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 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].

For research use only. We do not sell to patients.

WMJ-J-09 Chemical Structure

WMJ-J-09 Chemical Structure

CAS No. : 2416914-29-7

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WMJ-J-09 Related Antibodies

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PIM1 PIM2 PIM3

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Description

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].

In Vitro

WMJ-J-09 (compound WMJ-J-09) (0-10 μM, 48 h, CRC cells) (0-20 μM, 72 h, HNSCC cells) selectively kills cancer cells in a concentration- and time-dependent manner, and exerts no significant toxicity on non-tumor FHC cells[1][2].

WMJ-J-09 (5 μM, 24 h, HCT116 cells) (10 μM, 48 h, FaDu cells) arrests the cell cycle of cancer cells at the G2/M phase and induces apoptosis[1][2].

WMJ-J-09 (5 μM, 24 h, HCT116 cells) (10 μM, 24 h, FaDu cells) disrupts microtubule assembly[1][2].

WMJ-J-09 (5 μM, 6-24 h, HCT116 cells) (10 μM, 24 h, FaDu cells) inhibits survivin at the transcriptional level[1][2].

WMJ-J-09 (0-10 μM, 24 h, HCT116 cells) (0-20 μM, 48 h, FaDu cells) regulates signaling pathways in cancer cells, inhibits HDACs to modulate key proteins, and promotes cancer cell apoptosis[1][2].

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

WMJ-J-09 Related Antibodies

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).
In Vivo

WMJ-J-09 (compound WMJ-J-09) (20 mg/kg, i.p, daily for 19 days) inhibits CRC tumor growth by inhibiting cancer cell proliferation and is well tolerated in the HCT116 xenograft mice model[1].

WMJ-J-09 (20 mg/kg, i.p, daily for 23 days) inhibits the growth of HNSCC transplanted tumors and has good safety[2].

MedChemExpress (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.
Molecular Weight

445.53

Formula

C22H27N3O5S
CAS No.
SMILES

O=C(NO)CCCCCCC(NC1=CC(N(S(C2=CC=CC=C2)(=O)=O)CC3)=C3C=C1)=O
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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WMJ-J-09 Related Classifications

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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:

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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