New dual-action compound reduces pancreatic cancer cell growth
“Our data demonstrates that SB-216 effectively inhibits PDAC cell growth through inhibiting oncogenic microtubules and mitochondrial function”
2026-02-10
(Press-News.org)
“Our data demonstrates that SB-216 effectively inhibits PDAC cell growth through inhibiting oncogenic microtubules and mitochondrial function.”
BUFFALO, NY — February 10, 2026 — A new research paper was published in Volume 13 of Oncoscience on January 28, 2026, titled “Dual targeting of oncogenic microtubules and mitochondria in PDAC.”
In this study led by first author Michael W. Spinrad with corresponding author, Evan S. Glazer from The University of Tennessee Health Science Center, researchers found that an experimental compound, SB-216, reduced the growth of pancreatic ductal adenocarcinoma (PDAC) cells. The research addresses a critical need for new therapeutic approaches in PDAC, an aggressive cancer that is often resistant to existing treatments.
Pancreatic ductal adenocarcinoma is one of the leading causes of cancer-related death worldwide. Its treatment is challenging due to poor response to chemotherapy and a high rate of metastasis. In this study, researchers investigated whether targeting two specific cellular systems: microtubules, which support cell division, and mitochondria, which produce energy, could slow the growth of PDAC cells more effectively than standard approaches. To do this, they used two compounds: SB-216 and Veru-111.
SB-216 is part of a class of compounds that bind to tubulin, a building block of microtubules. In cell-based assays, SB-216 suppressed the expression of microtubule-associated proteins, particularly βIII- and βIVb-tubulin, which are often overexpressed in pancreatic cancer and associated with drug resistance. This suppression was associated with reduced cell viability and diminished cell proliferation.
The compound also interfered with mitochondrial function by lowering the expression of BRD4, a protein involved in energy regulation and gene expression. Treated PDAC cells showed decreased oxygen consumption, indicating mitochondrial dysfunction. This energy disruption was associated with increased markers of mitophagy and autophagy, cellular processes that help clear damaged components and regulate cell survival.
Compared to Veru-111, SB-216 demonstrated a stronger and more sustained effect on reducing PDAC cell viability. Both compounds act on similar targets, but SB-216 was more effective in this model. By acting on two critical systems at once, it may reduce the chance for cancer cells to adapt and survive.
“This novel approach simultaneously targets two hallmarks of cancer and patient demise.”
These findings were generated in vitro and represent early-stage preclinical research. Further studies in animal models will be needed to evaluate the compound’s safety, biological activity, and therapeutic potential in vivo. Overall, this study contributes to ongoing efforts to develop more effective treatment strategies for pancreatic cancer by exploring compounds that act on multiple cancer-related pathways.
DOI: https://doi.org/10.18632/oncoscience.641
Correspondence to: Evan S. Glazer- esglazer@umich.edu
Abstract video: https://www.youtube.com/watch?v=Naj0XD1e_DI
Keywords: cancer, pancreatic ductal adenocarcinoma, bromo- and extra-terminal domain, mitochondrial stress, mitophagy, mitochondria
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About Oncoscience:
Oncoscience is a peer-reviewed, open-access, traditional journal covering the rapidly growing field of cancer research, especially emergent topics not currently covered by other journals. This journal has a special mission: freeing oncology from publication costs. It is free to readers and authors.
Oncoscience is indexed and archived by PubMed, PubMed Central, Scopus, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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[Press-News.org] New dual-action compound reduces pancreatic cancer cell growth
“Our data demonstrates that SB-216 effectively inhibits PDAC cell growth through inhibiting oncogenic microtubules and mitochondrial function”
