Pep(1)

Pep(1) is a synthetic peptide derived from the N-terminal sequence (residues 1-23) of the Herpes Simplex Virus (HSV) glycoprotein D (gD). It is designed to function as an immune checkpoint inhibitor by targeting the Herpesvirus Entry Mediator (HVEM), a member of the tumor necrosis factor receptor (TNFR) superfamily. Pep(1) competitively binds to HVEM at the same interface as the B and T Lymphocyte Attenuator (BTLA), thereby disrupting the formation of the inhibitory BTLA-HVEM complex. This interaction is a known mechanism of tumor immune escape, particularly in melanoma, where it suppresses T cell effector functions. By blocking this inhibitory signal, Pep(1) aims to restore and enhance T cell activation, proliferation, and the production of pro-inflammatory cytokines such as interferon-gamma (IFN-γ) and interleukin-2 (IL-2). The peptide has been investigated in ex vivo studies using samples from melanoma patients to evaluate its immunomodulatory potential.

Other names

gD(1-23)gD-derived peptide 1