2. Neuronal Signaling GPCR/G Protein
  3. Amyloid-β α-synuclein CGRP Receptor Amylin Receptor
  4. D-Trp-Aib

D-Trp-Aib is a dipeptide and amyloid-β inhibitor with a Kd of 29.6 nM. D-Trp-Aib triggers formation of non-toxic, non-β-sheet, amorphous amyloid β clusters from misfolded amyloid β monomers and toxic amyloid β oligomers, and reduces toxic amyloid β1-42 deposits. D-Trp-Aib inhibits amyloid fibril formation of α‑synuclein, IAPP and calcitonin. D-Trp-Aib can be used for the research of Alzheimer's disease.

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D-Trp-Aib

D-Trp-Aib Chemical Structure

CAS No. : 1123071-24-8

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D-Trp-Aib Related Antibodies

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Description

D-Trp-Aib is a dipeptide and amyloid-β inhibitor with a Kd of 29.6 nM. D-Trp-Aib triggers formation of non-toxic, non-β-sheet, amorphous amyloid β clusters from misfolded amyloid β monomers and toxic amyloid β oligomers, and reduces toxic amyloid β1-42 deposits. D-Trp-Aib inhibits amyloid fibril formation of α‑synuclein, IAPP and calcitonin. D-Trp-Aib can be used for the research of Alzheimer's disease[1][2].

In Vitro

D-Trp-Aib (Compound 1) binds to Aβ1-42 with an Kd of 29.6 ± 1.7 nM[1].
D-Trp-Aib triggers the formation of larger, non-toxic amorphous and globular clusters from Aβ1-42[1].
D-Trp-Aib partially prevents Aβ1-42-induced membrane potential depolarization[1].
D-Trp-Aib (0.1 nM-1 μM; 90 min) reverses Aβ1-42-induced LTP deficits in mouse hippocampal slices[1].
D-Trp-Aib (molar ratio 1:10-1:30, 50 h) inhibits amyloid fibril formation of α‑synuclein, IAPP and calcitonin, and disassembles preformed amyloid fibrils[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

D-Trp-Aib Related Antibodies
In Vivo

D-Trp-Aib (Compound 1) (0.5-2.0%; eye drops; three times daily; 3 months) produces a significant, dose-dependent reduction in toxic amyloid β1-42 deposits in the retina of an AMD mouse model[1].
D-Trp-Aib (0.5-2.0%; eye drops; three times daily; 1 month) reduces toxic amyloid β1-42 deposits and associated complement component C3b inflammation in the retina of an aged AMD mouse model[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6 (5-6 months old; age-related macular degeneration genetic model)[1]
Dosage: 0.5%; 2.0%
Administration: eye drops; three times daily; 3 months
Result: Caused a significant reduction in retinal amyloid β1-42 levels compared to vehicle-treated mice.
Produced a greater reduction in retinal amyloid β1-42 levels at 2.0% dose than at 0.5% dose.
Animal Model: C57BL/6 (24 months old; aged age-related macular degeneration model)[1]
Dosage: 0.5%; 2.0%
Administration: eye drops; three times daily; 1 month
Result: Reduced thick, linear amyloid β1-42 deposits along the Bruch's membrane to isolated, non-toxic aggregates, with no amyloid β1-42 staining in the retinal pigment epithelium.
Induced a corresponding colocalized reduction in C3b (a marker of amyloid β-induced inflammation) compared to controls.
Molecular Weight

289.34

Formula

C15H19N3O3
CAS No.
SMILES

C([C@H](C(NC(C(O)=O)(C)C)=O)N)C=1C=2C(NC1)=CC=CC2
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Purity & Documentation
References
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D-Trp-Aib Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

D-Trp-Aib1123071-24-8Amyloid-βα-synucleinCGRP ReceptorAmylin Receptorβ-amyloid peptideAβAbetaα-SynCalcitonin gene-related peptide receptor AMYRneuronal cellsmouse hippocampal slicesamyloid βneuro-sensory cellsnon-neuronal cellsAlzheimer's diseaseage-related macular degenerationcomplement component C3bglaucomaInhibitorinhibitorinhibit

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