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 (BCMA) 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.
| SparkCures ID | 340 |
|---|---|
| Developed By | AbbVie |
| Generic Name | ABBV-383 |
| Additional Names | TNB-383B |
| Treatment Classifications | |
| Treatment Targets |
View all active clinical trials around the US.
The following is a listing of clinical trials for patients with multiple myeloma who have received one to two prior lines of therapy.
The following is a listing of clinical trials for patients with multiple myeloma who have received three or more prior lines of therapy.
May 29, 2024
As of May 2023, 220 pts received ABBV-383 (median age: 68 yr [35–92]; median prior therapy lines: 5 [3‒23]). Median FU was 4.1 mo (0.8–5.2) at 60mg Q4W (n=21), 12.2 mo (1.3–34.4) at 40mg Q3W (n=55), and 24.2 mo (0.6–33.4) at 60mg Q3W (n=61). At 60mg Q4W, with the modified premedication regimen, CRS was reported in 43% of pts (38% G1, 5% G2), and ICANS in 5% of pts (G2). In Q3W cohorts, CRS was reported in 71% (40mg; 45% G1, 25% G2) and 70% (60mg; 51% G1, 18% G2, 2% G3) of pts. The incidence of G3/4 neutropenia, anemia, and thrombocytopenia was 14/24/10% at 60mg Q4W, 31/31/16% at 40mg Q3W, and 34/13/13% at 60mg Q3W. G3/4 infections occurred in 10/24/34% of pts at 60mg Q4W, 40mg and 60mg Q3W, respectively. ORR and ≥VGPR were 65/50% at 60mg Q4W, 64/53% at 40mg Q3W, and 60/52% at 60mg Q3W. Corresponding exposure-response (ER) analyses and correlative analyses further supported RP2D determination (separate abstract submissions).
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