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Cereblon (CRBN)

Cereblon (CRBN) is an intracellular multifunctional protein that functions as a component of an E3 ubiquitin ligase system and cooperates with other elements of the ubiquitin–proteasome pathway.

Rebuilt from PubMed 18 Sept 2026 · no new papers today

Where the papers sit

10 papers study cereblon (crbn) directly. The themes below are drawn from those 10. 1 new direction follows.

  • CRBN Ligand Design and Applications : CRBN ligand work spans binding characterization, PROTAC and prodrug design, radiolabeled imaging agents, and early biomarker evaluation. The field is broadening CRBN recruitment beyond therapy while clinical validation remains preliminary. 5 papers · 50%

  • Molecular Glue Degrader Development : Molecular glue research is moving toward scalable discovery and systematic carcinogenicity assessment. ERα degradation through HSP27-associated E3 ligase recruitment offers a route around endocrine-resistant breast cancer. 3 papers · 30%

  • CRBN-Mediated Protein Degradation : CRBN degraders are being applied to both BTK elimination and IKZF1/3 degradation. Mezigdomide links this strategy to restored cytokine production and reversal of T-cell exhaustion. 2 papers · 20%

NEW DIRECTION

CRBN is proposed as an early prognostic biomarker in paediatric sepsis

The paediatric sepsis prospective observational study protocol treats CRBN not as a component recruited by therapeutic degraders but as a measurable immune-related biomarker whose expression may predict disease trajectory and mortality in children with sepsis 42613111Aug. Whereas the other abstracts use CRBN chiefly as an intracellular binding partner or E3-ligase recruitment element for drug design and targeted protein degradation, this study gives it a clinical prognostic role in an acute infectious disease. If validated, that would shift CRBN from a pharmacological mechanism into a tool for early triage and outcome prediction.

Recent Findings on Cereblon (CRBN)

CRBN Translational Research: CRBN ligand engineering now connects structural characterization with radiolabeling, targeted protein degradation, and clinical biomarker development. The purified cereblon Thalidomide-Binding Domain retained lenalidomide binding, enabling NMR-based analysis of ligand interactions 42101529May. Bioorganometallic modification weakened CRBN binding, whereas [Re(η6-lena)2]+ retained measurable affinity and showed rapid blood clearance with predominant renal excretion in mice 42627009Aug. CRBN-recruiting PROTAC prodrugs used triazole quaternization, tertiary-amine alkylation, or hydroxyl-linker installation to control self-immolative release and cellular potency in multiple myeloma models 42554619Aug. C13p strengthened hFAAH–CRBN interactions through stepwise assembly, while hFAAH dissociated independently in most trajectories 42333818Jun. A prospective paediatric sepsis protocol will test whether CRBN mRNA and protein levels correlate with 28-day mortality, pSOFA scores, inflammation, and PICU outcomes 42613111Aug.

Molecular Glue Degraders: CRBN-based molecular glue discovery is moving toward scalable chemical assembly, phenotypic screening, and integrated safety assessment. A primary amine-based photoclick platform generated more than 1000 CRBN-centric molecules directly in multi-well plates and identified degraders of GSPT1, CK1α, and multiple targets 42149616May. Hydrophobic-tag degrader VI-10h used an ERα–HSP27–RING1 ternary complex to drive ERα proteasomal degradation and showed antitumor activity in endocrine-resistant breast cancer models 42189698May. Carcinogenicity assessment emphasizes the biological effects of the recruited E3 ubiquitin ligase alongside the primary target, while early-generation cereblon molecular glue degraders create challenges for translatability and traditional weight-of-evidence interpretation 42051197Apr. These findings support broader degrader screening while requiring compound-specific evaluation of E3-ligase biology and carcinogenicity risk.

CRBN-Based Protein Degradation: CRBN-mediated degradation is producing distinct therapeutic effects through BTK depletion and IKZF1/IKZF3 modulation. Novel CRBN-binding warheads enabled orally bioavailable BTK-targeting PROTACs that degraded wild-type and mutated BTK without concomitant activity against IKZF1, IKZF3, or GSPT1 42720469Sep. The lead compounds ISM-PR25 and ISM-PR44 showed subnanomolar BTK degradation in malignant B cells and degraded BTK in mouse circulating B cells after a single oral dose 42720469Sep. Mezigdomide instead targeted IKZF1 and IKZF3 simultaneously, reducing exhaustion-related markers and restoring proinflammatory cytokine expression in exhausted T cells 42118707May. Mezigdomide also enhanced target-cell killing with the BCMA-targeting T-cell engager alnuctamab, supporting combination treatment in multiple myeloma 42118707May.