| Bioactivity | HPOB is a highly potent and selective inhibitor of HDAC6 with an IC50 of 56 nM. HPOB displays >30 fold less potent against other HDACs. HPOB enhances the effectiveness of DNA-damaging anticancer agents in transformed cells but not normal cells. HPOB does not block the ubiquitin-binding activity of HDAC6[1]. | ||||||||||||
| Invitro | HPOB (8, 16, or 32 μM; 72 hours) inhibits growth, however, not viability, of normal or transformed cells[1].In normal (HFS) and transformed (LNCAP, U87, and A549) cells, HPOB causes accumulation of acetylated α-tubulin and acetylated peroxiredoxin, substrates of HDAC6, but not of acetylated histones. HPOB enhances etoposide-, doxorubicin-, and SAHA-induced transformed cell ((LNCAP, U87, and A549 cells) death but not normal cell death[1]. In LNCaP cells cultured with HPOB and etoposide, there was an increase in cleaved PARP, a marker of apoptosis. Combination of HPOB with etoposide increased the accumulation of DNA damage compared with etoposide alone as evidenced by accumulation of γH2AX in LNCaP cells[1].HPOB attenuates corticosterone-induced injury in rat adrenal pheochromocytoma PC12 cells by inhibiting mitochondrial GR translocation and the intrinsic apoptosis pathway[2]. Cell Proliferation Assay[1] Cell Line: | ||||||||||||
| Name | HPOB | ||||||||||||
| CAS | 1429651-50-2 | ||||||||||||
| Formula | C17H18N2O4 | ||||||||||||
| Molar Mass | 314.34 | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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