ArticleJournal of advanced research2026
Guaianolide dimer KGA-1002 targets GRP94 and triggers unfolded protein response-associated degradation of SKP2/AKT axis as a novel antihepatoma agent.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The trial behind it
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Who cites it
2 citing papers in PubMed.
- SKP2 in Cancer: From Molecular Regulation to Therapeutic Vulnerabilities and Translational Perspectives.Drug design, development and therapy · 2026Review
- Tectochrysin alleviates Ang II-induced pathological cardiac hypertrophy by binding to STING and inhibiting STING/NFκB-mediated inflammation.Frontiers in pharmacology · 2026Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionHepatocellular carcinoma (HCC) remains a highly lethal malignant tumor with limited treatment options. The guaianolide dimer KGA-1002 exhibited significant inhibitory effects on HCC cells, but the specific target and mechanism remain unclear.
objectivesTo further evaluate the antiHCC efficacy of KGA-1002 and clarify its molecular target and mechanism.
methodsBrdU, flow cytometry, Transwell, and colony formation assays were utilized to evaluate the in vitro antiHCC efficacy of KGA-1002. Drug affinity responsive target stability (DARTS) and bioinformatics analyses were applied to identify its target. The binding site was confirmed through Mass spectra analysis and amino acid mutation. Knockdown cell lines were used to validate the GRP94-dependent effects of KGA-1002. Pulldown assays were performed to detect protein-protein interactions. Xenograft tumor models were employed to examine the in vivo efficacy and mechanism.
resultsKGA-1002 inhibited the proliferation and metastasis of HCC cells, induced apoptosis and cell-cycle arrest at the G0/G1 phase. GRP94 was identified as its direct target, and Ser
conclusionKGA-1002 was identified as a highly promising lead compound for antiHCC. Its mechanism involved triggering UPR-associated degradation and disrupting the GRP94-AKT interaction. KGA-1002 simultaneously induced apoptosis and ferroptosis in HCC cells through the GRP94/AKT/SKP2/P21 signaling axis.
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