Blisibimod for treatment of systemic lupus erythematosus: with trials you become wiser

• Published in: Expert opinion on biological therapy Vol. 16; no. 5; p. 723
• Main Authors: Scheinberg, Morton A, Hislop, Colin M, Martin, Renee S
• Format: Journal Article
• Language: English
• Published: England 03-05-2016
• Subjects: B-Cell Activating Factor - antagonists & inhibitors; Clinical Trials as Topic; Glomerulonephritis, IGA - drug therapy; Humans; Lupus Erythematosus, Systemic - drug therapy; Recombinant Fusion Proteins - pharmacokinetics; Recombinant Fusion Proteins - pharmacology; Recombinant Fusion Proteins - therapeutic use; B lymphocyte; BAFF; systemic lupus erythematosus; IgA nephropathy
• ISSN: 1744-7682
• DOI: 10.1517/14712598.2016.1169270

Blisibimod is a potent and selective inhibitor of B cell activating factor (BAFF), a mediator of differentiation, maturation and survival of B cells. It has a unique tetravalent, 'peptibody' structure and resulting high potency, and is currently in clinical evaluation for the treatment of SLE. The importance of BAFF in the pathogenesis of systemic lupus erythematosus (SLE) is under intense investigation. The anti BAFF monoclonal antibody belimumab was approved by the FDA for the treatment of SLE.
The general properties of blisibimod are reviewed including pharmacokinetic and pharmacodynamic properties in patients with SLE, efficacy and safety in the phase 2 PEARL-SC and open-label extension trials, and the focus in the ongoing phase 3 trial (CHABLIS-SC1) on the hypothesized 'responder' population. In addition, the rationale for evaluating blisibimod in patients with IgA nephropathy, a common nephritic disease for which there is no approved therapy, is presented.
Blisibimod's unique tetravalent, peptibody structure and resulting high potency, and the deliberate focus of the Phase 3 clinical development program on the 'responder populations' identified in completed trials in SLE raise the possibility that blisibimod will become an important medication for treatment of SLE and IgA nephropathy.