E7107
E7107 is a pre-mRNA spliceosome inhibitor and apoptosis (Apoptosis) inducer. E7107 binds to spliceosome-associated protein 130, inhibits spliceosome assembly and pre-mRNA splicing, regulates cellular protein expression, induces G1 and G2/M phase cell cycle arrest, triggers DNA damage, alters R-loop levels, reduces CHEK2 expression, impairs transcriptional elongation, and shifts MCL1 splicing toward pro-apoptotic isoforms. E7107 inhibits tumor growth in xenograft models and reduces leukemia burden. E7107 can be used in the research of advanced solid tumors, acute myeloid leukemia, T-cell acute lymphoblastic leukemia, and triple-negative breast cancer.
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- CAS. Nr.: 630100-90-2
- Formel: C40H66N2O9
- Molecular Weight:718.97
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
Beschreibung
IC50 & Target
[1]|
MCL1 |
In Vitro
E7107 (1-20 nM) inhibits the growth of unspecified tumor cell lines (including drug-resistant cell lines) in vitro with nanomolar potency ranging from 1 to 20 nM[1].
E7107 (0.1-5 nM) inhibits SRSF2 mutant-specific aberrant splicing of EZH2 in K052 cells in a dose-dependent manner[2].
E7107 (0.05 nM-10 μM; 48 h) regulates the viability of K052 and TF-1 leukemia cells[2].
E7107 (100 nM; 4-24 h) induces intron retention in specific transcripts, regulates the expression of splicing variants associated with immune response, ribosomal function and mitosis, and shifts MCL1 splicing toward pro-apoptotic isoforms[4].
E7107 (24 h) reduces the cell viability of basal A-type triple-negative breast cancer (TNBC) cell lines (BT20, HCC70, MB468, HCC1143, HCC1954, HCC1187) and induces apoptosis by activating PARP1 and caspase-3[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human leukemia cell lines (SRSF2-mutant K052 and SRSF2-wildtype TF-1)
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Concentration:0.05 nM, 10 μM
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Incubation Time:48 h
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Result:Alters cell viability in human K052 and TF-1 leukemia cells.
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Cell Line:human basal-A triple-negative breast cancer MB468 cells
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Concentration:100 nM
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Incubation Time:4 h, 24 h
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Result:Caused marked intronic retention, shown by accumulation of unspliced transcripts of DNAJB1, BRD2, and RIOK3 after 4 h and 24 h.
Activated the protein-coding isoform of CXCL8, induced intron-retaining transcripts of ribosomal proteins RPS7, RPS24, and RPS29, and suppressed protein-coding variants of E2F1, SPC24, and B9D2 transcripts after 24 h.
Altered MCL1 splicing to favor the proapoptotic splice variant in MB468 cells.
In Vivo
E7107 (5 mg/kg; intravenous injection; daily; 8 total administrations) reduces leukemia burden, improves survival outcomes, and exhibits extremely low toxicity in a CUTLL1 xenograft model of T-cell acute lymphoblastic leukemia[3].
E7107 (5 mg/kg; intravenous injection; daily; 8 total administrations) reduces leukemia burden (assessed by spleen size and weight) in NOTCH1-ΔE-Cherry+ T-cell acute lymphoblastic leukemia xenograft models[3].
E7107 (5 mg/kg; intravenous injection; once daily) inhibits the growth of HCC1187 basal subtype A triple-negative breast cancer (TNBC) xenografts in NU/J nude mice, reducing the average tumor volume by 80% after 22 days of treatment[4].
Compared with wild-type controls, E7107 (4 mg/kg; intravenous injection; once daily; for 10 consecutive days) preferentially reduces the leukemia burden and induces apoptosis in primary AML-derived xenografts with spliceosome mutations[2].
E7107 (4 mg/kg; once daily; for 5 consecutive days) induces differential gene expression and splicing responses between Srsf2G12C-mutant and wild-type hematopoietic cells in stable bone marrow chimeras[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (CD45.1 recipient, sub-lethally irradiated; donor cells from Vav-Cre+ Srsf2P95H/+ or Vav-Cre+ Srsf2+/+)[2]
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Dosage:4 mg/kg
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Administration:i.v.; daily; 10 consecutive days
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Result:Decreased disease burden assessed by peripheral blood leukocyte count, GFP percentage, and histological analyses.
Extended survival in Srsf2P95H/+ mice.
Improved anemia and thrombocytopenia in both Srsf2+/+ and Srsf2P95H/+ mice, with slightly greater improvement in Srsf2P95H/+ mice.
Induced more severe widespread intron retention and cassette exon skipping in Srsf2P95H/+ versus Srsf2+/+ mice.
Triggered more pronounced exon skipping and intron retention within the catalytic domain of Dot1l and within Meis1 in Srsf2P95H/+ leukemic cells relative to Srsf2+/+ cells, correlating with reduced Dot1l catalytic activity and mild decreases in Meis1 protein.
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Animal Model:NOD-scid IL2rnull (NSG) (6-week-old, gamma-irradiated 200 cGy)[2]
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Dosage:4 mg/kg
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Administration:i.v.; daily; 10 consecutive days
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Result:Reduced human leukemic burden significantly in all spliceosome-mutant AML patient-derived xenografts, with less robust responses in spliceosome-wildtype AMLs.
Decreased hCD45+ hCD34+ hematopoietic stem/progenitor subsets significantly in two of three spliceosome-mutant AMLs, while spliceosome-wildtype AMLs showed less substantial reductions in leukemic cells and hCD45+ hCD34+ subsets.
Induced substantially increased apoptosis only in spliceosome-mutant PDX samples, despite reducing cell proliferation regardless of mutational status.
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Animal Model:NOD.Cg-Prkdcscid (8-week-old female; T-cell acute lymphoblastic leukemia luciferase-expressing CUTLL1 cell tail vein xenograft)[3]
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Dosage:5 mg/kg
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Administration:i.v.; daily; 8 total doses (5 consecutive days, 2-day rest, 3 consecutive days)
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Result:Reduced leukemic burden (measured by fold change in luciferase radiance between days 10 and 20).
Prolonged mouse survival compared to vehicle control.
Showed no significant toxicity in body weight, organ weight, blood populations, or gastrointestinal tissues.
Chemical Information
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CAS. Nr. 630100-90-2
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Molecular Weight 718.97
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Formel C40H66N2O9
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SMILES
[C@H]([C@H](CC)O)(C)[C@@]1([C@@H](C[C@@](/C=C/C=C(\C)/[C@@H]2[C@@H](C)/C=C/[C@H](OC(=O)N3CCN(CC3)C4CCCCCC4)[C@](C)(O)CC[C@@H](O)CC(=O)O2)(C)O)O1)[H]
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
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Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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