CLR01 is a molecular tweezer. CLR01 reduces aggregated, pathologic, and seeding-competent α-synuclein in experimental multiple system atrophy. CLR01 inhibits aberrant superoxide dismutase 1 (SOD1) self-assembly in vitro and in the G93A-SOD1 mouse model of ALS. CLR01 inhibits Ebola and Zika virus infection. CLR01 Stabilizes a Disordered Protein-Protein Interface. CLR01, Modulates Aggregation of the Mutant p53 DNA Binding Domain and Inhibits Its Toxicity.
c-ABL-IN-3, a highly effective c-Abl inhibitor, exhibits promising potential for studying neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and Parkinson's disease (PD), as well as cancer [1]. The activation of c-Abl has been strongly implicated in a range of diseases, notably cancer [1]. It offers valuable opportunities for research in these fields [1].
C-ABL-IN-2 is a highly effective inhibitor of the c-Abl protein, which plays a significant role in the development of several diseases, including cancer. This compound exhibits promise for investigating neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS) and Parkinson's disease (PD), as well as cancer. (Source: WO2020260871A1, compound 25) [1].