| 生物活性 | HDAC-IN-36 (compound 23 g) is an orally active and potentHDAC(histone deacetylase) inhibitor, with anIC50of 11.68 nM (HDAC6). HDAC-IN-36 promotesapoptosis,autophagyand suppresses migration. HDAC-IN-36 shows anti-tumor and anti-metastatic activity, and can be used for breastcancerresearch[1]. |
| IC50& Target | HDAC6 11.68 nM (IC50) | HDAC10 13.24 nM (IC50) | HDAC3 79.17 nM (IC50) | HDAC1 86.93 nM (IC50) | HDAC2 97.32 nM (IC50) | HDAC8 378.2 nM (IC50) | HDAC4 >1000 nM (IC50) | HDAC5 >1000 nM (IC50) | HDAC7 >1000 nM (IC50) | HDAC9 >1000 nM (IC50) | HDAC11 >1000 nM (IC50) |
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体外研究
(In Vitro) | HDAC-IN-36 (compound 23 g) (0-10, 24 h) exhibits good antiproliferative activity in MDA-MB-231 cells, promotes the acetylation of α-Tubulin and HSP90[1].
HDAC-IN-36 (0-10, 24 h) induces apoptosis in MDA-MB-231 cells in a dose-dependent manner, and mainly induces mitochondrial-dependent apoptosis[1].
HDAC-IN-36 (0-10, 24 h) inhibits MDA-MB-231 cells migration in a dose-dependent manner, increases the expression of E-cadherin and decreases the expression of MMP-2 obviously[1].
HDAC-IN-36 (0-10, 24 h) induces noteworthy autophagy, increases the expression of Beclin1, LC3II and decreases the expression of SQSTM1/p62[1].
Cell Viability Assay | Cell Line: | MDA-MB-231 cells[1] | | Concentration: | 0, 2.5, 5, 10 μM | | Incubation Time: | 24 h | | Result: | Exhibited good anti-proliferative activity in MDA-MB-231 cells, with IC50of 1.32 ± 0.13 μM, increased the acetylation level of intracellular proteins, and promoted the acetylation of α-Tubulin and HSP90. |
Apoptosis Analysis | Cell Line: | MDA-MB-231 cells[1] | | Concentration: | 0, 2.5, 5, 10 μM | | Incubation Time: | 24 h | | Result: | Induced apoptosis in MDA-MB-231 cells in a dose-dependent manner. |
Cell Autophagy Assay | Cell Line: | MDA-MB-231 cells[1] | | Concentration: | 0, 2.5, 5, 10 μM | | Incubation Time: | 24 h | | Result: | Induced noteworthy autophagy with increased aggregation of LC3 puncta. |
Western Blot Analysis | Cell Line: | MDA-MB-231 cells[1] | | Concentration: | 0, 2.5, 5, 10 μM | | Incubation Time: | 24 h | | Result: | Mainly induced mitochondrial-dependent apoptosis, up-regulated the expression of Bax and downregulated the expression of Bcl-2, and increased the cleavage of caspase3, caspase8 and caspase9; increased the expression of E-cadherin and decreased the expression of MMP-2 obviously; increased the expression of Beclin1, LC3II and decreased the expression of SQSTM1/p62. |
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体内研究
(In Vivo) | HDAC-IN-36 (compound 23 g) (Zebrafish tumor xenograft model; 0-5 μg/mL, 3 days) shows potent anti-tumor and anti-metastatic activity, and improvesin vivoanti-tumor efficacy[1].
HDAC-IN-36 (Beagles, 20 mg/kg, Orally, once) shows a significant improvement in pharmacokinetic parameters[1].
Pharmacokinetic Parameters of HDAC-IN-36 in male Beagles[1].
| Parameters | 23g (20 mg/kg) | | T1/2(h) | 1.24 ± 0.21 | | Tmax(h) | 0.79 ± 0.33 | | Cmax(μg/L) | 120.36 ± 15.53 | | AUC0-t(μg/L*h) | 1275.35 ± 70.17 | | AUC0-∞(μg/L*h) | 1289.40 ± 88.91 |
| Animal Model: | Zebrafish (MDA-MB-231-derived xenograft model, Wild-type AB strain)[1] | | Dosage: | 0, 2.5, 5 μg/mL | | Administration: | 3 days | | Result: | Inhibited tumor formation and migration in a dose-dependent manner, and improvedin vivoanti-tumor efficacy. |
| Animal Model: | Beagles (female, 8-10 kg, n = 4)[1] | | Dosage: | 20 mg/kg (dissolved 0.5% sodium carboxyl methyl cellulose (CMC-Na) aqueous solution) | | Administration: | Orally, once (Pharmacokinetic Analysis) | | Result: | Showed a significant improvement in pharmacokinetic parameters with T1/2value of 1.24 h. |
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| 运输条件 | Room temperature in continental US; may vary elsewhere. |
| 储存方式 | Please store the product under the recommended conditions in the Certificate of Analysis. |
