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.

SparkCures ID 340
Developed By AbbVie
Generic Name ABBV-383
Additional Names TNB-383B
Treatment Classifications
Treatment Targets

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

A Phase 1 First-in-Human Study of Tnb-383B, a BCMA x CD3 Bispecific T-Cell Redirecting Antibody, in Patients with Relapsed/Refractory Multiple Myeloma

December 13, 2021

As of 10 May 2021, 103 pts (dose escalation, n=73; dose expansion, n=30) have been treated with TNB-383B (0.025–120 mg). The RP2D of 60 mg Q3W was selected on the basis of tolerability, safety, PK, and clinical activity. Pt demographics and baseline characteristics are summarized in Table 1. Three dose-limiting toxicities were reported in dose escalation (platelet count decreased: grade [Gr] 4, 60 mg; cytokine release syndrome [CRS]: Gr 3, 90 mg and 120 mg); none were reported as serious.

Treatment-related AEs (TRAEs) were reported in 79 (77%) pts, with Gr ≥3 and serious AEs occurring in 33 (32%) and 23 (22%) pts, respectively. The most common TRAEs (Table 2) include CRS (n=54, 52%), neutropenia (n=18, 17%), and fatigue (n=14, 14%). At the RP2D (n=39), the Gr ≥3 CRS rate was 3% (n=1). Onset of CRS typically occurred on the same or next day following the first dose and all pts recovered using tocilizumab or standard supportive care measures. Treatment-emergent AEs (TEAEs) of infusion-related reactions were reported in 8 (8%) pts and infections occurred in 29 (28%) pts; pneumonia (n=5, 5%) and upper respiratory tract infection (n=4, 4%) were the most common. Five deaths from TEAEs were reported; all were unrelated to study drug. Forty-two (40%) pts discontinued treatment due to disease progression.

In the dose-escalation cohorts of ≥40 mg Q3W (n=24), the objective response rate (ORR) was 79% (19/24), with a very good partial response or better (≥VGPR) rate of 63% (15/24), and a complete response (CR) rate of 29% (7/24) at the data cutoff date; these pts have the longest follow-up (ie, mature data) with median time on study of 6.1 months (Figure 1). At doses ≥40 mg in the combined dose-escalation and -expansion cohorts (n=44), the observed ORR, ≥VGPR, and CR rates were 64% (28/44), 43% (19/44), and 16% (7/44), respectively; these pts have shorter follow-up (ie, immature data) with median time on study of 3.1 months. Twenty-nine (66%) of the 44 pts administered ≥40 mg were triple-class refractory and reported an ORR of 55% (16/29).


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