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Merck
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SML3342

Sigma-Aldrich

Trofinetide Trifluoroacetate

≥95% (HPLC)

Sinónimos:

Gly-2–methylPro–Glu Trifluoroacetate, Gly-2MePro-Glu Trifluoroacetate, Glycyl-2-methyl-L-prolyl-L-Glutamic acid Trifluoroacetate, NNZ 2566 Trifluoroacetate, NNZ-2566 Trifluoroacetate

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About This Item

Fórmula empírica (notación de Hill):
C13H21N3O6 · xC2HF3O2
Peso molecular:
315.32 (free base basis)
UNSPSC Code:
51111800
NACRES:
NA.77

Quality Level

assay

≥95% (HPLC)

form

powder

color

white to off-white

storage temp.

−20°C

Biochem/physiol Actions

Trofinetide is a more enzymatically stable analogue of the N-terminal tripeptide of IGF-1(GPE) that exhibits potent neuroprotective effects in varies animal models of neurodegenerative diseases and traumatic brain injury. Trofinetide treatment provides clinically meaningful improvement in Rett syndrome (RTT) and Fragile X syndrome (FXS).

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3


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Michael J Bickerdike et al.
Journal of the neurological sciences, 278(1-2), 85-90 (2009-01-23)
The N-terminal cleavage product of human insulin-like growth factor-1 (IGF-1) in the brain is the tripeptide molecule Glypromate (Gly-Pro-Glu). Glypromate has demonstrated neuroprotective effects in numerous in vitro and in vivo models of brain injury and is in clinical trials
Elizabeth Berry-Kravis et al.
Pediatric neurology, 110, 30-41 (2020-07-15)
We analyze the safety and tolerability of trofinetide and provide a preliminary evaluation of its efficacy in adolescent and adult males with fragile X syndrome. This study was an exploratory, phase 2, multicenter, double-blind, placebo-controlled, parallel group study of the
Casandra M Cartagena et al.
Neuromolecular medicine, 15(3), 504-514 (2013-06-15)
The tripeptide glycine-proline-glutamate analogue NNZ-2566 (Neuren Pharmaceuticals) demonstrates neuroprotective efficacy in models of traumatic brain injury. In penetrating ballistic-like brain injury (PBBI), it significantly decreases injury-induced upregulation of inflammatory cytokines including TNF-α, IFN-γ, and IL-6. However, the mechanism by which

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