Sep 14, 2022 · Here we investigate the interaction between α-synuclein fibrils and anle138b, a clinical drug candidate for disease modifying therapy in neurodegeneration and a promising scaffold for positron...

Here we describe the novel oligomer modulator anle138b [3- (1,3-benzodioxol-5-yl)-5- (3-bromophenyl)-1H-pyrazole], an aggregation inhibitor we developed based on a systematic high-throughput screening campaign combined with medicinal chemistry optimization.

Emrusolmin (development code Anle138b) is an experimental drug for the treatment of neurodegenerative diseases.

Small aggregates (oligomers) of α-synuclein have been shown to be the most relevant neurotoxic species and are targeted by anle138b, an orally bioavailable small molecule compound which shows strong disease-modifying effects in animal models of synucleinopathies.

Results: We observed a reversal of motor function to healthy control levels when PLP-hαSyn mice were treated with both doses of anle138b. Histological and molecular analyses showed a significant reduction in α-synuclein oligomers and glial cytoplasmic inclusions in animals fed with anle138b compared to nontreated mice.

• Anle138b Modulates α-Synuclein Oligomerization and Prevents Motor Decline and Neurodegeneration in a Mouse Model of Multiple System Atrophy. Publication published on Wiley Online Library. Please follow this link for the complete publication.

Here we investigate the interaction between α-synuclein fibrils and anle138b, a clinical drug candidate for disease modifying therapy in neurodegeneration and a promising scaffold for positron emission tomography tracer design.

Mar 10, 2016 · Here we analyzed whether anle138b improves motor skills and reduces neuronal loss, as well as oligodendroglial α-syn aggregation in the PLP-α-syn transgenic mouse challenged with the mitochondrial toxin 3-nitropropionic acid (3-NP) to model full-blown MSA.

Jun 1, 2023 · We apply this approach to α-synuclein (αS) aggregates in complex with the small molecule anle138b, which is a clinical drug candidate for disease modifying therapy.

In this work, we examine the efficacy of the diphenylpyrazole (DPP) compound anle138b in an animal model of Aβ deposition. Oral application of anle138b ameliorates Aβ‐induced deficits in synaptic plasticity and memory formation.