This article explains how MOG-induced experimental autoimmune encephalomyelitis (EAE) is induced and measured in mice, what a sponsor should fix in the protocol, and where its interpretation stops. A reviewed source is explicit that chronic EAE is not multiple sclerosis (MS) and that no animal model reproduces every aspect of the human disease.[S3]
A standard protocol immunizes C57BL/6 mice with a peptide from myelin oligodendrocyte glycoprotein (MOG), using complete Freund’s adjuvant (CFA), with pertussis toxin (PTX) as part of the induction schedule.[S1][S2] The study then measures neurologic signs and tissue or immune endpoints in the induced mouse condition. These measurements characterize EAE in the animal; they do not diagnose or reproduce MS in a patient.[S3]
Use the model to test a defined hypothesis within the induced immune and neurologic phenotype, such as whether an intervention changes the prespecified score or tissue endpoint. A treatment effect in EAE is nonclinical evidence and does not establish efficacy in MS.[S3]
| Endpoint family | Commissioning decision |
|---|---|
| Clinical score | Use one written scale, define the observation schedule, blinding, handling of moribund animals, and the primary analysis before the study starts.[S4] |
| Histopathology | Specify tissues, levels, stains, scoring rules, and whether the reader is blinded. |
| Immune analysis | Specify compartments, cell panels, collection timepoints, and whether the analysis is primary or exploratory. |
The useful question is not whether a laboratory offers “EAE,” but whether its exact induction and readout plan fits the mechanism under study. Require the strain and substrain, MOG peptide, CFA formulation, PTX schedule, scoring rubric, randomization, blinding, humane endpoints, and analysis plan in the protocol.
| Score | Hooke protocol definition[S4] |
|---|---|
| 0 | No clinical signs |
| 1 | Limp tail |
| 2 | Limp tail and weakness of hind legs |
| 3 | Limp tail and complete paralysis of hind legs |
| 4 | Limp tail, complete hind-leg paralysis, and partial front-leg paralysis |
| 5 | Moribund or dead |
Mendel, Kerlero de Rosbo, and Ben-Nun reported MOG35-55-induced EAE in H-2b mice in 1995.[S1] The paper supports the induction claim. It should not be cited as evidence that the resulting T-cell response or neurologic signs are equivalent to MS in people.[S3]
Record the exact mouse strain and peptide because the 1995 study describes an H-2b-restricted encephalitogenic MOG epitope.[S1] Treat any change of substrain, immunization material, or schedule as a design change that may alter the induced phenotype.
Biocytogen’s US-facing product page describes EAE induction with MOG35-55/CFA and intraperitoneal PTX, with PTX administered 2 and 24 hours after immunization, and shows data for C57BL/6J and C57BL/6N mice (company website, accessed September 3, 2026).[S6] This listing confirms an available protocol example; it is not a recommendation of the company or service.
| Published item | Verified detail | Sponsor check |
|---|---|---|
| Induction service example | MOG35-55/CFA; PTX given intraperitoneally at 2 and 24 hours; C57BL/6J and C57BL/6N examples.[S6] | Confirm cohort design, scoring rubric, tissues, blinding, exclusions, and deliverables in the proposal. |
Hooke Laboratories, Inc. states that its kit contains MOG35-55/CFA emulsion and pertussis toxin for EAE induction (company website, accessed September 3, 2026).[S5] The product record establishes kit contents, not that the kit is appropriate for a particular program.
A usable proposal identifies the mouse substrain, MOG peptide, CFA and PTX formulations, dosing schedule, scoring scale, observer blinding, tissue plan, humane endpoints, and primary analysis. The resulting study can show what happened in that EAE protocol. It cannot establish efficacy or safety in people with MS.
In non-clinical development, the choice of contract research organization shapes the quality of the data and the time it takes to reach the next decision. Below, three CROs are introduced by the type of study they support: pharmacology (efficacy) studies, safety studies, and pharmacokinetic (PK/PD) studies. Each summary describes the services the company offers so that you can match a provider to your target and development objective.
SMC Laboratories is a specialized non-clinical CRO focused on in vivo pharmacology and efficacy studies using disease-relevant animal models, particularly in fibrosis, inflammation, metabolic diseases, and oncology.
SMC Laboratories offers models covering the liver, lung, kidney, intestine, and oncology. Its portfolio includes the proprietary STAM™ model for MASH, fibrosis, and hepatocellular carcinoma.
Study plans are developed around the target biology, mechanism of action, disease stage, and development objective. Pharmacological endpoints can be combined with histopathology, biomarkers, and disease-specific readouts.
With experience from more than 1,000 studies for clients in 30 countries, SMC Laboratories supports programs from target validation and candidate selection through in vivo proof-of-concept studies.
Charles River provides non-clinical toxicology and safety assessment services for programs ranging from exploratory safety studies to IND-enabling development.
Services include single- and repeat-dose toxicology, dose-range finding, and general toxicology studies across multiple species and administration routes.
Charles River supports both non-GLP and GLP studies, allowing sponsors to progress from early safety characterization to studies intended for regulatory submissions.
Toxicology studies can be integrated with toxicokinetics, clinical pathology, histopathology, and safety pharmacology to support interpretation and IND-enabling safety packages.
Inotiv provides integrated PK/PD, DMPK, and bioanalytical services to characterize drug exposure and its relationship with pharmacological response.
PK studies characterize exposure, half-life, clearance, and other pharmacokinetic parameters needed to understand how a candidate behaves in the selected model.
Pharmacokinetic data can be combined with pharmacodynamic endpoints and bioanalysis to evaluate the relationship between drug exposure and pharmacological response.
Integrated DMPK, pharmacology, and safety information supports candidate comparison, dose selection, dosing-frequency optimization, and decisions about subsequent preclinical development.