A novel colchicine-binding site inhibitor suppresses triple-negative breast cancer growth and metastasis and synergizes with anti-PD-L1 immunotherapy in an immunogenic cancer model

/M arrest and apoptosis and can bypass taxane resistance. SP-1-39, a novel CBSI, exhibits potent anti-cancer activity in a paclitaxel-resistant prostate cancer in vivo model, confirming its capacity to overcome chemoresistance. We also discovered that SP-1-39 upregulates PD-L1 expression in vitro, suggesting synergy with immune checkpoint blockade. This study evaluates the anti-metastatic activity of SP-1-39 in metastatic TNBC and the therapeutic potential of combining SP-1-39 with anti-PD-L1 immune checkpoint inhibition in a PD-L1-responsive colon cancer model. Our findings provide preclinical evidence supporting SP-1-39 as a promising therapeutic agent for TNBC and other solid tumors, either as a single agent or in combination with immunotherapy.

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Publication Details

Journal
Biomedicine & Pharmacotherapy
Published
2026-04-10
DOI
https://doi.org/10.1016/j.biopha.2026.119353
Primary Topic
Inflammasome and immune disorders
Type
article
Field-Weighted Citation Impact
0.00

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article

A novel colchicine-binding site inhibitor suppresses triple-negative breast cancer growth and metastasis and synergizes with anti-PD-L1 immunotherapy in an immunogenic cancer model

Duane D. Miller, Damilola Oluwalana, Gustavo A. Miranda‐Carboni, Raisa I. Krutilina et al.
Biomedicine & Pharmacotherapy
Inflammasome and immune disorders
article

A novel colchicine-binding site inhibitor suppresses triple-negative breast cancer growth and metastasis and synergizes with anti-PD-L1 immunotherapy in an immunogenic cancer model

Duane D. Miller, Damilola Oluwalana, Gustavo A. Miranda‐Carboni, Raisa I. Krutilina, Kelli L. Adeleye, Satyanarayana Pochampally, Tiffany N. Seagroves, Yang Xie, Lily Waltz, Wei Li
article en

Abstract

/M arrest and apoptosis and can bypass taxane resistance. SP-1-39, a novel CBSI, exhibits potent anti-cancer activity in a paclitaxel-resistant prostate cancer in vivo model, confirming its capacity to overcome chemoresistance. We also discovered that SP-1-39 upregulates PD-L1 expression in vitro, suggesting synergy with immune checkpoint blockade. This study evaluates the anti-metastatic activity of SP-1-39 in metastatic TNBC and the therapeutic potential of combining SP-1-39 with anti-PD-L1 immune checkpoint inhibition in a PD-L1-responsive colon cancer model. Our findings provide preclinical evidence supporting SP-1-39 as a promising therapeutic agent for TNBC and other solid tumors, either as a single agent or in combination with immunotherapy.

Biomedicine & PharmacotherapyVol. 198
Tulane University (US), St. Jude Children's Research Hospital (US), University of Tennessee Health Science Center (US)
Drug Discovery Center, College of Pharmacy, Health Science Center, University of Tennessee, National Institutes of Health, National Cancer Institute
Good health and well-being
Openalex Percentile: Top 26%
Inflammasome and immune disorders
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