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Atara Biotherapeutics, Inc (Symbol: ATRA) is a pioneering company in the healthcare sector, specializing in the development of transformative therapies for patients combating serious diseases, including cancer, kidney disease, and autoimmune disorders. Founded in August 2012, Atara Biotherapeutics is driven by a mission to provide better treatment options for patients, inspired by Atara Ciechanover, who tragically passed away from cancer in 2012.
The company's research is founded on groundbreaking discoveries related to activin, myostatin, and other growth factors that can alter disease progression. Atara's innovative approach has led to the development of several promising product candidates:
- Pinta 745
- STM 434
- ATA 842
Moreover, Atara Biotherapeutics is collaborating with the prestigious Memorial Sloan Kettering Cancer Center (MSK) to develop three cutting-edge T-cell product candidates:
- Epstein-Barr Virus (EBV)-targeted Cytotoxic T Lymphocytes (CTLs)
- Cytomegalovirus (CMV)-targeted CTLs
- Wilms Tumor 1 (WT1)-targeted CTLs
These T-cell therapies are designed to tackle the underlying mechanisms of various diseases, offering hope for conditions that are currently challenging to treat.
Atara's product pipeline also includes Tab-cel, ATA188, and ATA3219 (CAR T platform). Each of these candidates targets specific mechanisms of disease, aiming to provide effective and innovative treatment solutions.
The company operates within the US healthcare sector, managing its business as a single operating and reportable segment focused on therapeutic development. Atara Biotherapeutics continues to make strides in its mission, marked by recent achievements and partnerships that underscore its commitment to improving patient outcomes.
Stay updated with the latest news and developments from Atara Biotherapeutics to gain insights into their ongoing projects and performance in the stock market.
Atara Biotherapeutics has announced promising preclinical data for ATA3219, an allogeneic CD19-targeted CAR T therapy aimed at treating B-cell driven autoimmune diseases such as systemic lupus erythematosus (SLE) and multiple sclerosis (MS). The data, to be presented at the ISCT 2024 Annual Meeting, show that ATA3219 effectively depletes CD19+ B-cells and induces lower levels of pro-inflammatory cytokines compared to autologous CD19 CAR T cells.
ATA3219 incorporates multiple clinically validated technologies, including a modified CD3ζ signaling domain and a less differentiated phenotype. A Phase 1 clinical trial for lupus nephritis (LN) and severe SLE without lymphodepletion is expected to begin in Q4 2024, with initial data anticipated in 2025.
Atara Biotherapeutics has submitted a Biologics License Application (BLA) to the U.S. FDA for tabelecleucel (tab-cel®), targeting Epstein-Barr virus positive post-transplant lymphoproliferative disease (EBV+ PTLD) in patients aged two and older.
This marks the first allogeneic T-cell therapy BLA submission for the FDA. If approved, tab-cel would be the first FDA-approved therapy for EBV+ PTLD, potentially triggering milestone payments of up to $80 million from Pierre Fabre Laboratories.
Supported by data from over 430 patients, including a 48.8% Objective Response Rate from the ALLELE study, tab-cel has shown a favorable safety profile. The BLA submission is part of a broader global partnership with Pierre Fabre, which includes double-digit tiered royalties on net sales and reimbursement for development costs.
Atara Biotherapeutics announced its first-quarter 2024 financial results and operational progress, highlighting key advancements in its lead CAR T program, ATA3219, for oncology and autoimmune diseases. The company plans to submit a BLA for tab-cel in Q2 2024 and initiate studies for lupus nephritis and non-Hodgkin’s lymphoma. Atara's cash runway extends into 2027, enabling key pipeline readouts.
Atara Biotherapeutics, Inc. granted 4,150 restricted stock units to a newly hired employee under the Nasdaq Listing Rule 5635(c)(4). The stock units vest over four years, subject to continuous employment.
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