CAS 1447799-33-8 Reltecimod

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CAS 1447799-33-8 Reltecimod
Details
CAS: 1447799-33-8
Core structure: Synthetic targeted peptide that specifically blocks the triggering receptor expressed on myeloid cells 1 (TREM-1) signaling pathway, inhibits excessive inflammatory response, sequence-optimized for improved metabolic stability
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Related documents
COA/MS/HPLC Report
Peptide Dissolution and Storage Guide
Category
Anti-inflammatory Peptide / TREM-1 Pathway Selective Inhibitor
Category
Pharmaceutical Peptides
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Product name CAS:1447799‑33‑8:Reltecimod
Description Reltecimod is a new‑generation synthetic peptide targeting the inflammatory pathway. It binds triggering receptor expressed on myeloid cells 1 (TREM‑1) with high specificity, blocks its interaction with ligands, inhibits downstream inflammatory signaling pathways such as NF‑κB, reduces excessive release of pro‑inflammatory cytokines such as TNF‑α, IL‑1β and IL‑6, and alleviates cytokine storm and tissue damage in severe conditions such as sepsis and septic shock, without affecting normal immune defense function. Applied in mechanism research of severe infection, sepsis, inflammatory diseases and novel anti‑inflammatory peptide drug development.
Peptide purity (HPLC, %) 95%/98%/99%
Theoretical molecular weight (Da) ~1310 (subject to actual synthetic batch)
Structure type Targeted synthetic peptide, TREM‑1 pathway inhibitor

 

Product Basic Information Table

 

Product Standard English Name Product Abbreviation / Alias Function Tags (comma-separated) Core Structure Molecular Formula Exact Mass (Da) Average MW (Da) Structure Type Target
Reltecimod Reltecimod; TREM-1 inhibitory peptide TREM-1 pathway inhibition, Anti-cytokine storm, Sepsis research, Severe infection, Targeted anti-inflammatory peptide, Immune regulation Linear synthetic peptide backbone with optimized TREM-1 targeting binding sequence Large peptide, subject to actual batch MS - ~1310 (theoretical) Synthetic targeted peptide Triggering Receptor Expressed on Myeloid cells 1 (TREM-1)

 

Physicochemical Solubility & Storage Parameters

Product Code Appearance Long-term Storage Conditions Short-term Storage Conditions Liquid Stability Solid Powder Stability
PEP-REL001 white powder Store at -20℃, sealed, dry & protected from light, aliquoted; avoid repeated freeze-thaw cycles Stable for 2 weeks at 2-8℃ sealed & dry; ice pack shipping recommended Stable for 48 h at 4℃; stable for 2 weeks at -20℃ in aliquots. **Good water solubility, freely soluble in water and physiological buffer**. Linear peptide easily degraded by endopeptidases with rapid activity decay at room temperature Stable for 2 years at -20℃ under dry & dark conditions

 

Functional Description

 

Product Code Frontend Short Summary (for search list display) Detailed Biological Function Description Applicable Research Areas (comma-separated) Targets / Pathways
PEP-REL001 TREM-1-targeted anti-inflammatory peptide that blocks inflammatory cascade and alleviates sepsis cytokine storm to protect tissues Reltecimod specifically binds to TREM-1 receptors on the surface of myeloid cells, competitively blocks their binding to endogenous ligands, thereby inhibits the inflammatory signaling cascade downstream of the receptor, downregulates the activation of pro-inflammatory pathways such as NF-κB and MAPK, significantly reduces the release of pro-inflammatory mediators such as TNF-α, IL-1β, IL-6 and HMGB1, and alleviates tissue and organ damage caused by excessive inflammatory response. Unlike broad-spectrum anti-inflammatory drugs, it only targets amplified inflammatory pathways and does not inhibit basal immune defense, so infection clearance capacity is not affected. It shows significant protective effects in severe inflammatory models such as sepsis, septic shock and acute respiratory distress syndrome. Sepsis research, Severe infection models, Cytokine storm mechanism, Acute organ injury, Targeted anti-inflammatory drugs, Innate immune regulation Triggering Receptor Expressed on Myeloid cells 1 (TREM-1); NF-κB/MAPK inflammatory pathway; Inflammatory cascade blockade pathway

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