SMER-28 | Autophagy inducer
NMR (Conforms)
Available Options
| Size : | Price | Quantity | |
|---|---|---|---|
| 5 mg | $42.00 | ||
| 25 mg | $172.00 |
SMER28 (CAS 307538-42-7) Induces autophagy via an mTOR-independent pathway. Enhances clearance of ß-amyloid protein in cell lines and primary neuronal culture models.1-3 May be a useful lead compound for the development of new therapeutics for neurodegenerative diseases.4 Induces the release of articular cartilage vesicles from healthy articular chondrocytes in a dose- and time-dependent manner.5 Promotes reprogramming of fibroblasts to neural stem-like cells.6 Cell permeable.
References/Citations:
1) Tian et al. (2011), A small-molecule enhancer of autophagy decreases levels of Abeta and APP-CTF via Atg5-dependent autophagy pathway; FASEB J., 25 1934
2) Tian et al. (2014), The convergence of endosomal and autophagosomal pathways; implications for APP-CTF degradation; Autophagy, 10 694
3) Shen et al. (2011), Novel cell- and tissue-based assays for detecting misfolded and aggregated protein accumulation within aggresomes and inclusion bodies; Cell Biochem. Biophys., 60 173
4) Renna et al. (2010), Chemical inducers of autophagy that enhance the clearance of mutant proteins in neurodegenerative diseases; J. Biol. Chem., 285 11061
5) Rosenthal et al. (2015), Autophagy modulates articular cartilage vesicle formation in primary articular chondrocytes; J. Biol. Chem., 290 13028
6) Zhang et al. (2016), Pharmacological Reprogramming of Fibroblasts into Neural Stem Cells by Signaling-Directed Transcriptional Activation; Cell Stem Cell., 18 653
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
SMER28 (CAS 307538-42-7) Induces autophagy via an mTOR-independent pathway. Enhances clearance of ß-amyloid protein in cell lines and primary neuronal culture models.1-3 May be a useful lead compound for the development of new therapeutics for neurodegenerative diseases.4 Induces the release of articular cartilage vesicles from healthy articular chondrocytes in a dose- and time-dependent manner.5 Promotes reprogramming of fibroblasts to neural stem-like cells.6 Cell permeable.
References/Citations:
1) Tian et al. (2011), A small-molecule enhancer of autophagy decreases levels of Abeta and APP-CTF via Atg5-dependent autophagy pathway; FASEB J., 25 1934
2) Tian et al. (2014), The convergence of endosomal and autophagosomal pathways; implications for APP-CTF degradation; Autophagy, 10 694
3) Shen et al. (2011), Novel cell- and tissue-based assays for detecting misfolded and aggregated protein accumulation within aggresomes and inclusion bodies; Cell Biochem. Biophys., 60 173
4) Renna et al. (2010), Chemical inducers of autophagy that enhance the clearance of mutant proteins in neurodegenerative diseases; J. Biol. Chem., 285 11061
5) Rosenthal et al. (2015), Autophagy modulates articular cartilage vesicle formation in primary articular chondrocytes; J. Biol. Chem., 290 13028
6) Zhang et al. (2016), Pharmacological Reprogramming of Fibroblasts into Neural Stem Cells by Signaling-Directed Transcriptional Activation; Cell Stem Cell., 18 653
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