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Lactobacillus reuteri GMNL-89
- Development stage
- Preclinical
- Lead developer
- GenMont Biotech
- Modality
- Synthetic Biology Platforms → Engineered Microbial Therapeutics → Microbiome Therapeutics, Fresh FMT → Fecal Microbiota Transplantation (FMT) → Microbiome Therapeutics, Yeast Strains → Single Strain Products → Live Biotherapeutic Products → Microbiome Therapeutics, Bacterial Strains → Single Strain Products → Live Biotherapeutic Products → Microbiome Therapeutics, Defined Consortia → Multi-strain Products → Live Biotherapeutic Products → Microbiome Therapeutics, Frozen FMT → Fecal Microbiota Transplantation (FMT) → Microbiome Therapeutics, Genetically Modified Bacteria → Engineered Microbial Therapeutics → Microbiome Therapeutics, Microbial Metabolites → Microbiome-Derived Products → Microbiome Therapeutics, Microbial Proteins → Microbiome-Derived Products → Microbiome Therapeutics, Complex Communities → Multi-strain Products → Live Biotherapeutic Products → Microbiome Therapeutics
- Administration
- Oral
01
Overview
Lactobacillus reuteri GMNL-89 is a specific probiotic strain developed by GenMont Biotech. It has been investigated for its potential therapeutic effects in autoimmune and inflammatory conditions, specifically systemic lupus erythematosus (SLE). In preclinical models, GMNL-89 has demonstrated the ability to reduce systemic inflammation and oxidative stress. Its mechanism of action involves the suppression of the mitogen-activated protein kinase (MAPK) and NF-κB signaling pathways, leading to a reduction in the production of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α). Additionally, it has been shown to mitigate hepatic inflammation and apoptosis in lupus-prone mice. Unlike some other Lactobacillus strains, GMNL-89 does not appear to significantly influence the differentiation of CD4+CD25+FoxP3+ regulatory T cells.
- Other names
- L. reuteri GMNL-89
02
Targets
IL-6 (Interleukin 6)MEKTNFA (Tumor necrosis factor alpha (soluble))MYD88 (Myeloid differentiation primary response protein MyD88)TLR (Toll-like receptors)NF-κB
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