2. Cell Cycle/DNA Damage Cytoskeleton Apoptosis
  3. Microtubule/Tubulin Apoptosis Caspase
  4. SMU-G4

SMU-G4 is a Tubulin polymerization inhibitor. SMU-G4 induces G2/M phase cell cycle arrest, triggers Apoptosis, and upregulates the expression of Cleaved-Caspase 3. SMU-G4 exhibits in vivo anti-tumor activity in melanoma xenograft models. SMU-G4 can be used for research related to melanoma.

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SMU-G4

SMU-G4 Chemical Structure

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SMU-G4 Related Antibodies

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Description

SMU-G4 is a Tubulin polymerization inhibitor. SMU-G4 induces G2/M phase cell cycle arrest, triggers Apoptosis, and upregulates the expression of Cleaved-Caspase 3. SMU-G4 exhibits in vivo anti-tumor activity in melanoma xenograft models. SMU-G4 can be used for research related to melanoma[1].

IC50 & Target[1]

Caspase-3

 

In Vitro

SMU-G4 (multiple concentrations; 48 h) potently inhibits the proliferation of B16-F10, A549, and HepG2 cancer cells with IC50 values of 4 nM, 1.5 nM, and 44.8 nM, respectively[1].
SMU-G4 (1.5-3 μM) potently inhibits in vitro tubulin polymerization in a concentration-dependent manner, with near-complete suppression at 3 μM[1].
SMU-G4 (6.25-25 nM; 6 h) dose-dependently disrupts the microtubule network in HepG2 cells after 6 h of treatment[1].
SMU-G4 (6.25-12.5 nM; 24 h) induces concentration-dependent G2/M phase cell cycle arrest in B16-F10 cells, with 61.46% of cells in G2/M phase after 24 h treatment with 12.5 nM[1].
SMU-G4 (6.25-12.5 nM; 24 h) induces concentration-dependent apoptosis in B16-F10 cells, with 18.90% of cells apoptotic after 24 h treatment with 12.5 nM[1].
SMU-G4 (1-12 nM; 24 h) dose-dependently increases Cleaved-Caspase 3 expression in B16-F10 cells after 24 h of treatment[1].
SMU-G4 (6.25-25 nM; 24 h) dose-dependently inhibits B16-F10 cell migration, achieving a 70.78% inhibition rate after 24 h treatment with 25 nM[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

SMU-G4 Related Antibodies

Cell Proliferation Assay[1]

Cell Line: B16-F10 mouse melanoma cells, A549 human non-small cell lung cancer cells, HepG2 human hepatocellular carcinoma cells
Concentration: multiple concentrations
Incubation Time: 48 h
Result: Potently inhibited proliferation of B16-F10 cells with an IC50 of 4 nM.
Potently inhibited proliferation of A549 cells with an IC50 of 1.5 nM.
Potently inhibited proliferation of HepG2 cells with an IC50 of 44.8 nM.

Immunofluorescence[1]

Cell Line: HepG2 human hepatocellular carcinoma cells
Concentration: 6.25 nM, 12.5 nM, 25 nM
Incubation Time: 6 h
Result: Induced a progressive, dose-dependent collapse of the HepG2 cell microtubule network, phenocopying the effects of CA-4 and colchicine.

Cell Cycle Analysis[1]

Cell Line: B16-F10 mouse melanoma cells
Concentration: 6.25 nM, 12.5 nM
Incubation Time: 24 h
Result: Increased the percentage of B16-F10 cells in G2/M phase from 4.67% (control) to 29.96% at 6.25 nM.
Increased the percentage of B16-F10 cells in G2/M phase to 61.46% at 12.5 nM, which was comparable to CA-4 at 6.25 nM (63.44%) and far superior to colchicine at 25 nM (11.21%).

Apoptosis Analysis[1]

Cell Line: B16-F10 mouse melanoma cells
Concentration: 6.25 nM, 12.5 nM
Incubation Time: 24 h
Result: Increased the total percentage of apoptotic B16-F10 cells from 2.94% (control) to 14.38% at 6.25 nM.
Increased the total percentage of apoptotic B16-F10 cells to 18.90% at 12.5 nM.

Western Blot Analysis[1]

Cell Line: B16-F10 mouse melanoma cells
Concentration: 1 nM, 3 nM, 6 nM, 12 nM
Incubation Time: 24 h
Result: Induced a dose-dependent increase in Cleaved-Caspase 3 levels in B16-F10 cells.

Cell Migration Assay [1]

Cell Line: B16-F10 mouse melanoma cells
Concentration: 6.25 nM, 12.5 nM, 25 nM
Incubation Time: 24 h
Result: Inhibited B16-F10 cell migration with an inhibition rate of 31.95% at 6.25 nM.
Inhibited B16-F10 cell migration with an inhibition rate of 61.88% at 12.5 nM, which was comparable to CA-4 at 12.5 nM (62.53%) and substantially more effective than colchicine at 12.5 nM (15.77%).
Inhibited B16-F10 cell migration with an inhibition rate of 70.78% at 25 nM.
In Vivo

SMU-G4 (15-30 mg/kg; daily; for 10 consecutive days) exhibits potent dose-dependent in vivo anti-tumor efficacy in a mouse melanoma model without significant systemic toxicity[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6 (female, 5 weeks old, subcutaneous implantation of 4×105 B16-F10 cells)[1]
Dosage: 15 mg/kg; 30 mg/kg
Administration: daily; 10 days
Result: Achieved a tumor growth inhibition (TGI) value of 74.4% at 15 mg/kg.
Increased TGI to 81.91% at 30 mg/kg.
Recorded no significant body weight loss or observable signs of toxicity over the 10-day period.
Molecular Weight

349.38

Formula

C20H19N3O3
SMILES

CN(N=C1C#N)C(C1=C2)=CC=C2/C=C\C3=CC(OC)=C(OC)C(OC)=C3
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

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Purity & Documentation
References
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SMU-G4 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

SMU-G4Microtubule/TubulinApoptosisCaspaseporcine tubulinmelanoma xenograft modelsmelanoma cellsA549HepG2B16-F10G2/M phase cell cycle arrestmicrotubule dynamicscolchicine-binding siteapoptosisInhibitorinhibitorinhibit

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