COG449
(Synonyms: OP449)
COG449 (OP449) is a cell-penetrating peptide that binds to SET, prevents the formation of the SET-PP2A complex, and restores PP2A phosphatase activity. COG449 decreases the phosphorylation levels of AKT308, ERK1/2, NFkB p65, and c-MYC S62, and reduces c-MYC stability and target gene expression. COG449 induces apoptosis, autophagy, and histone H3 hyperacetylation, and decreases the levels of SET, CIP2A, SETBP1, and Mcl-1. COG449 reduces cancer cell viability and decreases tumor mass in xenograft models. COG449 can be used for research on various cancers such as oral squamous cell carcinoma, T-cell acute lymphoblastic leukemia, B-CLL, non-Hodgkin lymphoma, and breast cancer.
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- 화학식: C418H712N146O82S4
- 분자량:9223.31
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Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
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Biological Activity
제품 설명
COG449 (OP449) is a cell-penetrating peptide that binds to SET, prevents the formation of the SET-PP2A complex, and restores PP2A phosphatase activity. COG449 decreases the phosphorylation levels of AKT308, ERK1/2, NFkB p65, and c-MYC S62, and reduces c-MYC stability and target gene expression. COG449 induces apoptosis, autophagy, and histone H3 hyperacetylation, and decreases the levels of SET, CIP2A, SETBP1, and Mcl-1. COG449 reduces cancer cell viability and decreases tumor mass in xenograft models. COG449 can be used for research on various cancers such as oral squamous cell carcinoma, T-cell acute lymphoblastic leukemia, B-CLL, non-Hodgkin lymphoma, and breast cancer[1][2][3][4][5][6][7].
IC50 & Target
[2]|
ERK1 |
ERK2 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| WSU-HN13 | IC50 |
5.94 μM
|
Reduction in cell viability of human HN13 head and neck squamous cell carcinoma cells assessed after incubation for 72 hrs by resazurin assay.
Reduction in cell viability of human HN13 head and neck squamous cell carcinoma cells assessed after incubation for 72 hrs by resazurin assay.
|
32569675 |
| HN12 | IC50 |
5.11 μM
|
Reduction in cell viability of human HN12 head and neck squamous cell carcinoma cells assessed after incubation for 72 hrs by resazurin assay.
Reduction in cell viability of human HN12 head and neck squamous cell carcinoma cells assessed after incubation for 72 hrs by resazurin assay.
|
32569675 |
| HN-6 | IC50 |
9.17 μM
|
Reduction in cell viability of human HN6 head and neck squamous cell carcinoma cells assessed after incubation for 72 hrs by resazurin assay.
Reduction in cell viability of human HN6 head and neck squamous cell carcinoma cells assessed after incubation for 72 hrs by resazurin assay.
|
32569675 |
| CAL-27 | IC50 |
8.86 μM
|
Reduction in cell viability of human Cal27 head and neck squamous cell carcinoma cells assessed after incubation for 72 hrs by resazurin assay.
Reduction in cell viability of human Cal27 head and neck squamous cell carcinoma cells assessed after incubation for 72 hrs by resazurin assay.
|
32569675 |
| SCC-9 | IC50 |
6.26 μM
|
Reduction in cell viability of human SCC9 head and neck squamous cell carcinoma cells assessed after incubation for 72 hrs by resazurin assay.
Reduction in cell viability of human SCC9 head and neck squamous cell carcinoma cells assessed after incubation for 72 hrs by resazurin assay.
|
32569675 |
| Jurkat | IC50 |
1.25 μM
|
Inhibition of cell viability in human JURKAT T-ALL cells assessed by MTS assay after 72 hrs incubation.
Inhibition of cell viability in human JURKAT T-ALL cells assessed by MTS assay after 72 hrs incubation.
|
27705940 |
| LOUCY | IC50 |
1.25 μM
|
Inhibition of cell viability in human LOUCY T-ALL cells assessed by MTS assay after 72 hrs incubation.
Inhibition of cell viability in human LOUCY T-ALL cells assessed by MTS assay after 72 hrs incubation.
|
27705940 |
| RPMI 8402 | IC50 |
1.25 μM
|
Inhibition of cell viability in human RPMI-8402 T-ALL cells assessed by MTS assay after 72 hrs incubation.
Inhibition of cell viability in human RPMI-8402 T-ALL cells assessed by MTS assay after 72 hrs incubation.
|
27705940 |
| MOLT-4 | IC50 |
1.25 μM
|
Inhibition of cell viability in human MOLT-4 T-ALL cells assessed by MTS assay after 72 hrs incubation.
Inhibition of cell viability in human MOLT-4 T-ALL cells assessed by MTS assay after 72 hrs incubation.
|
27705940 |
| K562 | IC50 |
2.5 μM
|
Cytotoxicity against human K562 CML cells assessed as reduction in proliferation and increased apoptosis.
Cytotoxicity against human K562 CML cells assessed as reduction in proliferation and increased apoptosis.
|
blood.V118.21.3757.3757 |
| BaF3 | IC50 |
0.89 μM
|
Inhibition of proliferation of murine Ba/F3 cells expressing wild-type BCR-ABL1 incubated for 72 hrs by Cell Titer 96 Aqueous One solution assay.
Inhibition of proliferation of murine Ba/F3 cells expressing wild-type BCR-ABL1 incubated for 72 hrs by Cell Titer 96 Aqueous One solution assay.
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24436473 |
| BaF3 | IC50 |
1.62 μM
|
Inhibition of proliferation of murine Ba/F3 cells expressing imatinib-insensitive BCR-ABL1T315I point mutant incubated for 72 hrs by Cell Titer 96 Aqueous One solution assay.
Inhibition of proliferation of murine Ba/F3 cells expressing imatinib-insensitive BCR-ABL1T315I point mutant incubated for 72 hrs by Cell Titer 96 Aqueous One solution assay.
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24436473 |
| BaF3 | IC50 |
1.97 μM
|
Inhibition of proliferation of murine Ba/F3 cells expressing BCR-ABL1E255V/T315I compound mutant incubated for 72 hrs by Cell Titer 96 Aqueous One solution assay.
Inhibition of proliferation of murine Ba/F3 cells expressing BCR-ABL1E255V/T315I compound mutant incubated for 72 hrs by Cell Titer 96 Aqueous One solution assay.
|
24436473 |
| K562 | IC50 |
0.60 μM
|
Inhibition of proliferation of human CML K562 cells incubated for 72 hrs by Cell Titer 96 Aqueous One solution assay.
Inhibition of proliferation of human CML K562 cells incubated for 72 hrs by Cell Titer 96 Aqueous One solution assay.
|
24436473 |
| MOLM-14 | IC50 |
0.59 μM
|
Inhibition of proliferation of human AML MOLM-14 cells harboring FLT3-ITD incubated for 72 hrs by cell viability assay.
Inhibition of proliferation of human AML MOLM-14 cells harboring FLT3-ITD incubated for 72 hrs by cell viability assay.
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24436473 |
| GDM-1 | IC50 |
0.82 μM
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Inhibition of proliferation of human AML GDM-1 cells with CSF1R overexpression incubated for 72 hrs by cell viability assay.
Inhibition of proliferation of human AML GDM-1 cells with CSF1R overexpression incubated for 72 hrs by cell viability assay.
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24436473 |
| HL-60 | IC50 |
0.94 μM
|
Inhibition of proliferation of human AML HL-60 cells harboring NRASQ61L incubated for 72 hrs by cell viability assay.
Inhibition of proliferation of human AML HL-60 cells harboring NRASQ61L incubated for 72 hrs by cell viability assay.
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24436473 |
| CMK | IC50 |
1.73 μM
|
Inhibition of proliferation of human AML CMK cells harboring JAK3A572V incubated for 72 hrs by cell viability assay.
Inhibition of proliferation of human AML CMK cells harboring JAK3A572V incubated for 72 hrs by cell viability assay.
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24436473 |
| UT7 | IC50 |
1.78 μM
|
Inhibition of proliferation of human AML UT7 cells incubated for 72 hrs by cell viability assay.
Inhibition of proliferation of human AML UT7 cells incubated for 72 hrs by cell viability assay.
|
24436473 |
In Vitro
Anti-cancerApoptosisAutophagyOthersCytokines & Chemokines
Anti-cancer
COG449 (0-7.0 μM; 72 h) reduces cell viability in HN13, HN12, HN6, Cal27, and SCC9 OSCC cell lines with IC50 values of 5.94 μM, 5.11 μM, 9.17 μM, 8.86 μM, and 6.26 μM, respectively, and reduces viability in NOK-SI and NOK-SI/SET cells with IC50 values of 8.95 μM and 9.16 μM, respectively[1].
COG449 (72 h) inhibits the growth of NOTCH-dependent and -independent T-ALL cells with an IC50 of 1.25 μM at 72 h[2].
COG449 (1 μM) reduces total c-MYC and phospho-S62 c-MYC levels in RPMI-8402 and JURKAT T-ALL cells[2].
COG449 (1 μM) reduces the phosphorylation of ERK1/2 and AKT in RPMI-8402 and JURKAT cells[2].
COG449 (1 μM) negatively affects c-MYC transcriptional activity and reduces the levels of SET, CIP2A, and SETBP1 in T-ALL cells[2].
COG449 (1 μM) reduces tyrosine phosphorylation of PP2Ac in T-ALL cells[2].
COG449 (24 h) induces dose-dependent cytotoxicity in breast cancer cell lines and immortalized MCF10A cells[4].
COG449 significantly reduces the anchorage-independent growth of MDA-MB-231, HCC38, SKBR3, MDA-MB-436, and MDA-MB-468 breast cancer cells[4].
COG449 (1-2 μM; 4 h) reduces pS62-MYC levels in MDA-MB-231, HCC38, MDA-MB-436, and MDA-MB-468 breast cancer cells[4].
COG449 (1 µM) increases PP2A activity by 45% in K562 and 32Dp210 CML cells[5].
COG449 is cytotoxic to K562 and LAMA CML cells, with IC50 values of 2.5 µM and 1.25 µM, respectively[5].
COG449 exhibits selective cytotoxicity against BCR-ABL-positive CML cells[5].
COG449 is cytotoxic to the TKI-resistant 32Dp210T315I mutant cell line, with an IC50 of 2.5 µM[5].
COG449 (2.5-5 µM) inhibits colony formation in primary CML CD34+ cells without affecting normal human CD34+ cells[5].
COG449 (72 h) selectively inhibits the growth of Ba/F3 cells expressing wild-type and mutant BCR-ABL1, as well as K562 and LAMA CML cell lines, with IC50 values ranging from 0.60 to 1.97 μM, while showing no effect on parental Ba/F3 cells[6].
COG449 (2.5 μM) effectively inhibits the growth of primary CML blast crisis cells harboring wild-type BCR-ABL1 (90% inhibition) and BCR-ABL1T315I (35% inhibition)[6].
COG449 (72 h) inhibits the growth of NOTCH-dependent and -independent T-ALL cells with an IC50 of 1.25 μM at 72 h[2].
COG449 (1 μM) reduces total c-MYC and phospho-S62 c-MYC levels in RPMI-8402 and JURKAT T-ALL cells[2].
COG449 (1 μM) reduces the phosphorylation of ERK1/2 and AKT in RPMI-8402 and JURKAT cells[2].
COG449 (1 μM) negatively affects c-MYC transcriptional activity and reduces the levels of SET, CIP2A, and SETBP1 in T-ALL cells[2].
COG449 (1 μM) reduces tyrosine phosphorylation of PP2Ac in T-ALL cells[2].
COG449 (24 h) induces dose-dependent cytotoxicity in breast cancer cell lines and immortalized MCF10A cells[4].
COG449 significantly reduces the anchorage-independent growth of MDA-MB-231, HCC38, SKBR3, MDA-MB-436, and MDA-MB-468 breast cancer cells[4].
COG449 (1-2 μM; 4 h) reduces pS62-MYC levels in MDA-MB-231, HCC38, MDA-MB-436, and MDA-MB-468 breast cancer cells[4].
COG449 (1 µM) increases PP2A activity by 45% in K562 and 32Dp210 CML cells[5].
COG449 is cytotoxic to K562 and LAMA CML cells, with IC50 values of 2.5 µM and 1.25 µM, respectively[5].
COG449 exhibits selective cytotoxicity against BCR-ABL-positive CML cells[5].
COG449 is cytotoxic to the TKI-resistant 32Dp210T315I mutant cell line, with an IC50 of 2.5 µM[5].
COG449 (2.5-5 µM) inhibits colony formation in primary CML CD34+ cells without affecting normal human CD34+ cells[5].
COG449 (72 h) selectively inhibits the growth of Ba/F3 cells expressing wild-type and mutant BCR-ABL1, as well as K562 and LAMA CML cell lines, with IC50 values ranging from 0.60 to 1.97 μM, while showing no effect on parental Ba/F3 cells[6].
COG449 (2.5 μM) effectively inhibits the growth of primary CML blast crisis cells harboring wild-type BCR-ABL1 (90% inhibition) and BCR-ABL1T315I (35% inhibition)[6].
Anti-cancer
Apoptosis
Autophagy
COG449 (10-20 μM; 2-6 h) alters multiple SET targets in HN12 and SCC9 cells and activates apoptosis and autophagy markers[1].
COG449 (10-20 μM; 2-6 h) modulates SET targets in NOK-SI and NOK-SI/SET cells and induces apoptosis and autophagy markers, with dose-dependent effects on histone H3 acetylation[1].
COG449 (10-20 μM; 2-6 h) modulates SET targets in NOK-SI and NOK-SI/SET cells and induces apoptosis and autophagy markers, with dose-dependent effects on histone H3 acetylation[1].
Anti-cancer
Apoptosis
COG449 (0.62-1.25 μM) increases PP2A activity in a dose-dependent manner in JURKAT, LOUCY, RPMI-8402, and MOLT-4 T-ALL cell lines[2].
Others
Apoptosis
Anti-cancer
COG449 is a SET-targeting agent that activates PP2A and reduces Mcl-1 levels by disrupting the SET-PP2A complex, and has shown activity in B-CLL and non-Hodgkin lymphoma[3].
COG449 (48 h) induces apoptosis in mouse and human CML cell lines[6].
COG449 (48 h) induces apoptosis in mouse and human CML cell lines[6].
Anti-cancer
Others
Anti-cancer
Cytokines & Chemokines
COG449 (24 h) attenuates BCR-ABL1 kinase signaling and leads to BCR-ABL1 degradation in K562 cells[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[1]
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Cell Line:HN13, HN12, HN6, Cal27, SCC9
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Concentration:0, 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 7.0 μM
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Incubation Time:72 h
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Result:Decreased cell viability in HN13, HN12, HN6, Cal27, and SCC9 cell lines in a dose-dependent manner.
Achieved IC50 values of 5.94 μM for HN13, 5.11 μM for HN12, 9.17 μM for HN6, 8.86 μM for Cal27, and 6.26 μM for SCC9.
Cell Viability Assay[1]
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Cell Line:NOK-SI, NOK-SI/SET
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Concentration:0, 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 7.0 μM
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Incubation Time:72 h
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Result:Decreased cell viability in NOK-SI and NOK-SI/SET cells.
Achieved IC50 values of 8.95 μM for NOK-SI and 9.16 μM for NOK-SI/SET.
Western Blot Analysis[1]
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Cell Line:HN12, SCC9
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Concentration:10, 20 μM
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Incubation Time:2, 4, 6 h
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Result:Induced a marked increase of p21 and reduction of pAKT308, pNFκB, and NFκB levels in HN12 cells.
Showed reduction of pNFκB, NFκB, and AKT, a decrease in ERK1/2 levels, and an increase of acetyl histone H3 levels in SCC9 cells.
Decreased PARP (full length) levels and increased LC3 lipidation (LC3-II) in both HN12 and SCC9 cells.
Western Blot Analysis[1]
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Cell Line:NOK-SI, NOK-SI/SET
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Concentration:10, 20 μM
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Incubation Time:2, 4, 6 h
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Result:Decreased the levels of pNFκB, NFκB, pAKT308, SET, and p53, and increased the levels of pERK and acetyl histone H3.
Increased the levels of acetyl-H3 histones at 10 μM, while 20 μM promoted a drastic reduction in these levels.
Reduced PARP (full length) in both cell lines.
Confirmed increased LC3 lipidation (LC3-II).
Observed an increase of LC3-II/LC3-I ratio in NOK-SI/SET cells.
Western Blot Analysis[4]
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Cell Line:MDA-MB-231, HCC38, MDA-MB-436, and MDA-MB-468 cells
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Concentration:1, 2 μM (MDA-MB-231); 0.5, 1 μM (HCC38); 1, 2 μM (MDA-MB-436); 1, 2 μM (MDA-MB-468)
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Incubation Time:4 h
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Result:Decreased pS62-MYC/GAPDH ratios from 1.0 to 0.72 (1 μM) and 0.50 (2 μM) in MDA-MB-231; from 1.0 to 0.64 (0.5 μM) and 0.54 (1 μM) in HCC38; from 1.0 to 0.70 (1 μM) and 0.42 (2 μM) in MDA-MB-436; from 1.0 to 0.60 (1 μM) and 0.39 (2 μM) in MDA-MB-468.
MYC/GAPDH ratios were 1.0, 1.13 (1 μM), and 1.08 (2 μM) in MDA-MB-231; 1.0, 1.05 (0.5 μM), and 1.17 (1 μM) in HCC38; 1.0, 0.78 (1 μM), and 0.56 (2 μM) in MDA-MB-436; 1.0, 0.68 (1 μM), and 0.38 (2 μM) in MDA-MB-468.
In Vivo
Anti-cancerApoptosis
Anti-cancer
Apoptosis
Anti-cancer
COG449 (5 mg/kg; i.p.; once every 3 days) significantly inhibits AML tumor growth in mice, reducing tumor burden by more than 2-fold compared with the vehicle control group[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:NOD/SCID/γ-chain null (NSG) (female, orthotopic xenografts of MDA-MB-231, MDA-MB-436, and MDA-MB-468 cells into the fourth mammary gland)[4]
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Dosage:5 mg/kg
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Administration:i.p.; three times per week; up to 40 days
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Result:Slowed tumor growth in MDA-MB-231, MDA-MB-436, and MDA-MB-468 xenografts compared with controls.
Increased the number of apoptotic cells in MDA-MB-231 tumors as measured by TUNEL assay.
Decreased the number of proliferating cells in MDA-MB-231 tumors as measured by Ki67 staining.
Was specifically detected in the tumors of treated mice.
Significantly increased PP2A activity in treated tumors compared with PBS-treated tumors.
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Animal Model:RAG2−/− γc−/− mice (20 g)[6]
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Dosage:5 mg/kg
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Administration:i.p.; every 3 days; starting 7 days post-implantation
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Result:Inhibited tumor growth measured over time.
Reduced tumor burden by more than 2-fold compared with vehicle-treated controls, with final tumor mass of 0.45 g versus 1.14 g for vehicle.
Related Protocols :
- RT-PCR
- Western Blot
- RNA extraction experimental
- Mammalian live/dead viability and cytotoxicity staining
- Annexin V plus membrane-impermeant dye apoptosis staining
- CCK-8/WST-8 Cell Proliferation Assay
- Breast Cancer Modeling
- Real Time qPCR (Q-PCR)
- Cell Viability Determination by MTT Colorimetric Assay
- Kinase activity and phosphorylation assays
- Detection of Apoptosis
- TUNEL staining for apoptotic DNA fragmentation
- Cell Cytotoxicity Assay
- Autophagy
- Patient-Derived Xenograft (PDX)
- Apoptosis Solutions
- Splenic/Portal-Vein Liver Metastasis Xenograft
- Protocol for Kinase activity and phosphorylation assays
- Lysosome and acidic-vesicle live-cell staining
- MTT Cell Proliferation Assay
- Subcutaneous Cell-Line-Derived Xenograft
- Macroautophagy Solutions
- Orthotopic Cell-Line Xenograft
- Intraperitoneal/Peritoneal Dissemination Xenograft
Chemical Information
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분자량 9223.31
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화학식 C418H712N146O82S4
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SMILES
O=C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCC(N)=O)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CCCCN)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CC1=CNC2=CC=CC=C12)C(N[C@@H](CC3=CC=CC=C3)C(N[C@@H](CCC(N)=O)C(N[C@@H](CC(N)=O)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCSC)C(N[C@@H](CCCCN)C(N[C@@H](CC4=CNC5=CC=CC=C45)C(N[C@@H](CCCCN)C(N[C@@H](CCCCN)C(N[C@@H](CSC(C6=O)CC(N6CCN7C(CC(SC[C@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC(C)=O)CCCNC(N)=N)=O)CCC(N)=O)=O)[C@H](CC)C)=O)CCCCN)=O)[C@H](CC)C)=O)CC8=CNC9=CC=CC=C98)=O)CC%10=CC=CC=C%10)=O)CCC(N)=O)=O)CC(N)=O)=O)CCCNC(N)=N)=O)CCCNC(N)=N)=O)CCSC)=O)CCCCN)=O)CC%11=CNC%12=CC=CC=C%12%11)=O)CCCCN)=O)CCCCN)=O)C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N)=O)CC(C)C)=O)CC(C)C)=O)CCCNC(N)=N)=O)CCCCN)=O)CCCNC(N)=N)=O)CC(C)C)=O)CCCCN)=O)CCCNC(N)=N)=O)CC(C)C)=O)CC%13=CNC=N%13)=O)CO)=O)C)=O)CC(C)C)=O)CCCNC(N)=N)=O)C(C)C)=O)CCCNC(N)=N)=O)CC(C)C)=O)C7=O)=O)=O)C(N[C@@H](CC(C)C)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](C(C)C)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CC(C)C)C(N[C@@H](C)C(N[C@@H](CO)C(N[C@@H](CC%14=CNC=N%14)C(N[C@@H](CC(C)C)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCCN)C(N[C@@H](CC(C)C)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCCN)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CC(C)C)C(N[C@@H](CC(C)C)C(N)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)C
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Synonyms
OP449
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Sequence
Ac-Arg-Gln-Ile-Lys-Ile-Trp-Phe-Gln-Asn-Arg-Arg-Met-Lys-Trp-Lys-Lys-Cys-Leu-Arg-Val-Arg-Leu-Ala-Ser-His-Leu-Arg-Lys-Leu-Arg-Lys-Arg-Leu-Leu-NH2 (BMOE-linked Cys17 dimer)
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Sequence Shortening
Ac-RQIKIWFQNRRMKWKKCLRVRLASHLRKLRKRLL-NH2 (BMOE-linked Cys17 dimer)
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
순도&문서
References
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Calculators
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COG449 Related Classifications
HY-P12219 Related Classifications
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Keywords
- COG449
- OP449
- COG 449
- COG-449
- OP 449
- OP-449
- Phosphatase
- Akt
- ERK
- NF-κB
- c-Myc
- Apoptosis
- Autophagy
- Histone Acetyltransferase
- SET antagonist
- SET-PP2A complex
- chronic myeloid leukemia
- histone H3 hyperacetylation
- T-cell acute lymphoblastic leukemia
- oral squamous cell carcinoma
- apoptosis
- autophagy
- PP2A phosphatase activity
- PP2A activator
- Inhibitor
- inhibitor
- inhibit