ArticleScientific reports2026
Absence of synergistic effects by CDK12/13 inhibition in combination with cisplatin or olaparib in ovarian cancer cells.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The identification of novel molecular drivers and the development of new state-of-the-art therapies are critical challenges in ovarian cancer (OC) treatment. Cyclin-dependent kinase 12 (CDK12) is a promising target, as it's functional activity promotes genomic stability. Here, we examined the anticancer efficacy of the dual CDK12/13-inhibitor SR-4835 in platinum-sensitive and -resistant OC cell lines, as well as its potential as a drug partner for platinum or olaparib combination therapy. SR-4835 exhibited potent anti-proliferative effects on most OC cell lines with IC50 values within the nanomolar range. A tendency for increased sensitivity of the cisplatin-resistant compared to their sensitive, parental cell lines was observed. Transcriptome analyses indicated gross changes in gene expression in numerous signaling pathways by SR-4835. Gene downregulation was in part due to alternative exon usage, which correlated with the number of intronic polyadenylation sites per gene and gene length. Furthermore, SR-4835 lead to the downregulation of key homologous recombination pathway genes rendering a BRCAness phenotype. However, the combination of SR-4835 with cisplatin or olaparib primarily exhibited an additive, not synergistic, effect. In summary, the present findings indicate that CDK12/13 inhibitor SR-4835 has potent anti-cancer effects accompanied by a BRCAness induction, but fails to achieve synergistic effects with cisplatin or olaparib in OC cells.
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