Molecular Mechanisms of Cereblon-Interacting Small Molecules in Multiple Myeloma Therapy.
CELMoDs
Cereblon
IMiDs
multiple myeloma
thalidomide
Journal
Journal of personalized medicine
ISSN: 2075-4426
Titre abrégé: J Pers Med
Pays: Switzerland
ID NLM: 101602269
Informations de publication
Date de publication:
11 Nov 2021
11 Nov 2021
Historique:
received:
18
10
2021
revised:
08
11
2021
accepted:
08
11
2021
entrez:
27
11
2021
pubmed:
28
11
2021
medline:
28
11
2021
Statut:
epublish
Résumé
Thalidomide analogues (or immunomodulatory imide drugs, IMiDs) are cornerstones in the treatment of multiple myeloma (MM). These drugs bind Cereblon (CRBN), a receptor for the Cullin-ring 4 ubiquitin-ligase (CRL4) complex, to modify its substrate specificity. IMiDs mediate CRBN-dependent engagement and proteasomal degradation of 'neosubstrates', Ikaros (IKZF1) and Aiolos (IKZF3), conveying concurrent antimyeloma activity and T-cell costimulation. There is now a greater understanding of physiological CRBN functions, including endogenous substrates and chaperone activity. CRISPR Cas9-based genome-wide screening has further elucidated the complex cellular machinery implicated in IMiD sensitivity, including IKZF1/3-independent mechanisms. New-generation IMiD derivatives with more potent anti-cancer properties-the CELMoDs (Cereblon E3 ligase modulators)-are now being evaluated. Rational drug design also allows 'hijacking' of CRL4
Identifiants
pubmed: 34834536
pii: jpm11111185
doi: 10.3390/jpm11111185
pmc: PMC8623651
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Subventions
Organisme : Australian Medical Research Future Fund
ID : GNT1160133
Organisme : Family of My Laurence Bode
ID : NA
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