ABBV-383 is a type of drug known as an immunotherapeutic drug. Immunotherapy is a form of cancer treatment that uses the immune system to attack cancer cells, similar to the way it attacks bacteria or viruses. This type of therapy works by activating immune cells circulating in your body. Simply put, immunotherapy is a tool to trigger your body to treat the cancer itself. ABBV-383 has been developed in a laboratory to make powerful ‘killer’ T-cells from your own immune system attack multiple myeloma cells in your body.
ABBV-383 is a ‘bispecific’ antibody, meaning that it interacts with two molecules in your body. One molecule is called B-Cell Maturation Antigen (BMCA) and is found on your multiple myeloma cells. The second is called CD3 and is present on your killer T-cells. When CD3 is engaged on a T cell, it turns the T-cell on and makes it kill whatever cell triggered the activation. Because ABBV-383 sticks very strongly to your myeloma cells, nearby T-cells should specifically attack your tumor cells.
View all active clinical trials around the US.
The following is a listing of clinical trials for patients with multiple myeloma who have received three or more prior lines of therapy.
January 08, 2022
As of 8 Jan 2022, 124 pts were treated: 73 pts in ESC (0.25–120 mg; 40mg, n=6; 60mg, n=9) and 51 pts in EXP at 60 mg. Pts in 40mg ESC (n=6) and 60mg ESC+EXP cohorts (n=60) had a median age of 64 (range 56-76) and 68 years (range 35-92), received 4 (range 3-10) and 5 (range 3-12) prior lines of therapy, and 67% and 83% of pts were triple refractory, respectively. Pt demographics and baseline characteristics are shown in Table 1. Median follow-up was 17.4 and 8.4 months in 40mg ESC and 60mg ESC+EXP cohorts, with 50% and 45% continuing Tx, respectively. All 3 pts in 40mg ESC cohort and 23 of 33 pts in 60mg ESC+EXP cohort discontinued Tx due to PD.
Tx-emergent AEs (TEAE) were reported in 100% (50% grade [G]≥3) of pts in 40mg ESC cohort (n=6) and 98% (78% G≥3) of pts in 60mg ESC+EXP cohort (n=60), with 0 and 1 DLT-associated TEAE, and AE-led study drug discontinuation in 0% and 5% pts, respectively. CRS occurred in 83% (0% G≥3) of pts receiving 40mg in ESC and 72% (2% G≥3) of pts receiving 60mg in ESC+EXP. Infections occurred in 50% (17% G≥3) of 40mg ESC cohort and 43% (22% G≥3) of 60mg ESC+EXP cohort. In 40mg ESC and 60mg ESC+EXP cohorts, the incidence of neutropenia was 67% (67% G≥3) and 40% (35% G≥3), anemia was 33% (17% G≥3) and 32% (12% G≥3), and thrombocytopenia was 33% (0% G≥3) and 25% (12% G≥3), respectively.
Clinical response for all pts (N=122), 40mg ESC (n=6), and 60mg ESC+EXP cohorts (n=58) is shown in Figure 1. In the triple-refractory subpopulation of 40mg ESC cohort (n=4), ORR was 75% with rates of complete response + stringent complete response (≥CR) and very good partial response or better (≥VGPR) of 50% and 75%, respectively. An ORR of 54%, ≥CR of 29%, and ≥VGPR of 40% was observed in the triple-refractory subpopulation of 60mg ESC+EXP cohort (n=48). Median DOR and PFS, analyzed by Kaplan-Meier method, were not reached (NR) in any cohort.