SVC112 (0-10 μM, 72 hours) exhibited broad growth inhibitory effects on 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) inhibited the synthesis of new proteins in MV-4-11, NCI-H929, HCT116, FaDu, DLD-1 and SW948 cells [1]. SVC112 (1 μM, 6–24 h) can induce apoptosis in AML and myeloma cell lines (AML-EOL-1, MV-4-11, OCI-AML-3, NCI-H929, RPMI-8226 and U226B1 cells), but has no effect on CRC and HNSCC cell lines (HCT116 and FaDu cells) [1]. The sensitivity of SVC112 (1 μM, 6 h) to different colorectal cancer cell lines (DLD-1 and SW948 cells) varies and is related to c-Myc status [1]. When SVC112 (0.2–0.4 μM) is used in combination with Ulixertinib (1 μM), its growth-inhibiting effect is usually enhanced [1]. SVC112 (5-1000 nM, 2 h) inhibited protein synthesis and proliferation in Det562 and FaDu HNSCC cells and enhanced their radioactive effects [2]. SVC112 (0.1-1000 nM) inhibited cap-independent translation of capless luciferase mRNA in vitro using rabbit reticulocyte lysate (IC50 = 81 nM) [2]. SVC112 (1-10000 nM) showed antiproliferative effects on 036C, 067C, 049C and 013C cells with IC50 values of 3.8 nM, 9.3 nM, 24.1 nM and 50.5 nM, respectively [2]. SVC112 (10-1000 nM, 10 days) reduced the spheroidization ability of 013C, 036C, 049C and 067C head and neck squamous cell carcinoma (HNSCC) cell lines [2]. SVC112 (100 nM, 0–24 h) depletes proteins by affecting translation rather than transcription, and its translational repression is stronger in 013C, 036C, 049C, and 067C HNSCC cell lines than in autologous non-cancer cells [2]. SVC112 (100–1000 nM, 6–48 h) induces reversible protein depletion while having a more durable effect on cancer stem cell (CSC) properties [2]. SVC112 (100–1000 nM, 24 h) exhibits antispheroidization activity in 013C, 036C, 067C, and 049C cells, which can be rescued by exogenous Sox2 expression [2]. SVC112 (100 nM, 12–24 h) enhances the radiation effect by delaying DNA repair in 013C, 036C, 067C, and 049C cells [2].

SVC112 (60 mg/kg, intraperitoneal injection, once daily for 3 weeks) showed efficacy in mouse MV-4-11, AML-EOL-1 and HCT116 cell xenograft models [1]. SVC112 (15 mg/kg, intraperitoneal injection, once daily for 3 weeks) in combination with Ulixertinib inhibited the growth of mouse DLD1 cell xenografts [1]. SVC112 (60 mg/kg, intraperitoneal injection, twice weekly for 28 days) alone or in combination with radiotherapy inhibited tumor growth in CUHN036, CUHN047, CUHN004 and CUHN013 PDX models [2].

Apoptosis analysis [1] Cell Types: MV-4-11, NCI-H929, HCT116 and FaDu cells
Tested Concentrations: 1 μM
Incubation Duration: 6 hours
Experimental Results: Strong apoptosis was induced in MV-4-11 and NCI-H929 cells, but not in HCT116 and FaDu cells.

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Western Blot Analysis [1]
Cell Types: 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
Tested Concentrations: 1 μM
Incubation Duration: 6, 24 hours
Experimental Results: PARP lysis was induced in AML and myeloma cell lines (AML-EOL-1, MV-4-11, OCI-AML-3, NCI-H929, RPMI-8226 and U226B1 cells), accompanied by depletion of MCL-1 and c-Myc, but this phenomenon was not observed in other cell lines. Despite the absence of the unstable proteins MCL-1 and c-Myc, CRC and HNSCC cell lines (HCT116 and FaDu cells) showed little sign of PARP lysis.

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Apoptosis analysis [2]
Cell Types: Det562 and FaDu HNSCC cells
Tested Concentrations: 5, 20, 50, 100, 200, 500, 1000 nM
Incubation Duration: 2 hours
Experimental Results: The expression of Myc and Cyclin D1 was reduced in Det562 and FaDu HNSCC cells.

Animal/Disease Models: 107 MV-4-11 cells/mouse were subcutaneously injected into the right posterior side of BALB/c nude mice (6-8 weeks old females); 5 × 106 MV-4-11 cells/mouse were dissolved in 100 µL PBS and injected into NOG mice (6-8 weeks old females) via the tail vein; 1 × 10⁶ AML-EOL-1, MV-4-11 or 5 × 10⁵ HCT116 cells were mixed with Matrigel at a 1:1 ratio, with a total volume of 100 µL, and subcutaneously injected into the right posterior abdomen of nude mice (nu/nu, 5-8 weeks old females) [1].
Doses: 60 mg/kg, with intraperitoneal injection of QDX5 (five times a week). <
Route of Administration:Intraperitoneal injection, once daily for 3 weeks.
Experimental
Experimental Results:Significant tumor growth control was demonstrated in all three models. Survival was significantly prolonged in mice carrying MV-4-11 and AML-EOL-1 xenografts. No significant changes in body weight were observed.

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Animal/Disease Models:1 × 10⁶ DLD-1 cells were mixed with Matrigel at a 1:1 ratio, with a total volume of 100 µL, and injected subcutaneously into the right posterior abdomen of nu/nu mice (5-8 weeks old females) [1].
Doses: 15 mg/kg in combination with Ulixertinib (50 mg/kg).
Route of Administration: Intraperitoneal injection, once daily for 3 weeks.
Experimental Results: Compared with the vector control group, the combination with Ulixertinib significantly inhibited tumor growth, while monotherapy had no significant effect.

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Animal/Disease Models:Tumor tissue blocks were implanted into the bilateral abdomens of 6- to 10-week-old female athymic nude mice (Foxn1nu) [2].
Doses: 60 mg/kg or combined with radiotherapy (3 Gy).
Route of Administration: Intraperitoneal injection, twice weekly for 28 days.
Experimental Results: Alone, it inhibited the growth of CUHN036 (T/C = 0.45) and CUHN047 (T/C = 0.37). Combined with radiotherapy, it inhibited the growth of CUHN047 (T/C = −0.02), CUHN036 (T/C = 0.08), and CUHN004 (T/C = 0.19). When used in combination with radiotherapy (2 Gy twice a week) and cisplatin (1 mg/kg weekly), FaDu enhanced its inhibitory effect on xenograft tumors. Myc expression in CUHN036 tumors was suppressed, and the combination therapy suppressed Myc expression in both CUHN036 and CUHN047 tumors. The number of cancer stem cells (CSCs) was reduced.

[1]. Sensitivity to an inhibitor of translation elongation in solid and hematologic cancers. Sci Rep. 2025 Jul 1;15(1):21328.

[2]. 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.

C40H47BRN6O9

835.74

Typically exists as solids at room temperature

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

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)