IB-DMD compound showed potential for reducing skeletal muscular fibrosis and muscle damage, improving muscular function, and reducing muscle tearing.
Duchene Muscular Dystrophy and Fibrosis
Route of Administration:
Oral & Injectable
Mechanism of Action:
- Inhibits NFkB and Connective Tissue Growth Factor (CTGF)
- Lowered levels of serum Creatine Kinase
- Reduces pro-fibrosis cytokines TGF-β1 and PAI-1 in CTGF, Fibronectine, and Collagen
- Increases cell migration through fibrosis inhibition
- In-vitro research had shown IB-DMD to inhibit NFkB and expression of CTGF (pro-fibrotic factor); reduce collagen, fibronectin.
- Improves skeletal muscle strength: Increases isometric force, twitch force, and recovery score
- Significantly improve whole animal functional capacity as determined by the ability to treated dystrophic mice to run in a treadmill.
- Significantly decreases cumulative skeletal muscle damage, improves the architecture of dystrophic skeletal muscles, decreases tissue damage, and lowered levels of serum CK
- Reduces Skeletal Muscle Fibrosis Proteins: fibronectin, collagen I, and collagen II
- Reduces Pro-fibrosis Factors: TGF-β1 and CTGF
- Reduces inflammatory Markers: macrophages, eosinophils, lymphocytes CD4+ and CD8+
- Increases efficacy of cellular therapies
- Extend lifespan of dystrophic mice.
Skeletal Muscle (2014), 4:6 Andrographolide attenuates skeletal muscle dystrophy in mdx mice and increases efficiency of cell therapy by reducing fibrosis