2. MAPK/ERK Pathway Epigenetics Cell Cycle/DNA Damage PI3K/Akt/mTOR Apoptosis Cytoskeleton JAK/STAT Signaling
  3. p38 MAPK HDAC AMPK MDM-2/p53 Microtubule/Tubulin Pim Survivin Apoptosis
  4. WMJ-J-09

WMJ-J-09 是 HDAC 抑制剂，对其的IC50为 7.5 nM (HDAC1)，21.3 nM (HDAC2)，18.4 nM (HDAC3)，90.9 nM (HDAC8)，3.9 nM (HDAC6)，8715.7 nM (HDAC4)。WMJ-J-09 在癌细胞中可以阻滞细胞周期并诱导细胞凋亡 (Apoptosis)。WMJ-J-09 通过LKB1-AMPK-p38MAPK-p63-存活素信号级联反应诱导癌细胞死亡。WMJ-J-09 通过抑制 HDAC 酶活性，导致关键蛋白乙酰化，进而调控癌细胞死亡。WMJ-J-09可以用于结直肠癌和头颈部鳞状细胞癌的研究[1][2]。

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WMJ-J-09 Chemical Structure

WMJ-J-09 Chemical Structure

CAS No. : 2416914-29-7

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WMJ-J-09 相关抗体

Top Publications Citing Use of Products

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p38 MAPK p38α p38β MAPK13 p38δ p38γ

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HDAC HDAC1 HDAC2 HDAC3 HDAC4 HDAC5 HDAC6 HDAC7 HDAC8 HDAC9 HDAC10 HDAC11 HD1 HD2

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NUAK1 NUAK2 AMPK AMPK α1β1γ1 AMPK α2β1γ1 AMPK α1β2γ1 AMPK α2β2γ1

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PIM1 PIM2 PIM3

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

WMJ-J-09 is an HDAC inhibitor with IC50 values of 7.5 nM (HDAC1), 21.3 nM (HDAC2), 18.4 nM (HDAC3), 90.9 nM (HDAC8), 3.9 nM (HDAC6) and 8715.7 nM (HDAC4). WMJ-J-09 blocks the cell cycle and induces apoptosis in cancer cells. WMJ-J-09 induces cancer cell death through the LKB1-AMPK-p38MAPK-p63-survivin signaling cascade.WMJ-J-09 inhibits HDAC enzyme activity, leading to acetylation of key proteins and thereby regulating cancer cell death. WMJ-J-09 can be used in HCT116 cells and FaDu cells research[1][2].

体外研究
(In Vitro)

WMJ-J-09 (compound WMJ-J-09) (0-10 μM, 48 h, CRC cells) (0-20 μM, 72 h, HNSCC cells) 具有浓度和时间依赖性，选择性杀伤癌细胞，对非肿瘤 FHC 细胞无显著毒性[1][2]。
WMJ-J-09 (5 μM, 24 h, HCT116 cells) (10 μM, 48 h, FaDu cells) 在G2/M期阻滞癌细胞的细胞周期，诱导细胞凋亡[1][2]。
WMJ-J-09 (5 μM, 24 h, HCT116 cells) (10 μM, 24 h, FaDu cells) 破坏微管组装[1][2]。
WMJ-J-09 (5 μM, 6-24 h, HCT116 cells) (10 μM, 24 h, FaDu cells) 在转录水平抑制Survivin[1][2]。
WMJ-J-09 (0-10 μM, 24 h, HCT116 cells) (0-20 μM, 48 h, FaDu cells) 在癌细胞中可以控制信号通路，并抑制 HDAC 来调控关键蛋白，促进癌凋亡[1][2]。

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

WMJ-J-09 相关抗体:

Cell Viability Assay[1][2]

Cell Line: HCT116 cells, FHC cells; FaDu cells, SCC9 cells, SCC25 cells
Concentration: 0.1 μM, 0.5 μM, 1 μM, 2.5 μM, 5 μM, 10 μM (HCT116 cells, FHC cells); 0.5 μM, 1 μM, 2.5 μM, 5 μM, 10 μM, 20 μM (FaDu cells, SCC9 cells, SCC25 cells)
Incubation Time: 48 h (HCT116 cells, FHC cells); 72 h (FaDu cells, SCC9 cells, SCC25 cells)
Result: Reduced the viability of CRC cells (with significant inhibition at 10 μM and an IC50 of approximately 5 μM).
Had the strongest inhibitory effect on cell viability at 10 μM, and the survival rate of FaDu cells dropped to about 30 % after treatment with 20 μM for 72 h.

Apoptosis Analysis[1][2]

Cell Line: HCT116 cells; FaDu cells
Concentration: 5 μM (HCT116 cells); 10 μM (FaDu cells)
Incubation Time: 24 h (HCT116 cells); 48 h (FaDu cells)
Result: Increased the proportion of early apoptotic (LR quadrant) and late apoptotic (UR quadrant) cells.
Increased cleaved caspase-3 and PARP cleavage fragments.
Significantly increased the proportion of sub-G1 phase (apoptotic cells), with approximately 40 % at 20 μM.

Cell Cycle Analysis[1][2]

Cell Line: HCT116 cells; FaDu cells
Concentration: 5 μM (HCT116 cells); 0.1 μM, 0.5 μM, 1 μM, 2.5 μM, 5 μM, 10 μM, 20 μM (FaDu cells)
Incubation Time: 24 h
Result: Reduced the proportion of cells in the S phase and increased the proportion of cells in the G2/M phase and sub-G1 phase (apoptosis peak).
Increased the proportion of cells in the G2/M phase (from 12 % to 28 % at 10 μM) and decreased the number of cells in the S phase.

Immunofluorescence[1][2]

Cell Line: HCT116 cells; FaDu cells
Concentration: 5 μM (HCT116 cells); 10 μM (FaDu cells)
Incubation Time: 24 h
Result: Disrupted the cytoskeleton through α-tubulin acetylation.

RT-PCR[1][2]

Cell Line: HCT116 cells; FaDu cells
Concentration: 5 μM (HCT116 cells); 10 μM (FaDu cells)
Incubation Time: 6-24 h (HCT116 cells); 6 h (FaDu cells)
Result: Inhibited survivin expression at the transcriptional level.

Western Blot Analysis[1][2]

Cell Line: HCT116 cells, HCT116 p53-/- cells, HCT116-p53 wildtype cells; FaDu cells
Concentration: 0.1 μM, 0.5 μM, 1 μM, 2.5 μM, 5 μM, 10 μM (HCT116 cells, HCT116 p53-/- cells, HCT116-p53 wildtype cells); 2.5 μM, 5 μM, 10 μM, 20 μM (FaDu cells)
Incubation Time: 24 h (HCT116 cells, HCT116 p53-/- cells, HCT116-p53 wildtype cells); 48 h (FaDu cells)
Result: Increased p21 protein, acetylated and phosphorylated p53, decreased survivin protein, and increased α-tubulin acetylation.
Activated phosphorylation of the LKB1/p38MAPK pathway.
Acetylated survivin and degraded it in the proteasome.
Increased p21 protein significantly, while cyclin D1 and survivin proteins decreased.
Increased the phosphorylation levels of LKB1 (Ser 428), AMPK (Thr 172), p38MAPK (Thr 180/Tyr 182), and p63 (Ser 160/162) over time, and increased cleaved caspase-3 and PARP (apoptosis markers).
体内研究
(In Vivo)

WMJ-J-09 (化合物WMJ-J-09) (20 mg/kg, i.p, 每日一次，持续19天) 通过抑制癌细胞增殖来抑制 CRC 肿瘤生长，并且在 HCT116 异种移植小鼠模型中耐受性良好[1]。

WMJ-J-09 (20 mg/kg, i.p, 每日一次，持续23天) 可抑制头颈部鳞状细胞癌移植瘤的生长，且安全性良好[2]。

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

Animal Model: HCT116 xenograft model established in nude male mice(4 weeks)[1]
Dosage: 20 mg/kg
Administration: Daily intraperitoneal injection (i.p.), at the corresponding doses for 19 days
Result: Inhibited tumor growth, with tumor volume and weight significantly lower than those in the control group.
Inhibited tumor proliferation, as indicated by reduced Ki67 immunohistochemical staining within the tumor.
Exhibited low toxicity, with no significant change in mouse body weight.
Animal Model: DaFu xenograft model established in nude male mice(4 weeks, 25g)[2]
Dosage: 20 mg/kg
Administration: Daily intraperitoneal injection (i.p.), at the corresponding doses for 23 days.
Result: Significantly inhibited tumor growth, with the average tumor weight in the treatment group lower than that in the control group.
Exhibited low toxicity, with no significant change in mouse body weight.
分子量

445.53

Formula

C22H27N3O5S
CAS 号
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

WMJ-J-09 相关分类

  • 摩尔计算器

  • 稀释计算器

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  • 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:

WMJ-J-092416914-29-7p38 MAPKHDACAMPKMDM-2/p53Microtubule/TubulinPimSurvivinApoptosisHistone deacetylasesAMP-activated protein kinasePim kinasescolorectal cancerhead and neck squamous cell carcinoma(HNSCC)FaDu cellsHCT116 cellsaliphatic hydroxamateliver kinase B1 (LKB1)Histone deacetylase (HDAC)p63P53survivinInhibitorinhibitorinhibit

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