ChemicalBook--->CAS DataBase List--->887255-16-5

887255-16-5

887255-16-5 Structure

887255-16-5 Structure
IdentificationBack Directory
[Name]

L-Proline, L-leucyl-L-glutaminyl-L-valyl-L-threonyl-L-α-aspartyl-L-serylglycyl-L-leucyl-L-tyrosyl-L-arginyl-L-cysteinyl-L-valyl-L-isoleucyl-L-tyrosyl-L-histidyl-L-prolyl-
[CAS]

887255-16-5
[Synonyms]

LQVTDSGLYRCVIYHPP (LP17)
LP17 TREM-1 inhibitory peptide
L-Proline, L-leucyl-L-glutaminyl-L-valyl-L-threonyl-L-α-aspartyl-L-serylglycyl-L-leucyl-L-tyrosyl-L-arginyl-L-cysteinyl-L-valyl-L-isoleucyl-L-tyrosyl-L-histidyl-L-prolyl-
[Molecular Formula]

C89H137N23O25S
[MOL File]

887255-16-5.mol
[Molecular Weight]

1961.27
Chemical PropertiesBack Directory
[density ]

1.47±0.1 g/cm3(Predicted)
[form ]

Solid
[pka]

3.43±0.20(Predicted)
[color ]

White to off-white
[Sequence]

Leu-Gln-Val-Thr-Asp-Ser-Gly-Leu-Tyr-Arg-Cys-Val-Ile-Tyr-His-Pro-Pro
Hazard InformationBack Directory
[Uses]

LQVTDSGLYRCVIYHPP (LP17) is a triggering receptor expressed on myeloid cells (TREM-1) inhibitory peptide. LQVTDSGLYRCVIYHPP substantially alleviates ischemia-induced infarction and neuronal injury. LQVTDSGLYRCVIYHPP can get access into brain and block TREM-1[1].
[in vivo]

LQVTDSGLYRCVIYHPP (LP17) (0.5 or 1 mg/kg; intranasal; daily for 3 days) alleviates ischemia-induced infarction and neuronal injury in mice[1].

Animal Model:Adult male C57BL/6J mice (20-25?g), mice cerebral ischemia/reperfusion (I/R) model induced by middle cerebral artery occlusion (MCAO)[1]
Dosage:0.5?mg/kg or 1?mg/kg
Administration:Intranasal administration, once daily for 3 consecutive days after MCAO
Result:Abolished ischemia-induced TREM-1 elevation at 1?mg/kg. Significantly reduced infarct volume by 27.3%, induced a markedly reduction in TUNEL positive cells and FJC positive neurons at 1?mg/kg. Rescued neurological deficits and cognitive dysfunction of MCAO mice. Inhibited microglial M1 polarization and neutrophil infiltration.
[References]

[1] Pengfei Xu, et al. Microglial TREM-1 receptor mediates neuroinflammatory injury via interaction with SYK in experimental ischemic stroke. Cell Death Dis. 2019 Jul 19;10(8):555. DOI:10.1038/s41419-019-1777-9
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