MYCMI-7 hydrobromide
MYCMI-7 hydrobromide is a potent and selective MYC/MYCN inhibitor, with a Kd of 4 μM for MYC and an IC50 of 10 μM for topoisomerase IIα (Topoisomerase IIα). MYCMI-7 hydrobromide binds directly to MYC, selectively inhibits the interactions of MYC:MAX and MYCN:MAX, reduces MYC-driven transcription levels, induces MYC/MYCN protein degradation, and blocks the binding of MYC to chromatin, thereby inducing tumor cell growth arrest, apoptosis and reducing cell viability, while only inducing G1 phase growth arrest in normal cells. MYCMI-7 hydrobromide can be used in research related to MYC-driven acute myeloid leukemia and breast cancer, MYCN-amplified neuroblastoma, glioblastoma, Burkitt's lymphoma, melanoma, colon cancer, osteosarcoma, cervical cancer and histiocytic lymphoma.
For research use only. We do not sell to patients.
- CAS No.: 102537-38-2
- Formula: C23H28N3·1/2HBr·Br
- Molecular Weight:466.84
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Biological Activity
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topoisomerase II alpha 10 μM (IC50) |
MYC 4 μM (Kd) |
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Cell Line
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Type | Value | Description | References |
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| MDA-MB-231 | GI50 |
5.800 μM
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Antiproliferative activity against human MDA-MB-231 breast cancer cells transfected with control siRNA assessed as reduction in cell viability incubated for unspecified time by resazurin assay.
Antiproliferative activity against human MDA-MB-231 breast cancer cells transfected with control siRNA assessed as reduction in cell viability incubated for unspecified time by resazurin assay.
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36874405 |
| MDA-MB-231 | GI50 |
5.763 μM
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Antiproliferative activity against human MDA-MB-231 breast cancer cells transfected with Top2α-targeting siTOP2A-1 assessed as reduction in cell viability incubated for unspecified time by resazurin assay.
Antiproliferative activity against human MDA-MB-231 breast cancer cells transfected with Top2α-targeting siTOP2A-1 assessed as reduction in cell viability incubated for unspecified time by resazurin assay.
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36874405 |
| MDA-MB-231 | GI50 |
5.803 μM
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Antiproliferative activity against human MDA-MB-231 breast cancer cells transfected with Top2α-targeting siTOP2A-2 assessed as reduction in cell viability incubated for unspecified time by resazurin assay.
Antiproliferative activity against human MDA-MB-231 breast cancer cells transfected with Top2α-targeting siTOP2A-2 assessed as reduction in cell viability incubated for unspecified time by resazurin assay.
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36874405 |
| MDA-MB-231 | GI50 |
5.491 μM
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Antiproliferative activity against untreated human MDA-MB-231 breast cancer cells assessed as reduction in cell viability incubated for unspecified time by resazurin assay.
Antiproliferative activity against untreated human MDA-MB-231 breast cancer cells assessed as reduction in cell viability incubated for unspecified time by resazurin assay.
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36874405 |
MYCMI-7 hydrobromide (0.5-10 μM; 72 h) induces growth arrest in normal human skin fibroblasts without reducing cell viability[1].
MYCMI-7 hydrobromide (1-100 μM; 10 min) potently inhibits the decatenation activity of recombinant human Top2α in cell-free assays[1].
MYCMI-7 hydrobromide (5 μM; 6 h) blocks the binding of MYC to the promoter of the ODC1 target gene in U-937 cells[1].
MYCMI-7 (1-6 h) hydrobromide reduces the formation of MYC:MAX complex and the expression of MYC protein in MCF7 cells in a time-dependent manner[1].
MYCMI-7 hydrobromide (5 μM; 17 h) downregulates the protein expression of MYC, MYCN, phosphorylated MYC, and MAX in MCF7, HeLa, Kelly, P493-6, HCT116, and neuroblastoma cell lines, and reduces the steady-state levels of wild-type and mutant MYC in U2OS cells[1].
MYCMI-7 (10-30 μM; 96 h) hydrobromide reduces the growth of H015.19 Rat1 fibroblasts in a concentration-dependent manner[1].
MYCMI-7 (0.1-6.25 μM; 2 h-2 weeks) hydrobromide inhibits anchorage-independent growth of SK-N-DZ MYCN-amplified neuroblastoma cells, potently reduces the growth capacity of MYC-translocated Daudi, Raji and Mutu Burkitt lymphoma cells after 24 hours, and strongly decreases anchorage-independent colony formation of MYC+HRAS-transformed primary REF[1].
MYCMI-7 hydrobromide reduces the growth of MDA-MB-231 cells with a GI50 of approximately 5.5-5.8 μM, and knockdown of Top2α does not alter the sensitivity of cells to MYCMI-7[1].
MYCMI-7 (0.5-12 μM; 72 h) hydrobromide potently inhibits the growth/activity of AML cells driven by MYC/BCL-XL, and suppresses the growth of MDA-MB-231 breast cancer cells in a concentration-dependent manner[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:MCF7, HeLa, P493-6, HCT116, Kelly, SK-N-DZ, CHP212, SK-N-AS, U2OS human cancer and fibroblast cell lines
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Concentration:5 μM
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Incubation Time:17 h; overnight (U2OS cells, post-24 h transfection)
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Result:Reduced MYC protein expression in MCF7, HeLa, P493-6, wild-type HCT116, and FBW7-/- HCT116 cells.
Reduced MYCN protein expression in Kelly neuroblastoma cells.
Reduced phosphorylated MYC and total MYC expression in FBW7-/- HCT116 cells to ~75% of DMSO control levels.
Reduced steady-state levels of wild-type and T58A/S62A mutant MYC in U2OS cells.
Reduced MAX protein expression in Kelly, SK-N-DZ, CHP212, and SK-N-AS neuroblastoma cells.
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Cell Line:H015.19 Rat1 fibroblasts (MYC-proficient)
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Concentration:10, 20, 30 μM
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Incubation Time:96 h
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Result:Reduced cell growth/viability to ~90% at 10 μM, ~45% at 20 μM, and ~25% at 30 μM relative to DMSO control.
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Cell Line:Daudi, Raji, and Mutu Burkitt's lymphoma cells (MYC-translocated)
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Concentration:6.25 μM
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Incubation Time:24 h
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Result:Reduced cell growth/viability to ~18% in Daudi cells, ~25% in Raji cells, and ~18% in Mutu cells relative to DMSO control.
All reductions showed statistically significant differences (p<0.01 to p<0.05).
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Cell Line:MYC/BCL-XL-driven acute myeloid leukemia (AML) cells
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Concentration:0, 0.5, 1, 2, 3, 4, 5, 6, 7, 8 μM
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Incubation Time:72 h
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Result:Reduced cell growth/viability in a concentration-dependent manner.
Achieved complete inhibition at concentrations ≥3 μM.
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Cell Line:MDA-MB-231 human breast cancer cells
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Concentration:0, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12 μM
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Incubation Time:72 h
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Result:Reduced cell growth/viability in a concentration-dependent manner.
Achieved near-complete inhibition at 10 μM.
MYCMI-7 (6.25 mg/kg; i.t.; twice weekly; 26 days) hydrobromid einhibits the growth of MDA-MB-231 breast cancer xenografts, reduces MYC expression levels, induces cell apoptosis, and significantly improves the survival rate of mice[1].
MYCMI-7 (6.25 mg/kg; i.t.; twice weekly; 20 days) hydrobromide inhibits the growth of MYCN-amplified SK-N-DZ neuroblastoma xenografts, reduces MYCN expression, and significantly improves the survival rate of mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL mice (sublethally irradiated)[1]
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Dosage:12.5 mg/kg
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Administration:i.p.; once daily; 15 days
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Result:Reduced GFP+ leukemic cells in bone marrow from ~4% to undetectable levels at day 15.
Reduced GFP+ leukemic cells in bone marrow from ~40% to ~10% at endpoint.
Significantly reduced MYC expression in leukemic spleen cells.
Increased cleaved caspase-3 and H3K9me3 expression in leukemic spleens.
Showed no significant difference in overall survival between groups.
Retained body weight with no severe side effects.
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Animal Model:NOD/SCID mice (6-8 weeks old)[1]
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Dosage:6.25 mg/kg
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Administration:i.t.; twice weekly; 26 days
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Result:Significantly slowed tumor growth, with a significant difference in tumor volume observed at day 11.
Significantly increased mouse survival.
Induced extensive necrosis/apoptosis in tumor tissue.
Reduced MYC expression in tumor tissue.
Increased cleaved caspase-3 and TUNEL staining in tumor tissue.
Reduced Ki67 staining (proliferation) in tumor tissue.
Reduced CD31 staining (microvascular density) in tumor tissue.
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Animal Model:NMRI nu/nu mice (6-8 weeks old)[1]
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Dosage:6.25 mg/kg
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Administration:i.t.; twice weekly; 30 days
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Result:Reduced tumor growth, with a significant difference in tumor volume observed at day 7.
Significantly increased mouse survival.
Induced massive apoptosis/necrosis and hemorrhage in tumor tissue.
Strongly reduced MYCN expression in tumor tissue.
Chemical Information
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CAS No. 102537-38-2
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Molecular Weight 466.84
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Formula C23H28N3·1/2HBr·Br
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SMILES
CC1=C(C2=C(C)C3=C1C=C[N+](CCN(CC)CC)=C3)NC4=C2C=CC=C4.[Br-].Br.[1/2]
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
MYCMI-7 hydrobromide Related Classifications
HY-187521 Related Classifications
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