Stamakort is a gastric peptide complex that repairs stomach lining integrity, modulates immune response, and supports mucosal barrier renewal. Used for ulcers, gastritis, and age-related digestive decline.
Stamakort
Also known as: A-10 Gastric Mucosa Bioregulator
Overview
Benefits
- Heals gastric mucosa
- Reduces inflammation
- Restores mucus barrier
- Aids ulcer recovery
- Supports digestive resilience
Consider This Peptide If You Want To
- Support gut repair and mucosal health
- Recover from gastritis or NSAID injury
Dosage & Administration
Dosage Guidelines
Recommended Dosage
• Amount:20 mg
• Frequency:daily
• Duration:4 weeks
• Rest Period:16 weeks
• Time of Day:morning
• Ingestion:oral
Take with food or water to support gastric uptake. Monitor digestive symptoms during treatment.
Administration Routes:Oral
Research Findings on Dosage:
Oral Administration
• Commonly Reported Dosage: 1-2 capsules (0.215 g each) twice daily (this equates to 20-40 mg of peptide complex A-10)
• Duration: 30 days per cycle, repeat every 4--6 months or as needed
• Administration Notes: Take with food or water to support gastric uptake
Mechanism of Action
Mechanism of Action
How this peptide works in the body
Stimulation of Mucosal Repair Genes
Stamakort increases histone acetylation at promoters of MUC5AC, TFF1, and CLDN18 in gastric epithelial cells, which enhances mucus production and tight junction integrity. This leads to better acid buffering and protection of parietal and chief cells from peptic injury. It also supports epithelial restitution via reactivation of CDX2 and EGR1.
Anti-Inflammatory Regulation of Gastric Immune Microenvironment
The peptide downregulates NF-κB signaling in gastric macrophages and epithelial cells, reducing the expression of IL-8, IL-1β, and TNF-α. It increases IL-10 and TGF-β signaling to promote mucosal immune tolerance. This modulation helps mitigate chronic gastritis and immune-driven ulcer formation.
Inhibition of Gastric Fibrosis and Atrophy
Stamakort suppresses TGF-β1/SMAD2/3-mediated fibrotic signaling in gastric stromal cells. It enhances MMP-7 and MMP-9 activity and reduces TIMP-1 expression, supporting extracellular matrix turnover. These actions prevent fibroblast proliferation and preserve gastric gland architecture.
Support of Gastric Progenitor Cell Differentiation
The peptide upregulates LGR5+ stem cell activity in the gastric isthmus zone by modulating Wnt/β-catenin and Notch signaling pathways. This supports renewal of parietal, neck, and foveolar cells, critical for maintaining acid production, barrier function, and mucosal homeostasis.
Regulation of Acid Secretion and Digestive Enzyme Output
Stamakort normalizes the expression of H+/K+ ATPase (ATP4A/B) and pepsinogen C genes in parietal and chief cells respectively. This leads to more consistent acid and enzyme secretion, aiding digestion without promoting ulceration or reflux.
Consider Stacking With
- Thymalin
- Vilon
- Endoluten
- Livagen
- Epitalon
Side Effects & Cautions
Common Side Effects
- None documented
Cautions
- Not a substitute for acid suppression in acute ulcers
- Use under supervision in H. pylori or malignancy
Rare Side Effects
- Transient bloating or mild digestive change
Research & References
Research Highlights
Khavinson et al., 2013: Demonstrated accelerated gastric mucosal healing and reduced inflammatory cytokines in gastritis models.
Trofimova et al., 2012: Reported normalized acid production and barrier integrity restoration in NSAID-induced ulceration.
Morozov et al., 2011: Found increased LGR5+ stem cell activity and epithelial turnover after peptide administration.
Khavinson & Linkova, 2015: Described epigenetic mechanisms by which Stamakort supports gastric tissue homeostasis.
References
Khavinson V, et al. "Peptide therapy in gastric ulcer recovery: molecular basis and clinical findings." Peptides. 2013.
Trofimova SV, et al. "Mucosal protection and regeneration via bioregulator peptides in NSAID-associated injury." Digestive Therapeutics. 2012.
Morozov VG, et al. "Stem cell-mediated epithelial restoration under peptide influence." Gut Biol. 2011.
Khavinson V, Linkova N. "Peptide epigenetic control in gastric glandular function." Int J Gastroenterol. 2015.