| Identification | Back Directory | [Name]
(2S,3S)-2-amino-3-methyl-N-(2-morpholin-4-ylethyl)pentanamide | [CAS]
102562-74-3 | [Synonyms]
LM11A-31
(LM11A 31)
(2S,3S)-2-Amino-3-methyl-N-(2-morpholinoethyl)pentanamide
Pentanamide, 2-amino-3-methyl-N-[2-(4-morpholinyl)ethyl]-, (2S,3S)- | [Molecular Formula]
C12H25N3O2 | [MDL Number]
MFCD13245016 | [MOL File]
102562-74-3.mol | [Molecular Weight]
243.35 |
| Chemical Properties | Back Directory | [Boiling point ]
418.8±40.0 °C(Predicted) | [density ]
1.033±0.06 g/cm3(Predicted) | [form ]
Solid | [pka]
15.24±0.46(Predicted) | [color ]
White to off-white |
| Hazard Information | Back Directory | [Uses]
LM11A-31, a non-peptide p75NTR (neurotrophin receptor p75) modulator, is an orally active and potent proNGF (nerve growth factor) antagonist. LM11A-31 is an amino acid derivative with high blood-brain barrier permeability and blocks p75-mediated cell death. LM11A-31 reverses cholinergic neurite dystrophy in Alzheimer's disease mouse models with mid- to late-stage disease progression[1][2]. | [in vivo]
LM11A-31 (oral gavage; 50 mg kg/day for 4 weeks) significantly mitigates proNGF accumulation and preserves BRB integrity[1].
LM11A-31 (orally; 50 or 75 mg/kg) administered for 3 months starting at 6-8 months of age prevents and/or reverses atrophy of basal forebrain cholinergic neurites and cortical dystrophic neurites in mid-stage male APPL/S mice[2].
| Animal Model: | Male C57BL/6 J mice[1]. | | Dosage: | 50 mg kg/day | | Administration: | Oral gavage; for 4 weeks | | Result: | Mitigated proNGF accumulation and preserved BRB integrity. |
| [References]
[1] Elshaer SL, et al. Modulation of the p75 neurotrophin receptor using LM11A-31 prevents diabetes-induced retinalvascular permeability in mice via inhibition of inflammation and the RhoA kinase pathway. Diabetologia. 2019 Aug;62(8):1488-1500. DOI:10.1007/s00125-019-4885-2
[2] Simmons DA, et al. A small molecule p75NTR ligand, LM11A-31, reverses cholinergic neurite dystrophy in Alzheimer's disease mouse models with mid- to late-stage disease progression. PLoS One. 2014 Aug 25;9(8):e102136. DOI:10.1371/journal.pone.0102136 |
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