Corynoxine B - CAS 17391-18-3
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Not Intended for Therapeutic Use. For research use only.
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Corynoxine B, a natural autophagy inducer, restores the deficient cytosolic translocation of HMGB1 and autophagy in cells overexpressing SNCA, which may be attributed to its ability to block SNCA-HMGB1 interaction. Corynoxine B exhibited prolongation of the thiopental-induced hypnosis on oral administration in mice.
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Corynoxine B
1.HMGB1 is involved in autophagy inhibition caused by SNCA/α-synuclein overexpression: a process modulated by the natural autophagy inducer corynoxine B.
Song JX1, Lu JH2, Liu LF1, Chen LL1, Durairajan SS1, Yue Z3, Zhang HQ1, Li M1. Autophagy. 2014 Jan;10(1):144-54. doi: 10.4161/auto.26751. Epub 2013 Jan 1.
SNCA/α-synuclein and its rare mutations are considered as the culprit proteins in Parkinson disease (PD). Wild-type (WT) SNCA has been shown to impair macroautophagy in mammalian cells and in transgenic mice. In this study, we monitored the dynamic changes in autophagy process and confirmed that overexpression of both WT and SNCA(A53T) inhibits autophagy in PC12 cells in a time-dependent manner. Furthermore, we showed that SNCA binds to both cytosolic and nuclear high mobility group box 1 (HMGB1), impairs the cytosolic translocation of HMGB1, blocks HMGB1-BECN1 binding, and strengthens BECN1-BCL2 binding. Deregulation of these molecular events by SNCA overexpression leads to autophagy inhibition. Overexpression of BECN1 restores autophagy and promotes the clearance of SNCA. siRNA knockdown of Hmgb1 inhibits basal autophagy and abolishes the inhibitory effect of SNCA on autophagy while overexpression of HMGB1 restores autophagy. Corynoxine B, a natural autophagy inducer, restores the deficient cytosolic translocation of HMGB1 and autophagy in cells overexpressing SNCA, which may be attributed to its ability to block SNCA-HMGB1 interaction.
2.Construction of tetracyclic 3-spirooxindole through cross-dehydrogenation of pyridinium: applications in facile synthesis of (±)-corynoxine and (±)-corynoxine B.
Xu J1, Shao LD, Li D, Deng X, Liu YC, Zhao QS, Xia C. J Am Chem Soc. 2014 Dec 31;136(52):17962-5. doi: 10.1021/ja5121343. Epub 2014 Dec 17.
A facile and straightforward method was developed to construct the fused tetracyclic 3-spirooxindole skeleton, which exists widely in natural products. The formation of the tetracyclic 3-spirooxindole structure was achieved through a transition-metal-free intramolecular cross-dehydrogenative coupling of pyridinium, which were formed in situ by the condensation of 3-(2-bromoethyl)indolin-2-one derivatives with 3-substituted pyridines. As examples of the application of this new methodology, two potentially medicinal natural products, (±)-corynoxine and (±)-corynoxine B, were efficiently synthesized in five scalable steps.
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CAS 17391-18-3 Corynoxine B

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