The tumor suppressor p53 is a transcription factor that prevents cancer development and is involved in regulation of various physiological processes. This is mediated both by induction of cell cycle arrest and apoptosis and by controlling the expression of a plethora of target genes, including secreted proteins.

Despite clear evidence demonstrating that the deletion of Nogo-receptor 1 (NgR1) can protect against axonal degeneration and thus progression of experimental autoimmune encephalomyelitis (EAE), an immunological role for this receptor is yet to yield mechanistic evidence. However, recently NgR has been suggested as an alternate receptor for the B-cell activating factor (BAFF) in the central nervous system (CNS).

Mutation in the p53 gene is a frequent alteration in human cancers which mostly leads to the acquiring of new oncogenic functions that promote tumorigenesis. In this study, we observed that bone marrow derived from mutant p53 mice exhibit higher ability to form tumors compared to WT-MSCs.

Interleukin-1 (IL-1), a central mediator of innate immunity and inflammation, plays a pivotal role in a broad spectrum of inflammatory diseases. RPH-104 is a novel IL-1 antagonist: a heterodimer comprised of human extracellular portions of IL-1RI and IL-1 receptor accessory protein, each linked to a mutant Fc portion of human IgG1. Aim: The aim of the studies is preclinical characterization of RPH-104.

Vanadium is a grey metal, with different states of oxidation (-1, 0, +2, +3, +4, and +5), and its most common form in commercial products is vanadium pentoxide (V2O5).