Preclinical studies on tissue regeneration, immunomodulation, and therapeutic mechanisms of MenSC-based therapies.
Menstrual blood-derived stem cells exert their regenerative effects through multiple interconnected mechanisms:
The primary therapeutic mechanism involves secretion of bioactive factors that stimulate endogenous repair processes:
MenSC-derived exosomes carry therapeutic cargo including miRNAs (miR-21, miR-24, miR-126) that modulate gene expression in recipient cells, promoting angiogenesis, reducing fibrosis, and enhancing tissue repair.
Myocardial infarction, heart failure, peripheral artery disease. MenSCs reduce infarct size, improve ejection fraction, and promote neovascularization.
Stroke, traumatic brain injury, spinal cord injury, neurodegenerative diseases. Cross blood-brain barrier; promote neural protection and regeneration.
Acute respiratory distress syndrome (ARDS), pulmonary fibrosis, COPD. Reduce inflammation and promote alveolar repair.
Osteoarthritis, bone defects, tendon injuries. Promote cartilage regeneration and bone formation through osteogenic differentiation.
Multiple sclerosis, rheumatoid arthritis, lupus, GvHD. Systemic immunomodulation without general immunosuppression.
Chronic wounds, diabetic ulcers, burns. Accelerate closure, enhance angiogenesis, reduce scarring.
Intramyocardial injection of MenSCs (1×10⁶ cells) 24 hours post-MI. Primary endpoints: ejection fraction (echo), infarct size (histology), capillary density. Preliminary results show 15-20% improvement in EF at 4 weeks compared to PBS control.
Intravenous MenSC administration (2×10⁶ cells) at 24h and 72h post-stroke. Evaluating functional recovery (mNSS score), infarct volume, and neurogenesis markers. Early data suggests reduced inflammation and improved motor function.
Topical application of MenSC-secretome in hydrogel formulation. Measuring wound closure rate, re-epithelialization, collagen deposition, and vascularization. Comparing cell-free secretome vs. live cell therapy.
Systemic MenSC administration for steroid-refractory acute GvHD. Primary endpoints: survival, clinical GvHD score, target organ histopathology. Exploring optimal dosing schedule and timing relative to transplant.
| Route | Indications | Dose Range | Advantages | Limitations |
|---|---|---|---|---|
| Intravenous | Systemic diseases, GvHD, autoimmune | 1-2 × 10⁶ cells/kg | Non-invasive, systemic distribution | Pulmonary first-pass effect |
| Intramyocardial | Heart failure, post-MI | 10-50 × 10⁶ cells | Direct delivery to target tissue | Invasive procedure required |
| Intrathecal | Spinal cord injury, MS | 1-5 × 10⁶ cells | CNS targeting | Invasive, limited distribution |
| Intra-articular | Osteoarthritis | 10-50 × 10⁶ cells | Local delivery, minimal systemic exposure | Joint access required |
| Topical | Wounds, burns | 1-5 × 10⁶ cells/cm² | Non-invasive, direct application | Limited penetration |
MenSCs have not shown tumorigenic potential in preclinical studies. Unlike embryonic stem cells or induced pluripotent stem cells, MSCs have limited proliferation capacity and undergo senescence after 10-15 passages. No teratoma formation has been reported with MSC therapies.
MSCs are considered "immunoprivileged" due to low expression of MHC class I and absence of MHC class II and co-stimulatory molecules. This allows for allogeneic (off-the-shelf) use without matching. However, repeated dosing may elicit immune responses.
Systemic IV administration can result in pulmonary entrapment of large cells. Using smaller cells, optimizing dosing, and considering alternative routes can minimize this risk.
Current status: Completing IND-enabling studies with target IND submission in 2027 for cardiovascular indication.