1. Metabolic Enzyme/Protease
  2. E1/E2/E3 Enzyme
  3. Avadomide

Avadomide (Synonyms: CC 122)

Cat. No.: HY-100507 Purity: 99.53%
Handling Instructions

Avadomide (CC 122) est un modulateur oralement active de cereblon. Avadomide module l'activité de la ligase du cereblon E3 et induit l'apoptose des lignées cellulaires diffuses de lymphome à grandes cellules B (DLBCL). Avadomide présente de puissantes activités antitumorales et immunomodulatrices.

Avadomid (CC 122) ist ein oral aktiver cereblon-Modulator. Avadomid moduliert die Aktivität der Cereblon-E3-Ligase und induziert die apoptosis diffuser großzelliger B-Zell-Lymphom-Zelllinien (DLBCL). Avadomid weist starke antitumorale und immunmodulatorische Aktivitäten auf.

Avadomide (CC 122) is an orally active cereblon modulator. Avadomide modulates cereblon E3 ligase activity and induces apoptosis of diffuse large B-cell lymphoma (DLBCL) cell lines. Avadomide exhibits potent antitumor and immunomodulatory activities.

For research use only. We do not sell to patients.

Avadomide Chemical Structure

Avadomide Chemical Structure

CAS No. : 1015474-32-4

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10 mM * 1 mL in DMSO USD 99 In-stock
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Based on 2 publication(s) in Google Scholar

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Avadomide (CC 122) is an orally active cereblon modulator. Avadomide modulates cereblon E3 ligase activity and induces apoptosis of diffuse large B-cell lymphoma (DLBCL) cell lines. Avadomide exhibits potent antitumor and immunomodulatory activities[1][2].

In Vitro

Avadomide inhibits proliferation and induces apoptosis in ABC and GCB DLBCL. In DLBCL cell lines, Avadomide-induced degradation or short hairpin RNA-mediated knockdown of Aiolos and Ikaros correlates with increased transcription of IFN-stimulated genes independent of IFN-α, -β, and -γ production and/or secretion and results in apoptosis in both activated B-cell (ABC) and germinal center B-cell DLBCL.[1]

In Vivo

Treatment of female CB-17 SCID mice with Avadomide (CC122) at 3 or 30 mg/kg once daily significantly decreased tumor growth in OCI-LY10 ABC-DLBCL (P = .028 and P < .001, respectively) and WSU-DLCL2 GCB-DLBCL derived xenograft models (P < .01) compared with the vehicle control. In a separate study, we assessed the ability of Avadomide (CC122) to promote degradation of Ikaros and Aiolos in vivo. In the 21-day efficacy study of WSU-DLCL2 xenograft transplanted mice, tumors were excised 1, 6, or 24 hours post final dosing. Aiolos and Ikaros expression was interrogated through immunohistochemistry (IHC) and was found to be decreased 64% and 30%, respectively, compared with vehicle within 1 hour of treatment, with a maximal reduction of 94% and 69%, respectively, observed at 6 hours. Aiolos and Ikaros levels partially recovered 24 hours postdosing with protein level within 20% and 34% of vehicle, respectively. The 24-hour postdose Aiolos and Ikaros expression represents the trough compound level following multiple doses of Avadomide (CC122). When the 1-hour time point is compared with the 24-hour postdose time point, there is a significant reduction in Aiolos but not Ikaros expression; however, at the 6-hour time point, both transcription factors are significantly different from the 24-hour time point. Taken together, these data reveal that Avadomide (CC122) inhibited DLBCL tumor growth in vivo and that this activity was associated with the degradation of Aiolos and Ikaros in both ABC- and GCB-DLBCL xenograft models.[1]

Clinical Trial
Molecular Weight









Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : 33.33 mg/mL (116.42 mM; Need ultrasonic)

Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 3.4930 mL 17.4648 mL 34.9296 mL
5 mM 0.6986 mL 3.4930 mL 6.9859 mL
10 mM 0.3493 mL 1.7465 mL 3.4930 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.5 mg/mL (8.73 mM); Clear solution

*All of the co-solvents are provided by MCE.
Animal Administration

Female SCID mice (CB17/Icr-Prkdcscid, Charles River) were 8 weeks old, with body weights ranging from 15.0 to 23.2 g, on day 1 of these studies. Each SCID mouse was injected subcutaneously in the right flank with 5x106 OCI-LY10 cells (0.2 ml cell suspension). Tumors were calipered in two dimensions to monitor growth as their mean volume approached 100–150 mm3 . Fourteen days (WSU-DLCL2) or twenty-one days (OCI-LY10) after tumor cell implantation, mice were sorted into treatment groups (n=10/group). Tumors were callipered twice weekly during the study. Avadomide (CC122) was suspended in 0.5% carboxymethyl cellulose: 0.25% Tween-80 in de-ionized water. Vehicle and Avadomide (CC122) were each administered via oral gavage (p.o.) once daily for twenty-eight days (qd x28). [1]

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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AvadomideCC 122CC122CC-122E1/E2/E3 EnzymeApoptosisE1 activating enzymeE2 conjugating enzymeE3 ligating enzymeUbiquitin activating enzymeUbiquitin conjugating enzymeUbiquitin ligaseorallycereblonE3ligaseantitumorimmunomodulatorydiffuselargeB-celllymphomaDLBCLInhibitorinhibitorinhibit

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