For research use only. Not for therapeutic Use.
Iberdomide (CC-220) is an orally active and potent cereblon (CRBN) E3 ligase modulator (CELMoD) with an IC50 of ~150 nM for cereblon-binding affinity. Iberdomide, a derivative of Thalidomide (HY-14658), has antitumor and immunostimulatory activities[1][2].
Iberdomide (CC-220; 0.01, 0.1, 1, 10 μM; 72-96 hrs) has antiproliferative effects in a panel of multiple myeloma (MM) cell lines (EJM, H929, KMS11, KMS128M, KMS12PE, MM1.S, MM1.R, RPM-8226, U266 cells) across a range of concentrations[1].
Iberdomide (0.1 μM; 96 hrs) induces apoptosis in all MM cell lines[1].
Iberdomide (0.1 μM; 24, 48, 72 hrs) results in time-dependent increases in G0/G1 and sub-G1 cell cycle fractions on H929 cells[1].
Iberdomide leads to rapid Aiolos depletion in the KMS12BM line[1].
Iberdomide (0.1 μM) displays some anti-proliferative activity in two of the Pomalidomide-resistant (PR) lines with cereblon mutations (EJM/PR and H929/PR) along with decreased levels of cereblon protein[1].
Iberdomide (0.1-1000 nM; 72 hrs) equally induces PBMC-mediated killing of both parental MM1.S cells and MM1.S/PR cells[1].
Iberdomide (CC-220; 10 mg/kg; oral gavage) after 6 or 24 hours causes higher hCRBN expression in hC343 splenocytes correlated to deeper IKZF1/3 downregulation in WT (C57BL/6), hC123, or-343, (representing two different transgenic founder lines expressing hCRBN) and mCrbn-/- mice[2].
| Catalog Number | I007241 |
| CAS Number | 1323403-33-3 |
| Synonyms | (3S)-3-[7-[[4-(morpholin-4-ylmethyl)phenyl]methoxy]-3-oxo-1H-isoindol-2-yl]piperidine-2,6-dione |
| Molecular Formula | C25H27N3O5 |
| Purity | ≥95% |
| InChI | InChI=1S/C25H27N3O5/c29-23-9-8-21(24(30)26-23)28-15-20-19(25(28)31)2-1-3-22(20)33-16-18-6-4-17(5-7-18)14-27-10-12-32-13-11-27/h1-7,21H,8-16H2,(H,26,29,30)/t21-/m0/s1 |
| InChIKey | IXZOHGPZAQLIBH-NRFANRHFSA-N |
| SMILES | C1CC(=O)NC(=O)C1N2CC3=C(C2=O)C=CC=C3OCC4=CC=C(C=C4)CN5CCOCC5 |
| Reference | [1]. Chad C Bjorklund, et al. Iberdomide (CC-220) is a potent cereblon E3 ligase modulator with antitumor and immunostimulatory activities in lenalidomide- and pomalidomide-resistant multiple myeloma cells with dysregulated CRBN. Leukemia. 2020 Apr;34(4):1197-1201. [2]. Erin W Meermeier, et al. Tumor burden limits bispecific antibody efficacy through T cell exhaustion averted by concurrent cytotoxic therapy. Blood Cancer Discov. 2021 Jul;2(4):354-369. |
