product candidates


PRV-3279 is a humanized diabody (a bispecific scaffold biologic molecule) targeting the B-cell surface proteins, CD32B and CD79B.  Simultaneous engagement of the CD32B and CD79B receptors triggers inhibition of B cell function and suppression of autoantibody production, thereby regulating B cells without causing depletion.   

We are initially developing PRV-3279 for the interception of systemic lupus erythematosus (SLE), a chronic autoimmune disorder characterized by an abnormal overactivation of B cells and subsequent pathologic production of auto-antibodies.

PRV-3279 also has the potential to address a wide variety of other autoimmune conditions where B cells play a role, from large indications such as rheumatoid arthritis and multiple sclerosis, to orphan diseases such as idiopathic thrombocytopenic purpura, neuromyelitis optica, pemphigus or myasthenia gravis.

Additionally, we are developing PRV-3279 to prevent or reduce the immunogenicity of biotherapeutics, including but not limited to gene therapy vectors and transgenes.

Provention plans to initiate the Phase 2a portion of its PREVAIL (PRV-3279 EVAluation In Lupus) study evaluating PRV-3279 in lupus patients in 2021. Additional information on the clinical trial is available at (Number NCT03955666).

SLE Interception

Peer-Reviewed Publications

Doerfler et al. Targeted approaches to induce immune tolerance for Pompe disease therapy. Molecular Therapy – Methods & Clinical Development. (2016) 3, 15053.

Franks SE et al. Targeting B cells in treatment of autoimmunity. Curr Opin Immunol. 2016 Dec;43:39-45.

Veri MC et al. Therapeutic control of B cell activation via recruitment of Fcgamma receptor IIb (CD32B) inhibitory function with a novel bispecific antibody scaffold. Arthritis Rheum. 2010;62(7):1933-1943.

Su K et al. Expression profile of FcgammaRIIb on leukocytes and its dysregulation in systemic lupus erythematosus. J Immunol. 2007 Mar 1;178(5):3272-3280.