| Field | Specification |
|---|---|
| Target | |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C40H66N2O9 |
| SMILES | |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
E7107 inhibits the pre-mRNA spliceosome and induces apoptosis. It binds spliceosome-associated protein 130, blocking spliceosome assembly and pre-mRNA splicing, and this alters cellular protein expression, triggers G1 and G2/M phase cell cycle arrest, causes DNA damage, changes R-loop levels, lowers CHEK2 expression, hampers transcriptional elongation, and redirects MCL1 splicing toward pro-apoptotic isoforms. In xenograft models, it slows tumor growth and lowers leukemia burden, and it can be used in research on T-cell acute lymphoblastic leukemia, triple-negative breast cancer, acute myeloid leukemia, and advanced solid tumors[1][2][3][4]. It has the molecular formula C40H66N2O9 and a molecular weight of 718.97 g/mol.
Physical & Chemical Properties
| CAS Number | 630100-90-2 |
|---|---|
| Molecular Formula | C40H66N2O9 |
| Molecular Weight | 718.97 g/mol |
| 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] |
| Target | MCL1 |
| Signaling Pathway | Cell Cycle/DNA Damage; Apoptosis |
| Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with your institution's chemical hygiene plan.
In Vitro
E7107 (1-20 nM) suppresses the in vitro growth of unspecified tumor cell lines, drug-resistant lines included, at nanomolar potency spanning 1 to 20 nM[1]. In K052 cells, E7107 (0.1-5 nM) blocks SRSF2 mutant-specific aberrant splicing of EZH2 in a dose-dependent manner[2]. E7107 (0.05 nM-10 μM; 48 h) modulates the viability of K052 and TF-1 leukemia cells[2]. At 100 nM for 4-24 h, E7107 triggers intron retention in specific transcripts, alters expression of splicing variants tied to immune response, ribosomal function and mitosis, and moves MCL1 splicing toward pro-apoptotic isoforms[4]. E7107 (24 h) decreases viability of the basal A-type triple-negative breast cancer (TNBC) lines BT20, HCC70, MB468, HCC1143, HCC1954, and HCC1187, and drives apoptosis through activation of PARP1 and caspase-3[4].
Cell Viability Assay[2]
| Cell Line | human leukemia cell lines (SRSF2-mutant K052 and SRSF2-wildtype TF-1) |
|---|---|
| Concentration | 0.05 nM, 10 μM |
| Incubation Time | 48 h |
| Result | Alters cell viability in human K052 and TF-1 leukemia cells. |
RT-PCR[4]
| Cell Line | human basal-A triple-negative breast cancer MB468 cells |
|---|---|
| Concentration | 100 nM |
| Incubation Time | 4 h, 24 h |
| 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
Mice bearing acute myeloid leukemia (AML) driven by Srsf2-mutant MLL-AF9 show a lower disease burden and better survival after E7107 (4 mg/kg; intravenous injection; once daily; for 10 consecutive days). Moreover, splicing inhibition is stronger in the mutant leukemia than in wild-type leukemia, and aberrant splicing of target genes is more prominent[2]. A CUTLL1 xenograft model of T-cell acute lymphoblastic leukemia shows reduced leukemia burden, improved survival outcomes, and extremely low toxicity after E7107 (5 mg/kg; intravenous injection; daily; 8 total administrations)[3]. Leukemia burden, assessed by spleen size and weight, is reduced in NOTCH1-ΔE-Cherry+ T-cell acute lymphoblastic leukemia xenograft models given E7107 (5 mg/kg; intravenous injection; daily; 8 total administrations)[3]. E7107 (5 mg/kg; intravenous injection; once daily) restrains xenograft growth of HCC1187 cells (basal subtype A triple-negative breast cancer, TNBC) in NU/J nude mice, lowering the average tumor volume by 80% after 22 days of treatment[4]. In primary AML-derived xenografts with spliceosome mutations, leukemia burden is preferentially reduced and apoptosis is induced by E7107 (4 mg/kg; intravenous injection; once daily; for 10 consecutive days), relative to wild-type controls[2]. In stable bone marrow chimeras, E7107 (4 mg/kg; once daily; for 5 consecutive days) elicits responses in gene expression and splicing that differ between Srsf2G12C-mutant hematopoietic cells and wild-type hematopoietic cells[2].
| Animal Model | C57BL/6 (CD45.1 recipient, sub-lethally irradiated; donor cells from Vav-Cre+ Srsf2P95H/+ or Vav-Cre+ Srsf2+/+)[2] |
|---|---|
| Dosage | 4 mg/kg |
| Administration | i.v.; daily; 10 consecutive days |
| 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. |
| Animal Model | NOD-scid IL2rnull (NSG) (6-week-old, gamma-irradiated 200 cGy)[2] |
|---|---|
| Dosage | 4 mg/kg |
| Administration | i.v.; daily; 10 consecutive days |
| 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. |
| Animal Model | NOD.Cg-Prkdcscid (8-week-old female; T-cell acute lymphoblastic leukemia luciferase-expressing CUTLL1 cell tail vein xenograft)[3] |
|---|---|
| Dosage | 5 mg/kg |
| Administration | i.v.; daily; 8 total doses (5 consecutive days, 2-day rest, 3 consecutive days) |
| 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. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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