injury at 1-3h (before CK-MB) and cTnI/cTnT remaining elevated for 5-10 days. For research use only.
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