2. Cell Cycle/DNA Damage Epigenetics Apoptosis
  3. HDAC Apoptosis
  4. HDAC8-IN-15

HDAC8-IN-15 是一种选择性 HDAC8 抑制剂，其 IC50 为 0.40 μM。HDAC8-IN-15 可提高 HDAC8 底物 SMC3 的乙酰化水平，且不会改变 SMC3 的总蛋白水平。HDAC8-IN-15 可降低癌细胞活力、抑制集落形成、减缓细胞迁移、诱导细胞凋亡 (apoptosis)，并诱导细胞周期阻滞于 SubG1 期。HDAC8-IN-15 可用于神经母细胞瘤的相关研究。

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HDAC8-IN-15

HDAC8-IN-15 Chemical Structure

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HDAC8-IN-15 相关抗体

Top Publications Citing Use of Products

查看 HDAC 亚型特异性产品:

查看所有亚型
HDAC HDAC1 HDAC2 HDAC3 HDAC4 HDAC5 HDAC6 HDAC7 HDAC8 HDAC9 HDAC10 HDAC11 HD1 HD2

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

HDAC8-IN-15 is a selective HDAC8 inhibitor with an IC50 of 0.40 μM. HDAC8-IN-15 increases the acetylation level of the HDAC8 substrate SMC3 without altering the total protein level of SMC3. HDAC8-IN-15 reduces cancer cell viability, inhibits colony formation, slows cell migration, induces apoptosis, and causes cell cycle arrest at the SubG1 phase. HDAC8-IN-15 can be used in studies related to neuroblastoma[1].

IC50 & Target[1]

HDAC8

0.4 μM (IC50)

体外研究
(In Vitro)

HDAC8-IN-15 (Compound 9m) 对 IMR32 神经母细胞瘤细胞的增殖抑制作用 (IC50 = 9.92 μM) 比对 HCT-116 结肠癌细胞、MCF7 乳腺癌细胞及正常 HEK293 细胞的抑制作用更强[1]。
HDAC8-IN-15 (1-5 μM; 9-12 days) 可强效抑制 IMR32 神经母细胞瘤细胞的集落形成[1]。
HDAC8-IN-15 (1-5 μM; 0-48 h) 可抑制 IMR32 神经母细胞瘤细胞的迁移，该作用通过伤口愈合程度降低得到验证[1]。
HDAC8-IN-15 (1-5 μM; 48 h) 可剂量依赖性地诱导 IMR32 神经母细胞瘤细胞发生凋亡[1]。
HDAC8-IN-15 (1-5 μM; 48 h) 可在 IMR32 神经母细胞瘤细胞中诱导 G1 亚期细胞周期阻滞[1]。
HDAC8-IN-15 (1-5 μM; 24 h) 可提高 IMR32 神经母细胞瘤细胞中 SMC3 的乙酰化水平，这与 HDAC8 抑制作用一致[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

HDAC8-IN-15 相关抗体:

Cell Migration Assay[1]

Cell Line: IMR32 neuroblastoma cells
Concentration: 1 μM, 5 μM
Incubation Time: 0, 12 and 48 h
Result: Significantly reduced the percentage of wound closure over 48 h compared to untreated controls, indicating inhibited cell migration.

Apoptosis Analysis[1]

Cell Line: IMR32 neuroblastoma cells
Concentration: 1 μM, 5 μM
Incubation Time: 48 h
Result: Induced early apoptosis in ~5% of IMR32 cells and late apoptosis/necrosis in ~2% of cells at 1 μM.
Induced early apoptosis in ~11% of cells and late apoptosis/necrosis in ~5% of cells at 5 μM, compared to minimal apoptosis in untreated controls.

Cell Cycle Analysis[1]

Cell Line: IMR32 neuroblastoma cells
Concentration: 1 μM, 5 μM
Incubation Time: 48 h
Result: Increased the sub-G1 cell population to ~11.2% (from ~2.62% in controls) at 1 μM.
Increased the sub-G1 population to ~20.2% at 5 μM, indicating induction of cell cycle arrest at the sub-G1 phase.

Western Blot Analysis[1]

Cell Line: IMR32 neuroblastoma cells
Concentration: 1 μM, 5 μM
Incubation Time: 24 h
Result: Significantly increased Ac-SMC3 protein levels relative to untreated controls, while total SMC3 and β-actin levels remained unchanged.
分子量

545.89

Formula

C26H27Cl3N6O
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.
纯度 & 产品资料
参考文献

HDAC8-IN-15 相关分类

  • 摩尔计算器

  • 稀释计算器

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量   浓度   体积   分子量 *
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Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

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浓度 (start) × 体积 (start) = 浓度 (final) × 体积 (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

HDAC8-IN-15HDACApoptosisHistone deacetylasesHDAC8HDAC3colon cancer cellsbreast cancer cellsHDAC1neuroblastomaMCF7 breast cancerIMR32 neuroblastoma cellsSMC3HEK293 cellsInhibitorinhibitorinhibit

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