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Although studies with cereblon-based PROTACs are still scarce, it is expected that long-term clinical use of this type of degrader could lead to the emergence of mutations that prevent PROTAC from binding to cereblon, thus preventing poly-ubiquitination of the target protein
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σ-1 Receptor antisense and antagonists have been shown to block the acute locomotor stimulant effects of METH [4]
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