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CAS No. : 1429651-50-2
MCE 国际站:HPOB
产品活性:HPOB 是一种高效、选择性的 HDAC6 抑制剂,IC50 为 56 nM。HPOB 显示对其他 HDAC 的效力降低了 30 倍以上。HPOB 提高 DNA 损伤抗癌活性分子在转化细胞中的有效性。HPOB 不阻断 HDAC6 的泛素结合活性。
研究领域:Cell Cycle/DNA Damage | Epigenetics | Apoptosis
作用靶点:HDAC | Apoptosis
In Vitro: 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.
In Vivo: HPOB (300 mg/kg; i.p.; daily for 18 days) and SAHA (50 mg/kg) causes suppression of the growth of established CWR22 tumors.
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