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| CAS:2014384‑91‑7:Nangibotide | |
| Nangibotide (also known as LR12) is a specific antagonist peptide targeting triggering receptor expressed on myeloid cells 1 (TREM‑1). It competitively binds to TREM‑1 receptors, blocks endogenous ligand‑mediated receptor activation and downstream inflammatory signaling pathways, inhibits pro‑inflammatory cytokine storm and excessive myeloid cell activation, while not affecting the normal antibacterial immune defense of the body. It can significantly reduce excessive inflammatory injury and improve survival rate in models of sepsis, septic shock and severe inflammation. It is a cutting‑edge tool peptide for the study of severe inflammation and immune disorder mechanisms. | |
| 95%/98%/99% | |
| ~1400 (subject to actual synthetic batch) | |
| Function Tags (comma-separated) | ||||||||
| Nangibotide; LR12 | TREM-1 antagonism, Cytokine storm inhibition, Sepsis research, Immunomodulation, Severe anti-inflammation, Peptide drug | TREM-1 ligand homologous dodecapeptide with receptor binding core sequence | - | ~1400 (theoretical) | 12 |
| Long-term Storage | Short-term Storage | ||||
| PEP-NAN001 | Store at -20℃, sealed, dry & protected from light, aliquoted; avoid repeated freeze-thaw cycles and contamination | Stable for 2 weeks at 2-8℃ sealed & dry; ice pack shipping recommended | Stable for 72h at 4℃ under sterile conditions; prone to degradation and inactivation by serum proteases at room temperature**Good water solubility, freely soluble in neutral physiological buffer**. Linear short peptide easily degraded by proteases | Stable for 2 years at -20℃ under dry & dark conditions |
| Applicable Research Areas (comma-separated) | ||||
| PEP-NAN001 | TREM-1 receptor specific antagonist peptide that blocks excessive inflammatory cascade and alleviates severe inflammatory injury such as sepsis | Nangibotide competitively occupies TREM-1 receptors on myeloid cell surface by mimicking the binding sequence of endogenous ligands, blocks ligand-induced receptor dimerization and activation of downstream SYK and NF-κB inflammatory signaling pathways, inhibits the massive release of pro-inflammatory cytokines such as TNF- , IL-1 and IL-6, and alleviates cytokine storm and tissue organ damage. Different from broad-spectrum anti-inflammatory drugs, it only targets the TREM-1-mediated excessive inflammatory pathway, does not inhibit the normal pathogen-clearing immune function of the body, with lower infection risk. It is a novel targeted tool for the study of severe infection, sterile inflammation and other diseases. | Sepsis and septic shock, Severe inflammation research, Cytokine storm mechanism, Myeloid cell immunity, Acute organ injury, Anti-inflammatory peptide development | Triggering Receptor Expressed on Myeloid cells 1 (TREM-1); SYK/NF-κB inflammatory signaling pathway; Cytokine storm inhibitory pathway |
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