On October 6, 2026 Beactica Therapeutics AB, a Swedish precision medicine company, reported the selection of BEA-28 as a preclinical candidate for its TEAD programme, which is aimed at developing novel therapies for a range of aggressive, difficult-to-treat solid tumours, including cancers where resistance to existing treatments remains a major clinical challenge.
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BEA-28 is a first-in-class small molecule targeted degrader of the TEAD transcription factors, key effectors of the Hippo-YAP/TAZ pathway. Rather than blocking a binding pocket, BEA-28 removes the TEAD proteins and all their functions – an approach suited to cancers where pathway activity drives tumour growth or treatment resistance. In preclinical studies, BEA-28 showed robust tumour regressions at well-tolerated doses, and restored sensitivity to KRAS inhibitors in resistant models. The programme advances a biomarker-led, combination strategy, with a high unmet need cancer as the lead indication.
"Selecting BEA-28 as a preclinical candidate reflects the strength of our TEAD degrader programme and our confidence in the compound’s differentiated profile. The compound has met all predefined success criteria for this stage, and we believe it has the potential to address several hard-to-treat cancers through a clear biomarker-led strategy." said Dr Per Källblad, CEO of Beactica Therapeutics. "By moving this specific molecule into final candidate validation, we are executing on our mission to transition this program rapidly toward the clinic."
BEA-28 was selected after meeting predefined success criteria covering chemistry, in vitro and in vivo pharmacology, ADME and pharmacokinetic properties. The molecule will now advance into comprehensive candidate validation, including non-regulatory (pre-GLP) toxicology, scale-up chemistry, and advanced formulation profiling. Studies formally supporting IND-enabling requirements will be initiated following candidate drug nomination.
About BEA-28
BEA-28, closely related to P65-047, is a first-in-class, cereblon-recruiting small molecule degrader of the TEAD transcription factors, generated using Beactica’s Eclipsor platform and developed to shut down Hippo-YAP/TAZ-TEAD pathway activity implicated in tumour growth, immune evasion and resistance to targeted therapies. In preclinical studies, BEA-28 has shown deep responses in selected high-need lineages within a broad cancer cell line panel and reversed acquired resistance to KRAS-inhibitor treatment in cellular models. In vivo, BEA-28 achieved robust TEAD degradation in target tissue and induced tumour regression in xenograft models of mesothelioma and KRAS-mutant lung cancer at well-tolerated, once-daily doses. Beactica is developing BEA-28 alongside a biomarker-driven patient selection strategy intended to identify the tumours most likely to respond, with lead combination strategies planned in a non-mesothelioma high unmet need cancer alongside checkpoint inhibitors, and in KRAS-driven cancers alongside KRAS inhibitors. BEA-28 is investigational and has not been approved anywhere globally; its efficacy and safety in humans have not been established.
(Press release, Beactica, OCT 6, 2026, View Source [SID1234673238])