nep

Peptide fragment corresponding to residues 1 - 40 of Nogo-66, the domain of the myelin protein Nogo that inhibits axonal outgrowth. Acts as a competitive antagonist at the Nogo-66 receptor (NgR); blocks Nogo-66- and CNS myelin-induced inhibition of axonal

NEP(1-40) TFA is a peptide antagonist of the Nogo-66 receptor (NgR), which attenuates myelin-derived inhibition and mitigates injury-induced shifts in microglial morphology distributions [1].

TAT-NEP1-40, a blood-brain barrier (BBB) permeable peptide, confers protection to PC12 cells against oxygen and glucose deprivation (OGD) while promoting neurite outgrowth. Furthermore, it enhances neurologic outcomes post-ischemia by mitigating apoptosis in affected cerebral regions. This compound holds potential for central nervous system (CNS) injury research, including studies on axonal regeneration and post-stroke functional recovery [1].

TAT-NEP1-40 TFA, a blood-brain barrier-permeable peptide, safeguards PC12 cells against oxygen and glucose deprivation (OGD) and fosters neurite outgrowth. Additionally, it enhances neurological outcomes post-ischemia by curtailing apoptosis in ischemic cerebral tissues. This compound has utility in investigating central nervous system (CNS) injuries, encompassing axonal regeneration and functional recuperation following a stroke [1].

TAT-NEP1-40 acetate, a potential therapeutic for axonal regeneration and functional recovery post-stroke, safeguards PC12 cells from oxygen and glucose deprivation (OGD) and encourages neurite outgrowth. This compound also affords cerebral protection against ischemia/reperfusion injury by hindering neuronal apoptosis and can be effectively administered into rat brains [1] [2].

Tianeptine metabolite MC5, an active derivative of the atypical antidepressant tianeptine produced through β-oxidation, exhibits selective G protein activation in bioluminescence resonance energy transfer (BRET) assays. Utilizing HEK293T cells expressing the human μ-opioid receptor (MOR) over the human δ-opioid receptor (DOR; EC50s = 0.454 and >100 µM, respectively), it demonstrates specificity. Moreover, this metabolite reduces immobility in wild-type mice during the forced swim test at a dose of 30 mg/kg, an effect not observed in MOR knockout mice, suggesting its antidepressant-like activity is MOR-dependent.

GLP-1(28-36)amide, a C-terminal nonapeptide derived from the cleavage of GLP-1 by neutral endopeptidase (NEP), is an important compound that functions as an antioxidant primarily targeting the mitochondrion to inhibit mitochondrial permeability transition (MPT), displaying anti-diabetic properties and cardioprotection effects[1].

GLP-1(28-36)amide TFA, a C-terminal nonapeptide derived from GLP-1 cleavage by neutral endopeptidase (NEP), is an antioxidant that targets mitochondria and inhibits mitochondrial permeability transition (MPT), demonstrating anti-diabetic and cardioprotective effects [1].