Atara Biotherapeutics

Discussion in 'Men's Economics' started by Michael Scally MD, Jun 20, 2014.

  1. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Atara Biotherapeutics, an early-stage biotech targeting muscle loss in patients with end-stage renal disease, filed on Friday with the SEC to raise up to $50 million in an initial public offering. http://www.atarabio.com/

    The company lists Celgene (CELG) and Amgen (AMGN) among its primary shareholders.

    The Brisbane, CA-based company, which was founded in 2012, plans to list on the NASDAQ under the symbol ATRA.

    ATA 842 is a fully human antibody that binds to the growth factor myostatin and blocks its signal. ATA 842 is being studied to test if it can reverse cachexia in cancer patients. It may also have a role in other conditions where reversing weight loss has the potential to improve functional status and outcomes.

    Han HQ, Mitch WE. Targeting the myostatin signaling pathway to treat muscle wasting diseases. Current opinion in supportive and palliative care. 2011;5 (4):334-41. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3273421/

    Roth SM, Walsh S. Myostatin: A therapeutic target for skeletal muscle wasting. Current opinion in clinical nutrition and metabolic care. 2004;7 (3):259-63. http://www.ncbi.nlm.nih.gov/pubmed/15075916
     
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  2. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    [Fail] Atara Bio Announces Results From the Phase 2 Proof-of-Concept PINTA 745 Clinical Trial for Protein Energy Wasting in Patients With End Stage Renal Disease
    Atara Bio Announces Results From the Phase 2 Proof-of-Concept PINTA 745 Clinical Trial for Protein Energy Wasting in Patients With End Stage Renal Disease

    PINTA 745 is a peptibody, a peptide-antibody combination that binds to and blocks growth factors in the TGF-β pathway.

    Atara Biotherapeutics, Inc. (ATRA) today announced results from its Phase 2 proof-of-concept clinical trial for PINTA 745 for the treatment of protein energy wasting (PEW) in patients with end stage renal disease (ESRD).

    The trial did NOT meet its primary endpoint, defined as the percent change from baseline in Lean Body Mass (LBM) as measured by Dual Energy X-Ray Absorptiometry (DXA) at week 12 following weekly treatment with PINTA 745.

    PINTA 745 also did not improve physical function, measures of glycemic control and markers of inflammation. There were no treatment related serious adverse events observed in the trial.
     
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  3. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    [Open Access] Anti-Myostatin Antibody Increases Muscle Mass and Strength and Improves Insulin Sensitivity in Old Mice

    [Conflict of interest statement: These studies were funded in part by an investigator initiated grant to Kitt Falk Petersena from Atara Biotherapeutics, the manufacturer of ATA 842. Glenn Friedmand and Christopher M. Haqqd are employees of Atara and may own stock in the company.]

    Sarcopenia, or skeletal muscle atrophy, is a debilitating comorbidity of many physiological and pathophysiological processes, including normal aging.

    There are no approved therapies for sarcopenia, but the antihypertrophic myokine myostatin is a potential therapeutic target.

    Here, we show that treatment of young and old mice with an anti-myostatin antibody (ATA 842) for 4 wk increased muscle mass and muscle strength in both groups.

    Furthermore, ATA 842 treatment also increased insulin-stimulated whole body glucose metabolism in old mice, which could be attributed to increased insulin-stimulated skeletal muscle glucose uptake as measured by a hyperinsulinemic-euglycemic clamp.

    Taken together, these studies provide support for pharmacological inhibition of myostatin as a potential therapeutic approach for age-related sarcopenia and metabolic disease.

    Camporez JG, Petersen MC, Abudukadier A, et al. Anti-myostatin antibody increases muscle mass and strength and improves insulin sensitivity in old mice. Proc Natl Acad Sci U S A. http://www.pnas.org/content/early/2016/02/04/1525795113.full.pdf