2. Cell Cycle/DNA Damage Apoptosis PI3K/Akt/mTOR
  3. Zinc Finger Protein Apoptosis PI3K Akt
  4. PLAGL2-IN-1

PLAGL2-IN-1 is a inhibitor of pleiomorphic adenoma-like protein 2 (PLAGL2) with a Kd of 2.23 µM. PLAGL2-IN-1 suppresses PLAGL2 transcriptional activity, induces G0/G1 cell cycle arrest, and apoptosis, thereby inhibiting hepatocellular carcinoma (HCC) cell proliferation. PLAGL2-IN-1 disrupts extracellular matrix organization and suppresses the PI3K-AKT pathway by reducing AKT phosphorylation. PLAGL2-IN-1 inhibits tumor growth in an HCCLM3 xenograft mouse model. PLAGL2-IN-1 can be used for the research of HCC.

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

PLAGL2-IN-1

PLAGL2-IN-1 Chemical Structure

CAS No. : 3099026-16-8

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PLAGL2-IN-1 Related Antibodies

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Description

PLAGL2-IN-1 is a inhibitor of pleiomorphic adenoma-like protein 2 (PLAGL2) with a Kd of 2.23 µM. PLAGL2-IN-1 suppresses PLAGL2 transcriptional activity, induces G0/G1 cell cycle arrest, and apoptosis, thereby inhibiting hepatocellular carcinoma (HCC) cell proliferation. PLAGL2-IN-1 disrupts extracellular matrix organization and suppresses the PI3K-AKT pathway by reducing AKT phosphorylation. PLAGL2-IN-1 inhibits tumor growth in an HCCLM3 xenograft mouse model. PLAGL2-IN-1 can be used for the research of HCC[1].

IC50 & Target[1]

PLAGL2

2.23 μM (Kd)

In Vitro

PLAGL2-IN-1 (compound C8) (72 h) demonstrates broad-spectrum antiproliferative activity in a panel of cancer cells, with IC50s of 0.96 (A549), 1.35 (NCI-H1650), 1.03 (NCI-H460), 3.31 (MGC803), 3.28 (HGC27), 7.63 (SW620), 0.92 (HT29), 1.64 (MDA-MB-231), 2.21 (HCC1937), 1.43 (U87-MG), 24.96 (LN229), 8.83 (U937), 5.67 (K562), 5.33 (MEG01), 19.54 (Jurkat), 4.14 (PC-3), and 16.19 μM (SKOV3), respectively[1].
PLAGL2-IN-1 (0-1 μM, 14 days) inhibits colony formation of MHCC-97H and HCCLM3 cells in a concentration-dependent manner[1].
PLAGL2-IN-1 (10 μM, 48 h) induces apoptosis in MHCC-97H and HCCLM3 cells[1].
PLAGL2-IN-1 (5 μM, 24 h) induces G0/G1 phase arrest in MHCC-97H cells[1].
PLAGL2-IN-1 (0-10 μM, 48 h) inhibits cell migration and invasion in HCCLM3 and MHCC-97H cells in a dose-dependent manner, and demonstrates significant inhibition of cell division in HCCLM3 HCC cells[1].
PLAGL2-IN-1 (5-10 μM, 24-48 h) disrupts extracellular matrix organization and suppresses the PI3K-AKT pathway by reducing AKT phosphorylation in HCCLM3 cells[1].

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

PLAGL2-IN-1 Related Antibodies

Cell Proliferation Assay[1]

Cell Line: MHCC-97H and HCCLM3
Concentration: 0, 0.01, 0.1, 1 μM
Incubation Time: 14 days
Result: Resulted in a marked reduction incolony formation.
Showed concentration-dependent inhibition in both cells.

Apoptosis Analysis[1]

Cell Line: MHCC-97H and HCCLM3
Concentration: 10 μM
Incubation Time: 48 h
Result: Induced late-stage apoptosis in both cells.
Exhibited stronger pro-apoptotic effects than the 5μM 5-FU (HY-90006) positive control.

Cell Cycle Analysis[1]

Cell Line: MHCC-97H and HCCLM3
Concentration: 5 μM
Incubation Time: 24 h
Result: Induced G0/G1 phase arrest in MHCC-97H cells.
Did not induce cell cycle arrest in HCCLM3 cells.

Cell Migration Assay [1]

Cell Line: MHCC-97H and HCCLM3
Concentration: 0, 5, 10 μM
Incubation Time: 48 h
Result: Showed a dose-dependent inhibition of cell wound healing in HCCLM3 and MHCC-97H cells.
Inhibited cell migration in HCCLM3 and MHCC-97H cells.

Cell Invasion Assay[1]

Cell Line: MHCC-97H and HCCLM3
Concentration: 0, 5, 10 μM
Incubation Time: 48 h
Result: Inhibited cell invasion in HCCLM3 and MHCC-97H cells in a dose-dependent manner.

Immunofluorescence[1]

Cell Line: HCCLM3
Concentration: 5 μM
Incubation Time: 48 h
Result: Reduced the protein expression levels Vimentin.
Increased E-cadherin expression.

Western Blot Analysis[1]

Cell Line: HCCLM3
Concentration: 5, 10 μM
Incubation Time: 48 h
Result: Reduced theprotein expression levels of ZEB1, Vimentin, MMP2, and MMP9.
Increased E-cadherin expression.
Significantly inhibited PLAGL2-dependent AKT phosphorylation at both Thr308 and Ser473.
In Vivo

PLAGL2-IN-1 (compound C8) (15 mg/kg, i.p., daily for 19 days) significantly inhibits tumor growth in a HCCLM3 xenograft mouse model without observable toxicity[1].

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

Animal Model: Male BALB/C nude mice (6-8 weeks old) subcutaneously injected with HCCLM3 cells[1]
Dosage: 15 mg/kg
Administration: i.p., daily for 19 days
Result: Effectively inhibited tumor growth, with a TGI of 63.27%.
Significantly reduced tumor weight and volume.
Showed no observable toxicity in major organs but induced noticeable tumornecrosis.
Reduced expression of Ki-67 and α-SMA in tumor tissues.
Demonstrated a stable body weight during administration.
Molecular Weight

632.60

Formula

C30H35Cl2N5O4S
CAS No.
SMILES

O=S(C1=CC=C2C=CC=CC2=C1)(NC3=CC(C(N4CCN(C(C(Cl)Cl)=O)CC4)=O)=CC=C3N5CCN(C(C)C)CC5)=O
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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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PLAGL2-IN-1 Related Classifications

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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:

PLAGL2-IN-13099026-16-8Zinc Finger ProteinApoptosisPI3KAktPhosphoinositide 3-kinasePKBProtein kinase B3-(Phenylsulfonamido) benzamide derivativesHepatocellular carcinomaStructural optimizationPLAGL2Inhibitorinhibitorinhibit

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