Evidence map›Paper›PMID 41651798›Full record

ReviewEuropean journal of haematology2026

Targeting Ikaros and Aiolos: Next-Generation Cereblon E3 Ligase Modulators in MM.

Maria Eugenia Alvaro, Enrica Antonia Martino, Santino Caserta, Mamdouh Skafi, Antonella Bruzzese, Nicola Amodio, Eugenio Lucia, Virginia Olivito, Caterina Labanca, Francesco Mendicino and 3 more

Abstract readReview
In one paragraph

Review in European journal of haematology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Maria Eugenia AlvaroDepartment of Onco-Hematology, AO of Cosenza, Hematology Unit, Cosenza, Italy.
Enrica Antonia MartinoDepartment of Onco-Hematology, AO of Cosenza, Hematology Unit, Cosenza, Italy.
Santino CasertaDepartment of Onco-Hematology, AO of Cosenza, Hematology Unit, Cosenza, Italy.
Mamdouh SkafiEmergency and Internal Medicine Department, Saint Joseph Hospital, East Jerusalem, Palestine.
Antonella BruzzeseDepartment of Onco-Hematology, AO of Cosenza, Hematology Unit, Cosenza, Italy.
Nicola AmodioDepartment of Experimental and Clinical Medicine, University of Catanzaro, Catanzaro, Italy.
Eugenio LuciaDepartment of Onco-Hematology, AO of Cosenza, Hematology Unit, Cosenza, Italy.
Virginia OlivitoDepartment of Onco-Hematology, AO of Cosenza, Hematology Unit, Cosenza, Italy.
Caterina LabancaDepartment of Onco-Hematology, AO of Cosenza, Hematology Unit, Cosenza, Italy.
Francesco MendicinoDepartment of Onco-Hematology, AO of Cosenza, Hematology Unit, Cosenza, Italy.ORCID https://orcid.org/0000-0001-6339-632X
Ernesto VignaDepartment of Onco-Hematology, AO of Cosenza, Hematology Unit, Cosenza, Italy.
Fortunato MorabitoAIL Sezione di Cosenza, Cosenza, Italy.
Massimo GentileDepartment of Onco-Hematology, AO of Cosenza, Hematology Unit, Cosenza, Italy.ORCID https://orcid.org/0000-0002-5256-0726

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) remains an incurable plasma cell malignancy characterized by recurrent relapses and eventual refractoriness to standard agents, including proteasome inhibitors (PIs), immunomodulatory drugs (IMiDs), and anti-CD38 monoclonal antibodies. With frontline therapeutic strategies increasingly employing quadruplet induction regimens and prolonged lenalidomide maintenance, resistance to traditional IMiDs has become more prevalent, creating an urgent need for next-generation cereblon E3 ligase modulators (CELMoDs) capable of overcoming IMiD refractoriness and enhancing the immunologic microenvironment. Iberdomide (CC-220) and mezigdomide (CC-92480) are rationally engineered CELMoDs designed to achieve deeper degradation of Ikaros (IKZF1) and Aiolos (IKZF3), restore cereblon-mediated activity, and potentiate immune effector responses. This review explores the core biological features of these agents, detailing their mechanisms of action, preclinical and clinical activity, as well as safety profile. We examine how their pharmacodynamic properties differ from classical IMiDs, their relevance in triple-class and penta-refractory MM, and their integration into emerging combination strategies with monoclonal antibodies and T-cell-redirecting immunotherapies. Special emphasis is placed on ongoing and future trials that may refine their therapeutic positioning, alongside a critical appraisal of the limitations and future directions of this rapidly advancing drug class.

Indexed as

Adaptor Proteins, Signal TransducingAntineoplastic AgentsIkaros Transcription FactorMultiple MyelomaPeptide HydrolasesUbiquitin-Protein LigasesAnimalsDrug Resistance, NeoplasmHumansMolecular Targeted TherapyAdaptor Proteins, Signal TransducingAntineoplastic AgentsCRBN protein, humanIkaros Transcription FactorIKZF1 protein, humanIKZF3 protein, humanPeptide HydrolasesUbiquitin-Protein LigasesCereblon E3 ligase modulators (CELMoDs)IberdomideIMiD resistance/immunomodulationMezigdomidemultiple myeloma

Identifiers

PMID41651798
PMCPMC13141667

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.