HPOB

HPOB is a highly potent and selective inhibitor of histone deacetylase 6 (HDAC6) with IC50 of 56nM, >30 fold less potent against other HDACs. [1]
HDAC6 is one of the eleven human zinc-dependent HDACs with two catalytic domains and one ubiquitin-binding domain at the C-terminal. It exhibits various biological functions including regulation of microtubule dynamics and degradation of misfolded proteins. It involves in many cellular pathways related to normal and tumor cell growth, migration and death. [1]
In normal HFS and transformed LNCaP cells, HPOB inhibited cell growth but not viability, induced acetylation of α-Tubulin, but not histones. HPOB enhanced etoposide-, doxorubicin-, and SAHA-induced cell death in transformed cell but not in normal cell. HPOB enhanced the effectives of anticancer drugs via apoptotic pathway and activated DNA damage response in transformed cell. [1]
HPOB is well-tolerated in mice carrying human prostate cancer CWR22 xenograft and enhances cytotoxicity effects of anticancer drug SAHA in these animals. [1]
References:
1.  Lee JH, Mahendran A, Yao Y, Ngo L, Venta-Perez G, Choy ML, Kim N, Ham WS, Breslow R, Marks PA. Development of a histone deacetylase 6 inhibitor and its
biological effects. Proc Natl Acad Sci U S A. 2013 Sep 24;110(39):15704-9.

HPOB, an HDAC6 inhibitor, attenuates corticosterone-induced injury in rat adrenal pheochromocytoma PC12 cells by inhibiting mitochondrial GR translocation and the intrinsic apoptosis pathway.[Pubmed:27522966]

Neurochem Int. 2016 Oct;99:239-251.

High levels of glucocorticoids (GCs) have been reported to damage normal hippocampal neurons, and such damage has been positively correlated with major depression (MD) and chronic stress. Our previous study showed that HDAC6 might be a potential target to regulate GC-induced glucocorticoid receptor (GR) translocation to the mitochondria and subsequent apoptosis. In the present study, we investigated the effect of HPOB, a selective HDAC6 inhibitor, on corticosterone (Cort)-induced apoptosis and explored the possible mechanism of action of HPOB in rat adrenal pheochromocytoma (PC12) cells, which possesses typical neuron features and expresses high levels of glucocorticoid receptors. We demonstrated that pre-treatment with HPOB remarkably reduced Cort-induced cytotoxicity and confirmed the anti-apoptotic effect of HPOB via the caspase-3 activity assay and H33342/PI and TUNEL double staining. Mechanistically, we demonstrated that HPOB reversed the Cort-induced elevation of GR levels in the mitochondria and blocked concomitant mitochondrial dysfunction and the intrinsic apoptosis pathway. Furthermore, HPOB was shown to attenuate expression of the multi-chaperone machinery (Hsp90-Hop-Hsp70) and cooperate with mitochondrial translocase of the outer/inner membrane (TOM/TIM) complex recruitment by triggering hyperacetylation of Hsps through HDAC6 inhibition. Considering all of these findings, the neuroprotective effect of HPOB demonstrated the crucial role of HDAC6 inhibition in reducing Cort-induced apoptosis in PC12 cells. The data further suggested that the anti-apoptotic activity of HDAC6 inhibition against the mitochondria-mediated impairment pathway might be mechanistically linked to the hyperacetylation of Hsps and consequent suppression of GR translocation to the mitochondria.

HPOB is a highly potent and selective inhibitor of histone deacetylase 6 (HDAC6) with IC50 of 56 nM, >30 fold less potent against other HDACs.

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