SVC112
SVC112 is a translation elongation inhibitor that prevents the cyclic dissociation of EF2 from the ribosome, thereby inhibiting the elongation step of translation. SVC112 shows activity in growth inhibition among cancer cell lines of various origins (acute myeloid leukemia (AML), multiple myeloma (Myeloma), colorectal cancer (CRC), and head and neck squamous cell carcinoma (HNSCC)). SVC112 preferentially impedes ribosomal processing of mRNAs, and decreaseds CSC-related proteins including Myc and Sox2. SVC112 induces apoptosis in hematologic cancer cell lines, while phosphorylation of c-Myc correlates with sensitivity to SVC112 in colorectal cancer cell lines. SVC112 inactivates HNSCC stem cells in vitro and prevents the regrowth of HNSCC tumor xenografts in mice. SVC112 can be used for the study of HNSCC.
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- Formule: C40H47BrN6O9
- Masse moléculaire:835.74
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
SVC112 (0-10 μM, 72 h) shows a wide range of growth inhibition in different cancer cell lines : acute myeloid leukemia (AML-BDL-1, MV-4-11, HL-60 and MOLM-13 cells) (IC50 < 0.1 μM), (THP-1, NOMO-1, MONO-MAC-6 and U-937 cells) (IC50 = 0.1-0.5 μM), (Kasumi-3 and KG-1a cells) (IC50 > 1 μM); multiple myeloma (NCI-H929, L-363, RPMI-8226, OPM-2, U266, MM.15 and MM.1R cells) (IC50 < 0.1 μM), (LP-1 cells) (IC50 = 0.1-0.5 μM); colorectal Cancer (SW48, RKO, HCT116, WiDr and CL-34 cells) (IC50 < 0.1 μM), (HT29, MDST8, COLO201, GP2D, NCI-H747, SNU70, SW837 and SW403 cells) (IC50 = 0.1-0.5 μM), (DLD-1, T84, KM-12C, SW948, Q-11,HCT-15 and SW48 cells) (IC50 > 1 μM);head and neck squamous cell carcinoma (FaDu) (IC50 < 0.1 μM)[1]. SVC112 (1 μM, 2 h) inhibits de novo protein synthesis in MV-4-11, NCI-H929, HCT116, FaDu, DLD-1 and SW948 cells[1]. SVC112 (1 μM, 6-24 h) induces apoptosis in AML and Myeloma cell lines (AML-EOL-1, MV-4-11, OCI-AML-3, NCI-H929, RPMI-8226 and U226B1 cells), but not in CRC and HNSCC cell lines (HCT116 and FaDu cells)[1]. SVC112 (1 μM, 6h) exhibits differential sensitivity across colorectal cancer cell lines (DLD-1 and SW948 cells) that correlates with c-Myc status[1]. SVC112 (0.2-0.4 μM) exhibits generally enhanced growth inhibitory effects with the addition of Ulixertinib (HY-15816) (1 μM)[1]. SVC112 (5-1000 nM, 2 h) inhibits protein synthesis, proliferation, and enhances radiation effects in Det562 and FaDu HNSCC cells[2]. SVC112 (0.1-1000 nM) inhibits in vitro cap-independent translation of capless luciferase mRNA using rabbit reticulocyte lysates (IC50 = 81 nM)[2]. SVC112 (1-10000 nM) shows antiproliferative effects in 036C, 067C, 049C, and 013C，with IC50s of 3.8nM, 9.3 nM, 24.1 nM, and 50.5 nM, respectively[2]. SVC112 (10-1000 nM, 10 days) decreases sphere formation by 013C, 036C, 049C and 067C HNSCC cell lines[2]. SVC112 (100 nM, 0-24 h) depletes proteins by influencing translation but not transcription and inhibits translation more potently in 013C, 036C, 049C and 067C HNSCC cell lines than autologous non-cancer cells[2]. SVC112 (100-1000 nM, 6-48 h) induces reversible protein depletion while exerting longer-lasting effects on cancer stem cell (CSC) properties[2]. SVC112 (100-1000 nM, 24 h) shows anti-sphering effects in 013C, 036C, 067C and 049C cells which are rescued by exogenous Sox2 expression[2]. SVC112 (100 nM, 12-24 h) enhances the effects of radiation by delaying DNA repair in 013C, 036C, 067C and 049C cells[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:MV-4-11, NCI-H929, HCT116 and FaDu cells
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Concentration:1 μM
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Incubation Time:6 h
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Result:Induced robust apoptosis in MV-4-11and NCI-H929 cells, but not in HCT116 and FaDu cells.
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Cell Line:AML-EOL-1, MV-4-11, MOLM-13, OCI-AML-3, NCI-H929, RPMI-8226, U226B1, THP-1, NOMO-1, Kasumi-3, HCT116 and FaDu cells
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Concentration:1 μM
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Incubation Time:6, 24 h
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Result:Induced PARP cleavage concomitantly with depletion of MCL-1 and c-Myc in AML and Myeloma cell lines (AML-EOL-1, MV-4-11, OCI-AML-3, NCI-H929, RPMI-8226 and U226B1 cells), but not in CRC and HNSCC cell lines (HCT116 and FaDu cells).
Showed little sign of PARP cleavage despite loss of the unstable proteins MCL-1 and c-Myc.
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Cell Line:Det562 and FaDu HNSCC cells
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Concentration:5, 20, 50, 100, 200, 500, 1000 nM
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Incubation Time:2 h
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Result:Depleted Myc and Cyclin D1 in Det562 and FaDu HNSCC cells.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:107 MV-4-11 cells per mouse were inoculated by subcutaneous injection into the right hind flank of BALB/c nude mice (6-8 weeks old females); 5 × 106 MV-4-11 cells per mouse in 100 µL PBS were inoculated into the tail vein of NOG mice (6-8 weeks old females); 1 × 106 AML-EOL-1, MV-4-11 or 5×105 HCT116 cells per mouse mixed 1:1 with Matrigel in 100 µL total volume were inoculated by subcutaneous injection into the right hind flank of nu/nu mice (5-8 weeks old females)[1]
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Dosage:60 mg/kg with QDX5 (i.p. five times weekly)
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Administration:i.p., once daily for 3 weeks
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Result:Showed significant tumor growth control in all three models.
Provided significant survival benefit in mice bearing MV-4-11 and AML-EOL-1 xenografts.
Showed no significant changes in body weight.
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Animal Model:1 × 106 DLD-1 cells per mouse mixed 1:1 with Matrigel in 100 µL total volume were inoculated by subcutaneous injection into the right hind flank of nu/nu mice (5-8 weeks old females)[1]
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Dosage:15 mg/kg combined with Ulixertinib (50 mg/kg)
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Administration:i.p., once daily for 3 weeks
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Result:Reduced tumor growth significantly compared to vehicle controls when combined with Ulixertinib whereas the single drug treatments had no significant effects.
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Animal Model:Tumor pieces were implanted on both flanks of 6 to 10-week-old female Athymic Nude-Foxn1nu mice[2]
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Dosage:60 mg/kg or combined with radiation (3Gy)
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Administration:i.p. twice weekly for 28 days
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Result:Suppressed growth in CUHN036 (T/C = 0.45) and CUHN047 (T/C = 0.37) alone.
Inhibited growth in CUHN047 (T/C = −0.02), CUHN036 (T/C = 0.08), and CUHN004 (T/C = 0.19) when combined with radiation.
Increased inhibition of FaDu xenografts when combined with radiation (2Gy twice weekly) and Cisplatin (HY-17394) (1mg/kg weekly).
Suppressed Myc in CUHN036 and combination treatment suppressed Myc in CUHN036 and CUHN047 tumors.
Decreased CSC number.
Chemical Information
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Masse moléculaire 835.74
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Formule C40H47BrN6O9
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SMILES
COC1=CC=C(C=C1)C[C@@H](N(C)C([C@@H](C)NC([C@H](C)NC([C@H](CC2=CC(OC3=CC=C(C4)C=C3)=C(OC)C=C2Br)N5)=O)=O)=O)C(N[C@H](C)C(N(C)[C@@H]4C5=O)=O)=O
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
[1]. Gomes N, et al. Sensitivity to an inhibitor of translation elongation in solid and hematologic cancers. Sci Rep. 2025 Jul 1;15(1):21328. [Content Brief]
[2]. Keysar SB, et al. Inhibiting Translation Elongation with SVC112 Suppresses Cancer Stem Cells and Inhibits Growth in Head and Neck Squamous Carcinoma. Cancer Res. 2020 Mar 1;80(5):1183-1198. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
SVC112 Related Classifications
HY-175164 Related Classifications
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