[CAS NO. 1429651-50-2] HPOB
PRODUCTS SPECIFICATIONS [1429651-50-2]
DESCRIPTION [1429651-50-2]
Overview
| MDL | MFCD27952937 |
|---|---|
| Molecular Weight | 314.34 |
| Molecular Formula | C17H18N2O4 |
| SMILES | O=C(N(CCO)C1=CC=CC=C1)CC2=CC=C(C(NO)=O)C=C2 |
2 Publications Citing Use of MCE
Summary
HPOB is a highly potent and selective inhibitor of HDAC6 with an IC 50 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] .
IC50 & Target
|
HDAC6 0.056 μM (IC 50 ) |
HDAC3/NCOR2 1.7 μM (IC 50 ) |
HDAC8 2.8 μM (IC 50 ) |
HDAC1 2.9 μM (IC 50 ) |
HDAC10 3.0 μM (IC 50 ) |
HDAC2 4.4 μM (IC 50 ) |
In Vitro
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]
.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Proliferation Assay [1]
| Cell Line: | Normal human foreskin fibroblast (HFS), LNCaP, A549, U87 cells |
| Concentration: | 8, 16, or 32 μM |
| Incubation Time: | 72 hours |
| Result: | Inhibited cell growth of normal and transformed cells in a concentration-dependent manner but do not induce cell death of normal or transformed cells. |
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 [1] .
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
| Animal Model: | Nude mice (CWR22 human prostate cancer xenograf) [1] |
| Dosage: | 300 mg/kg |
| Administration: | I.p.; daily for 18 days |
| Result: | Combination with SAHA showed significant shrinkage of CWR22 tumors. |
Appearance
Solid
Shipping
Room temperature in continental US; may vary elsewhere.
Storage
| Powder | -20°C | 3 years |
|---|---|---|
| 4°C | 2 years | |
| In solvent | -80°C | 6 months |
| -20°C | 1 month |
Solvent & Solubility
DMSO : 50 mg/mL ( 159.06 mM ; Need ultrasonic)
Stock Solutions
| Concentration Solvent Mass | 1 mg | 5 mg | 10 mg |
|---|
| 1 mM | 3.1813 mL | 15.9063 mL | 31.8127 mL |
| 5 mM | 0.6363 mL | 3.1813 mL | 6.3625 mL |
| 10 mM | 0.3181 mL | 1.5906 mL | 3.1813 mL |
References
- [1] Lee JH et al. 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.
- [2] Li ZY et al. HPOB, an HDAC6 inhibitor, attenuates corticosterone-induced injury in rat adrenal pheochromocytoma PC12 cells by inhibiting mitochondrial GR translocation and the intrinsic apoptosis pathway. Neurochem Int. 2016 Oct;99:239-51.