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Updated: Apr 23, 2026

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
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QW-5-70 targets the colchicine site and demonstrates antitumor activity in P-gp-overexpressing cancer models

Yang Xie1, Ruida Hou1, Najah Albadari1

  • 1University of Tennessee Health Science Center Memphis, TN United States.

Molecular Cancer Therapeutics
|April 22, 2026
PubMed

Insights

A new drug, QW-5-70, effectively treats drug-resistant neuroblastoma and prostate cancer by targeting tubulin. This colchicine-binding-site inhibitor overcomes P-glycoprotein efflux, showing potent activity in preclinical models.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Drug resistance in neuroblastoma (NB) and castration-resistant prostate cancer (CRPC) is a major clinical challenge, often driven by efflux transporters like P-glycoprotein (P-gp) and altered tubulin dynamics.
  • Existing therapies like taxanes and vincristine face limitations due to these resistance mechanisms.

Purpose of the Study:

  • To develop and evaluate QW-5-70, a novel colchicine-binding-site inhibitor (CBSI), designed to overcome P-gp-mediated efflux and maintain potency against drug-resistant cancers.
  • To assess the efficacy of QW-5-70 in preclinical models of NB and CRPC, including multidrug-resistant cell lines and xenografts.

Main Methods:

  • QW-5-70 was tested in vitro and in vivo against various NB and prostate cancer cell lines, including vincristine-resistant (BE2C/VCR) and paclitaxel-resistant (PC-3/TxR) lines.
  • The study evaluated QW-5-70's mechanism of action, including tubulin polymerization inhibition, cell cycle arrest (G2/M), apoptosis induction, and effects on colony formation and migration.
  • In vivo efficacy was assessed in xenograft models, and combination studies were performed with DFMO and MLN8237.

Main Results:

  • QW-5-70 demonstrated low-nanomolar potency against both parental and drug-resistant cancer cells, unaffected by P-gp inhibition.
  • The compound effectively inhibited tumor growth in vivo in resistant xenograft models with acceptable tolerability.
  • Synergistic interactions were observed when QW-5-70 was combined with DFMO and MLN8237, enhancing anti-cancer effects.

Conclusions:

  • QW-5-70 is a potent CBSI that effectively circumvents P-gp-mediated drug resistance in NB and CRPC models.
  • It induces mitotic arrest and apoptosis, leading to significant antitumor activity in multidrug-resistant cancers.
  • QW-5-70 shows promise for further preclinical development as a monotherapy or in combination regimens.

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