Multiple Sclerosis (MS)

Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system, driven by genetic susceptibility, immune dysregulation, viral infection, and environmental factors. It causes multifocal demyelinating lesions, axonal injury, and disrupted nerve signal transmission in the brain, spinal cord, and optic nerves. GemPharmatech offers experimental autoimmune encephalomyelitis (EAE) models to support mechanistic and therapeutic MS research.

50+
HF Models
200+
Studies Completed
15+
ND-Enabling Studies

Advantages

Our Advantages

Industry-leading capabilities for Multiple Sclerosis research

Distinct EAE models covering divergent immune pathogenic mechanisms to match diverse drug targets

We provide two classic MOG-induced EAE models with divergent immune mechanisms for MS research: MOG35-55 EAE features Th1/Th17 T cell-driven pathology, while human MOG1-125 EAE triggers concurrent T/B cell and complement activation to mirror full-spectrum patient immune lesions.

Broad-spectrum evaluation capacity across all mainstream therapeutic modalities.

Both EAE models support efficacy assessment across multiple therapeutic modalities, covering the full MS drug pipeline: small molecules (fingolimod, BTK inhibitors), cell therapy (mesenchymal stem cells, MSCs), and therapeutic antibodies.

Customizable Study Design

Flexible protocols for acute and chronic heart failure studies, with options for surgical and pharmacological induction.

Model Library

Comprehensive Multiple Sclerosis models for preclinical research

Multiple Sclerosis

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Case Studies

Case Studies & Validation Data

Explore our validated Multiple Sclerosis studies demonstrating the efficacy of various therapeutic interventions.

MOG35-55 Induced Experimental Autoimmune Encephalomyelitis (EAE) Model

Efficacy evaluation of a VAV1-degrader 3 in the MOG35-55 induced EAE model using female B6 mice.

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Panel A Study design. EAE model was established by immunization with MOG35-55/CFA and PTX challenge. VAV1-degrader 3 was administered via oral gavage on Day 7.

Panel B VAV1-degrader 3 treatment significantly ameliorated body weight loss and the decrease in body weight percentage compared to the EAE model group.

Panel C VAV1-degrader 3 treatment significantly decreased EAE score and cumilative EAE score compared to the EAE model group.

Panel D Representative H&E-stained spinal cord sections. Note: perivascular cuffing (green arrows), neutrophils (black arrows), mononuclear cells (red arrows), and gliosis (orange arrows). Top row: Scale bar = 200 μm; bottom row: Scale bar = 100 μm.

Panel E VAV1 degrader 3 treatment showed a trend toward lower spinal cord H&E scores relative to the EAE model group.

Panel F Representative LFB-stained spinal cord sections. Note: demyelination (yellow arrows). Top row: Scale bar = 200 μm; bottom row: Scale bar = 100 μm.

Panel G VAV1-degrader 3 treatment significantly reduced spinal cord demyelination scores compared to the EAE model group.

Data are expressed as mean ± standard error (Mean ± SEM), n=8-10. Statistics performed using one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

hMOG1-125 Induced B cell Dependent EAE Model

Efficacy study of Fenebrutinib in the MOG1-125 induced B cell dependent EAE model using female B6 mice

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Panel A Study design. The B cell dependent EAE model was established by immunization with human MOG1-125/CFA and PTX challenge. Fenebrutinib, a BTK inhibitor, was administered via intraperitoneal (i.p.) injection on Day 0.

Panel B Fenebrutinib treatment significantly ameliorated body weight loss and the decreased body weight percentage compared to the EAE model group.

Panel C Fenebrutinib treatment significantly decreased EAE score and cumilative EAE score compared to the EAE model group.

Panel D Fenebrutinib treatment significantly inhibited cell number of total leukocytes, T cells, and plasma cells in brain compared to the EAE model group.

Panel E Representative H&E-stained spinal cord sections. Note: vascular cuffs (red arrows), neutrophils (blue arrows), lymphocytes (green arrows), and glial cell hyperplasia (purple arrows).

Panel F Fenebrutinib treatment significantly reduced spinal cord H&E scores compared to the EAE model group.

Panel G Representative LFB-stained spinal cord sections. Note: demyelination of nerve fibers (black arrows).

Panel H Fenebrutinib treatment significantly reduced spinal cord demyelination scores compared to the EAE model group.

Data are expressed as mean ± standard error (Mean ± SEM), n=3-5. Statistics performed using One-way ANOVA. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

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Browse our comprehensive catalog of over 30,000 mouse models covering various gene families, signaling pathways, and disease models. Use advanced filters to find the perfect model for your research.

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Systemic Sclerosis(SSc)

Systemic sclerosis (SSc), also known as scleroderma, is a rare autoimmune connective tissue disease associated with significant morbidity and mortality. It is characterized by autoimmunity and inflammation, vasculopathy, and fibrosis of the skin and internal organs. GemPharmatech offers bleomycin-induced, humanized bleomycin-induced, and HOCl-induced models to support mechanistic and therapeutic research on SSc.

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