2. MAPK/ERK Pathway Cell Cycle/DNA Damage Immunology/Inflammation
  3. MNK DNA/RNA Synthesis Interleukin Related Eukaryotic Initiation Factor (eIF)
  4. ETC-501

ETC-501 is a blood-brain barrier-permeable, orally active, and selective MNK1/MNK2 inhibitor, with an IC50 of 0.033 μM against MNK1 and 0.111 μM against MNK2. ETC-501 inhibits glioblastoma cell proliferation, impairs DNA damage repair function, delays cell cycle progression, and suppresses ribosome biogenesis. ETC-501 enhances Temozolomide (HY-17364)-induced cellular senescence, attenuates the senescence-associated secretory phenotype, and increases cellular sensitivity to Navitoclax (HY-10087). ETC-501 is applicable to research related to glioblastoma.

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ETC-501

ETC-501 Chemical Structure

CAS No. : 3094990-88-9

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ETC-501 Related Antibodies

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Description

ETC-501 is a blood-brain barrier-permeable, orally active, and selective MNK1/MNK2 inhibitor, with an IC50 of 0.033 μM against MNK1 and 0.111 μM against MNK2. ETC-501 inhibits glioblastoma cell proliferation, impairs DNA damage repair function, delays cell cycle progression, and suppresses ribosome biogenesis. ETC-501 enhances Temozolomide (HY-17364)-induced cellular senescence, attenuates the senescence-associated secretory phenotype, and increases cellular sensitivity to Navitoclax (HY-10087). ETC-501 is applicable to research related to glioblastoma[1].

In Vitro

ETC-501 (0-20 μM; 24 h) dose-dependently inhibits eIF4E phosphorylation and reduces Cyclin D1 protein levels in LN-229 and T98G glioblastoma cells[1].
ETC-501 (0-10 μM) inhibits the viability of LN-229 and T98G glioblastoma cells with GI50 values of 4.035 μM and 6.122 μM, respectively, and reduces the tumor sphere-forming capacity and stem cell frequency of patient-derived GPCs[1].
ETC-501 (0-10 μM; 4 h) impairs DNA synthesis in LN-229, T98G and U-87MG glioblastoma cells in a dose-dependent manner[1].
ETC-501 (8 h) impairs G1-to-S phase progression in Palbociclib (HY-50767)-synchronized LN-229 and U-87MG glioblastoma cells[1].
ETC-501 (5-10 μM; 14 days) induces cellular senescence in LN-229 and U-87MG glioblastoma cells[1].
ETC-501 (5-10 μM; 10 days) reduces the levels of key inflammatory cytokines and chemokines, including IL-6, IL-8 and CCL2[1].
ETC-501 (10 μM; 6 days) and TMZ (HY-17364) drives LN-229 glioblastoma cells into a senescence priming state, and significantly enhances their sensitivity to Navitoclax (HY-10087)-induced cell death and apoptosis[1].

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

ETC-501 Related Antibodies

Western Blot Analysis[1]

Cell Line: LN-229, T98G (human glioblastoma cell lines)
Concentration: 0, 0.1. 1, 2.5, 5, 10 and 20 μM
Incubation Time: 24 h
Result: Caused a dose-dependent reduction in phosphorylation of eIF4E without altering total eIF4E protein levels.
Reduced Cyclin D1 protein levels.
Parmacokinetics
Species Dose Route AUC T1/2
Mice[1] 10 mg/kg p.o. 4.51 h 3.84 h
In Vivo

ETC-501 (100 mg/kg; oral gavage; once daily; 21 days) enhances tumor cell senescence and attenuates the senescence-associated secretory phenotype when combined with TMZ (HY-17364) in NSG mice bearing orthotopic or subcutaneous glioblastoma, and the additional combination with Navitoclax (HY-10087) effectively eliminates senescent cells[1].

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

Animal Model: NOD-SCID gamma (NSG, NOD.Cg-PrkdcscidIl2rgtm1wjl/SzJ) (6-8-week-old male; subcutaneous glioblastoma model)[1]
Dosage: 100 mg/kg
Administration: oral gavage; daily; 21 days
Result: Reduced excised tumor p-eIF4E levels by ~50%.
Induced senescent tumor cells (SA-β-gal positive) when combined with TMZ, with non-statistically significant trend toward higher SA-β-gal and p21 levels compared to TMZ alone.
Resulted in widespread tumor necrosis, near absence of SA-β-gal-positive cells, and markedly reduced p21 expression when combined with TMZ and navitoclax.
Animal Model: NOD-SCID gamma (NSG, NOD.Cg-PrkdcscidIl2rgtm1wjl/SzJ) (6-8-week-old male; orthotopic intracranial glioblastoma model)[1]
Dosage: 100 mg/kg
Administration: oral gavage; daily; 21 days
Result: Reduced p-eIF4E levels in contralateral and ipsilateral brain tissue by ~60%.
Did not significantly extend survival compared to vehicle control when administered alone.
Showed non-statistically significant trend toward improved survival compared to TMZ alone, and induced senescence (SA-β-gal positive) in orthotopic tumors when combined with TMZ.
Did not improve survival beyond TMZ alone when combined with TMZ and navitoclax, with residual SA-β-gal-positive senescent cells detected post-treatment.
Molecular Weight

452.51

Formula

C26H24N6O2
CAS No.
SMILES

O=C(C1=CC=C(C2=NC3=C(C#CC4=CC=NC(N(C)C)=C4)C=NN3C=C2)C=C1)N5CCOCC5
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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ETC-501 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:

ETC-5013094990-88-9ETC501ETC 501MNKDNA/RNA SynthesisInterleukin RelatedEukaryotic Initiation Factor (eIF)Mitogen activated protein kinase interacting kinaseMAP kinase interacting kinaseMAPK interacting kinaseILMNK2ribosome biogenesistemozolomidecell cycle regulationMNK1glioblastoma cellsDNA damage repairMYC signalinginflammationDNA replicationInhibitorinhibitorinhibit

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