AP4-43 is an orally active CLK1, CLK4, PI3K, DDR1, EGFR and NEK4 inhibitor. AP4-43 reduces growth of mammalian colorectal cancer organoids. AP4-43 improves survival in a transgenic Drosophila model of KRAS -mutant colorectal cancer. AP4-43 can be used for the research of KRAS -mutant colorectal cancer [1].
In Vivo, AP4-43 (1-100 µM; p.o.; continuous feeding in media) enhances survival of a patient-matched Drosophila colorectal cancer model by targeting a multi-kinase network including CLK1 and NEK4, with synergistic efficacy observed when combined with reduced NEK4 gene dosage, reaching 78.5% survival in this context[1].
In Vitro, AP4-43 (10 pM-100 μM; 72 hr) inhibits the viability of SW620 human KRAS-driven colorectal cancer cells with an IC50 of 2.23 µM and SW837 cells with an IC50 of 15.41 µM[1]. AP4-43 (2 µM) reduces the growth of AKP mouse KRAS-mutant colorectal cancer organoids more effectively than 2 µM Regorafenib [1]. AP4-43 (2 µM; 24 hr) inhibits CLK1-dependent Wnt/β-catenin signalling and CLK4-dependent NF-κB activation in AKP mouse KRAS-mutant colorectal cancer organoids, without affecting PI3K-AKT or RAS-MAPK pathway activity[1].
References:
[1]. Badmos HA, et al. Chemical programming of kinase inhibitors in a modular chemputer-based system. Commun Biol. Published online March 27, 2026.
In Vivo, AP4-43 (1-100 µM; p.o.; continuous feeding in media) enhances survival of a patient-matched Drosophila colorectal cancer model by targeting a multi-kinase network including CLK1 and NEK4, with synergistic efficacy observed when combined with reduced NEK4 gene dosage, reaching 78.5% survival in this context[1].
In Vitro, AP4-43 (10 pM-100 μM; 72 hr) inhibits the viability of SW620 human KRAS-driven colorectal cancer cells with an IC50 of 2.23 µM and SW837 cells with an IC50 of 15.41 µM[1]. AP4-43 (2 µM) reduces the growth of AKP mouse KRAS-mutant colorectal cancer organoids more effectively than 2 µM Regorafenib [1]. AP4-43 (2 µM; 24 hr) inhibits CLK1-dependent Wnt/β-catenin signalling and CLK4-dependent NF-κB activation in AKP mouse KRAS-mutant colorectal cancer organoids, without affecting PI3K-AKT or RAS-MAPK pathway activity[1].
References:
[1]. Badmos HA, et al. Chemical programming of kinase inhibitors in a modular chemputer-based system. Commun Biol. Published online March 27, 2026.
















