2. Cell Cycle/DNA Damage Cytoskeleton Apoptosis
  3. Microtubule/Tubulin Apoptosis
  4. QW-5-70

QW-5-70 is a potent colchicine‑site tubulin inhibitor that blocks tubulin polymerization. QW-5-70 induces mitotic and G2/M cell cycle arrest, triggers mitochondrial apoptosis, and suppresses cancer cell colony formation and migration. QW-5-70 overcomes P‑glycoprotein‑mediated multidrug resistance and inhibits drug‑resistant tumor growth. QW-5-70 demonstrates strong in vitro and in vivo antitumor efficacy in neuroblastoma and prostate cancer models. QW-5-70 can be used for the research of high-risk neuroblastoma and castration-resistant prostate cancer.

For research use only. We do not sell to patients.

QW-5-70

QW-5-70 Chemical Structure

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QW-5-70 Related Antibodies

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Description

QW-5-70 is a potent colchicine‑site tubulin inhibitor that blocks tubulin polymerization. QW-5-70 induces mitotic and G2/M cell cycle arrest, triggers mitochondrial apoptosis, and suppresses cancer cell colony formation and migration. QW-5-70 overcomes P‑glycoprotein‑mediated multidrug resistance and inhibits drug‑resistant tumor growth. QW-5-70 demonstrates strong in vitro and in vivo antitumor efficacy in neuroblastoma and prostate cancer models. QW-5-70 can be used for the research of high-risk neuroblastoma and castration-resistant prostate cancer[1][2].

IC50 & Target[2]

β-Tubulin

 

In Vitro

QW-5-70 binds directly to the colchicine-binding site on purified tubulin with a Kd of 10.8 μM, inhibits tubulin polymerization, and disrupts microtubule networks[1][2].
QW-5-70 exhibits subnanomolar antiproliferative activity in parental and drug-resistant BE2C/VCR, PC-3/TxR, NB, and prostate cancer cells, and evades P-glycoprotein-mediated efflux[1].
QW-5-70 significantly reduces colony formation, impairs migration, induces G2/M cell cycle arrest and mitochondrial apoptosis in parental and drug-resistant BE2C/VCR, PC-3/TxR, NB, and prostate cancer cells. QW-5-70 enhances apoptosis and reduces clonogenic survival when combined with DFMO (HY-B0744) or MLN8237 (HY-10971)[1][2].
QW-5-70 inhibits viability of SK-N-BE(2)-C, BE2C/VCR, PC-3, and PC-3/TxR cells with IC50 values of 1.0 nM, 1.8 nM, 1.5 nM, and 1.5 nM, respectively[2].
QW-5-70 (0.1-15 μM) destabilizes microtubules in SK-N-BE(2)-C, NB-1691, and PC-3 cells, as shown by reduced polymerized β-tubulin and increased soluble β-tubulin levels[2].
QW-5-70 (2-5 nM) induces G2/M phase cell cycle arrest in SK-N-BE(2)-C, NB-1691, and PC-3/TxR cells, triggers mitotic arrest in BE2C/VCR and PC-3/TxR cells with increased p-Histone H3 (Ser10), cyclin B1, and p-CDK1 (Thr161) levels, and induces apoptosis in BE2C/VCR and PC-3/TxR cells, as evidenced by elevated cleaved caspase-3, cleaved PARP, and phosphorylated BCL2 (Ser70) levels, and reduced total BCL2 expression[2].

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

QW-5-70 Related Antibodies

Immunofluorescence[2]

Cell Line: SK-N-BE(2)-C, NB-1691, PC-3 cancer cells
Concentration: 2, 5 nM
Incubation Time: 24 h
Result: Caused disruption of normal microtubule networks in SK-N-BE(2)-C, NB-1691, and PC-3 cells, resulting in fragmented, disorganized microtubule structures compared to untreated control cells.

Western Blot Analysis[2]

Cell Line: BE2C/VCR, PC-3/TxR cancer cells
Concentration: 2, 5 nM
Incubation Time: 24 h
Result: Increased levels of phosphorylated histone H3 (p-Histone H3) and cyclin B1, and reduced levels of phosphorylated CDK1 (p-CDK1 (Thr161)) in BE2C/VCR and PC-3/TxR cells, consistent with induction of mitotic arrest.\n
Increased levels of cleaved caspase-3 (cCas3), cleaved PARP (cPARP), and BCL2-associated X protein (p-BCL2), and reduced levels of B-cell lymphoma 2 (BCL2) in BE2C/VCR and PC-3/TxR cells, consistent with induction of apoptosis.

Cell Viability Assay[2]

Cell Line: SK-N-BE(2)-C neuroblastoma cells
Concentration: 0.125, 0.25, 0.5, 1, 2 nM (QW-5-70 alone)
10, 30, 100, 300, 1000 μM (DFMO alone)
1 nM (QW-5-70) plus 100 mM (DFMO, combination)
Incubation Time: 24 h
Result: Combination treatment with QW-5-70 and DFMO reduced SK-N-BE(2)-C cell viability more effectively than either agent alone.
Increased levels of cleaved PARP compared to single-agent treatment when used at 1 nM plus DFMO at 100 mM, indicating enhanced apoptosis.
Exhibited an additive to synergistic interaction with DFMO as confirmed by synergy analysis.
In Vivo

QW-5-70 (15, 30 mg/kg; daily; 14 days) significantly suppresses the growth of Paclitaxel (HY-B0015)-resistant PC-3/TxR tumor xenografts in mice[2].
QW-5-70 (20 mg/kg; daily; 14 days) effectively suppresses the growth of Vincristine (HY-N0488A)-resistant BE2C/VCR tumor xenografts in mice with favorable tolerability[2].

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

378.38

Formula

C20H18N4O4
SMILES

O=C(C1=NC(C2=C(C=NN3)C3=CC=C2)=CN1)C4=CC(OC)=C(OC)C(OC)=C4
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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QW-5-70 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:

QW-5-70Microtubule/TubulinApoptosisprostate cancermitotic arrestcolchicine siteG2/M cell cycle arresttubulinP-glycoproteinmicrotubule networksneuroblastomamitochondrial apoptosisBE2C/VCRInhibitorinhibitorinhibit

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