Mezigdomide is a Cereblon (CRBN) binding compound currently under clinical investigation for multiple myeloma.

SparkCures ID 307
Developed By Celgene Corporation, a wholly owned subsidiary of Bristol Myers Squibb
Generic Name Mezigdomide
Additional Names CC-92480
Treatment Classifications

Clinical Trials

All Clinical Trials

View all active clinical trials around the US.

Early Relapse Multiple Myeloma

The following is a listing of clinical trials for patients with multiple myeloma who have received one to two prior lines of therapy.

Late Relapse Multiple Myeloma

The following is a listing of clinical trials for patients with multiple myeloma who have received three or more prior lines of therapy.

Smoldering Myeloma
Monoclonal Gammopathy of Undetermined Significance (MGUS)

Published Results

Mezigdomide (MEZI) Plus Dexamethasone (DEX) and Daratumumab (DARA) or Elotuzumab (ELO) in Patients (pts) with Relapsed/Refractory Multiple Myeloma (RRMM): Results from the CC-92480-MM-002 Trial

December 11, 2023

Results: As of the May 25, 2023 data cut, 57 pts were enrolled and had received MeziDd (B1: n = 23; B2: n = 16; B3: n = 18) at the 0.3 mg or 0.6 mg dose. Median age was 67 (range, 45–83) y, median time since initial diagnosis was 8.2 (1.0–15.8) y, and median number of prior regimens was 2 (2–5). Prior therapies included stem cell transplantation (15.8%), IMiD agents (100%), PIs (98.2%), and anti-CD38 mAbs (8.8%); 82.5% of pts were refractory to IMiD agents and 61.4% to PIs. Extramedullary plasmacytomas were present in 4 (7.0%) pts.

Forty-five of 57 (78.9%) pts continued treatment; the main reason for discontinuation was progressive disease (5 pts; 8.8%).

In the safety population (n = 56), ORR was 75.0% overall, with 2 (3.6%) stringent complete responses, 8 (14.3%) complete responses, 16 (28.6%) very good partial responses, and 16 (28.6%) partial responses (Figure). Duration of response and progression-free survival data were not yet mature.

Grade (Gr) 3/4 treatment-emergent adverse events (TEAEs) occurred in 43/56 (76.8%) pts and were mostly hematologic (Table). Gr 3/4 neutropenia occurred in 30 (53.6%) pts; Gr 3/4 thrombocytopenia occurred in 4 (7.1%) pts (3/4 pts were in subcohort B1-0.6 mg) and was not associated with bleeding. Gr 3/4 infections occurred in 11 (19.6%) pts and proved manageable in all cases (Table). Non-hematologic Gr 3/4 TEAEs were low. No Gr 3/4 TE or peripheral neuropathy was observed. MEZI dose reductions were needed for 7 (30.4%) pts in subcohort B1 (1 at 0.3 mg, 6 at 0.6 mg) and 1 (5.6%) pt in subcohort B3 (at 0.6 mg). In the evaluable population (n = 35), 5 (14.3%) pts had ≥ 1 dose-limiting toxicity. The maximum tolerated dose was not reached. MeziDd had pharmacodynamically active immune stimulation in T and NK cells in all 3 schedules and both doses.

Twenty pts received MeziEd at 0.3 mg (n = 11) or 0.6 mg (n = 9); median prior lines of therapy was 3 (2–4) and 3 (2–5), and most pts (72.7% and 100%) had prior anti-CD38 mAb exposure. ORRs were 36% and 56%, respectively. The safety profile was consistent with known TEAEs and was generally well tolerated, although 2 Gr 3 pulmonary embolisms occurred.

Conclusions: MeziDd showed promising efficacy and a manageable safety profile in pts with RRMM and 2–4 prior lines of therapy, as did MeziEd in pts with prior anti-CD38 mAb therapy. The immune activity of MEZI was consistent with previous preclinical reports. Improved safety and efficacy may be achieved by schedule and dose adjustments. These results support further evaluation of MEZI plus anti-myeloma mAbs in phase 1/2 and phase 3 studies. Updated results will be presented at the meeting.