产品
编 号：F160863
分子式：C17H18N2O4
分子量：314.34
分子式：C17H18N2O4
分子量：314.34
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
5mg
询价
询价
10mg
询价
询价
25mg
询价
询价
50mg
询价
询价
100mg
询价
询价
结构图
CAS No: 1429651-50-2
产品详情
生物活性：
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.
体内研究：
HPOB (300 mg/kg; i.p.; daily for 18 days) and SAHA (50 mg/kg) causes suppression of the growth of established CWR22 tumors.Animal Model:Nude mice (CWR22 human prostate cancer xenograf)
Dosage:300 mg/kg
Administration:I.p.; daily for 18 days
Result:Combination with SAHA showed significant shrinkage of CWR22 tumors.
体外研究：
HPOB (8, 16, or 32 μM; 72 hours) inhibits growth, however, not viability, of normal or transformed cells.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. 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.HPOB attenuates corticosterone-induced injury in rat adrenal pheochromocytoma PC12 cells by inhibiting mitochondrial GR translocation and the intrinsic apoptosis pathway.
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.
体内研究：
HPOB (300 mg/kg; i.p.; daily for 18 days) and SAHA (50 mg/kg) causes suppression of the growth of established CWR22 tumors.Animal Model:Nude mice (CWR22 human prostate cancer xenograf)
Dosage:300 mg/kg
Administration:I.p.; daily for 18 days
Result:Combination with SAHA showed significant shrinkage of CWR22 tumors.
体外研究：
HPOB (8, 16, or 32 μM; 72 hours) inhibits growth, however, not viability, of normal or transformed cells.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. 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.HPOB attenuates corticosterone-induced injury in rat adrenal pheochromocytoma PC12 cells by inhibiting mitochondrial GR translocation and the intrinsic apoptosis pathway.
产品资料
Copyright©2015-2024 沪ICP备2022026524号-1
沪公网安备