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Amyotrophic lateral sclerosis (ALS), also called Lou Gehrig’s disease, is centered around motor neuron deterioration. When these neurons die, muscles can’t function. Cholera toxin subunit B conjugated to Saporin (CTB-SAP) has a specificity towards motor neurons via GM1 ganglioside and has been used in different varieties to mimic complications in ALS.

Saporin as a Commercial Reagent: Its Uses and Unexpected Impacts in the Biological Sciences—Tools from the Plant Kingdom
Leonardo R. Ancheta, Patrick A. Shramm, Raschel Bouajram, Denise Higgins, and Douglas A. Lappi
Toxins (Basel). 2022 Mar; 14(3): 184.


Ciuro M et al. Mitigating the functional deficit after neurotoxic motoneuronal loss by an inhibitor of mitochondrial fission. Int J Mol Sci 25(13):7059, 2024. 

Objective: To use the Cholera Toxin B-Saporin (CTB-SAP) mouse animal model of Amyotrophic lateral sclerosis (ALS) to determine the efficacy of mitochondrial division inhibitor 1 (Mdivi-1) for its potential neuroprotective effect.

Summary: Mdivi-1 reduced motor deficits in the ALS model. It also showed neuroprotective effects on motoneurons and promoted plasticity. This could represent a translational approach for motoneuron disorders.

Usage: To establish the model, mice received two injections of the retrogradely transported, ribosome-inactivating toxin, CTB-SAP (Cat. #IT-14) into the medial and lateral right gastrocnemius muscles, respectively, with a toxin dose of 6 μg/2 μL in PBS per injection.

Related Products: CTB-SAP

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