ArticleDiscover oncology2026
A lipid nanoparticle-based peptide-proteolysis-targeting chimera degrades BCL6 for diffuse large B-cell lymphoma treatment.
Article in Discover oncology, 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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12 authors.
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Abstract
B-cell lymphoma 6 (BCL6) is an attractive drug target for diffuse large B-cell lymphoma (DLBCL). This study aimed to create a lipid nanoparticle (LNP)-based peptide-proteolysis-targeting chimera (PROTAC), specifically BCL6-PROTAC, to develop effective strategies for treating DLBCL via targeted degradation of the BCL6 protein. Molecular docking, SPR and cellular thermal shift assays revealed that F1324 (Ac-LWYTDIRMSWRVP-OH) is a high-affinity BCL6-binding peptide. PROTAC LNPs were synthesized by modifying F1324 and pomalidomide aptamers onto LNPs via a covalent chemical reaction in a certain proportion. The LNPs were characterized using dynamic light scattering and transmission electron microscopy. The ligand ratio (F1324:pomalidomide) used to verify the optimal BCL6 degradation was 1:5, as determined using western blotting. In vitro and in vivo studies revealed that BCL6-PROTAC significantly inhibited the proliferation of DLBCL cells. Target-specific uptake was used to evaluate the accumulation of BCL6-PROTAC in vivo. Toxicity in normal tissues was detected using H&E staining and serum indices. Overall, we developed a PROTAC that exhibited persistent and excellent BCL6 degradation ability in DLBCL, with an excellent safety profile. Thus, our BCL6 degrader provides a complementary approach to existing clinical‑stage candidates.
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