Preclinical Development of the Anti-LAG-3 Antibody REGN3767: Characterization and Activity in Combination with the Anti-PD-1 Antibody Cemiplimab in Human -Knockin Mice.

In the tumor microenvironment, multiple inhibitory checkpoint receptors can suppress T-cell function, thereby enabling tumor immune evasion. Blockade of one of these checkpoint receptors, PD-1, with therapeutic antibodies has produced positive clinical responses in various cancers; however, the efficacy of this approach can be further improved. Simultaneously targeting multiple inhibitory checkpoint receptors has emerged as a promising therapeutic strategy.

Characterization of the Anti-PD-1 Antibody REGN2810 and Its Antitumor Activity in Human Knock-In Mice.

The Programmed Death-1 (PD-1) receptor delivers inhibitory checkpoint signals to activated T cells upon binding to its ligands PD-L1 and PD-L2 expressed on antigen-presenting cells and cancer cells, resulting in suppression of T-cell effector function and tumor immune evasion. Clinical antibodies blocking the interaction between PD-1 and PD-L1 restore the cytotoxic function of tumor antigen-specific T cells, yielding durable objective responses in multiple cancers. This report describes the preclinical characterization of REGN2810, a fully human hinge-stabilized IgG4(S228P) high-affinity anti-PD-1 antibody that potently blocks PD-1 interactions with PD-L1 and PD-L2.

Brugada-like electrocardiographic pattern induced by lamotrigine toxicity.

Background: Brugada syndrome, a recognized cause of sudden cardiac death, is due to a defect of cardiac sodium channels. Many pharmotherapeutic agents induce an electrocardiographic (ECG) pattern that can be confused with Brugada syndrome in patients who may not have the disease.

Case Presentation: A 22-year-old Hispanic female presented for emergency evaluation with ataxia and alterations in consciousness.