Preferred Label : Oncolytic Type 2 Herpes Simplex Virus Expressing Anti-PD-L1/CD3 Bispecific Antibody
BS-006;
NCIt synonyms : Recombinant Oncolytic Type II Herpes Simplex Virus BS-006; Oncolytic HSV-2 Expressing PD-L1 x CD3 Bispecific Antibody BS-006; Recombinant Oncolytic Type II HSV BS-006; Oncolytic HSV-2 Expressing Anti-PD-L1/CD3 Bispecific Antibody BS-006; Oncolytic HSV-2 Expressing Anti-PD-L1/Anti-CD3 Bispecific T Cell Engager BS-006;
NCIt definition : A genetically engineered, ICP34.5- and ICP47-deleted oncolytic human herpes simplex
virus type 2 (HSV-2), derived from the HG52 strain and encoding a bispecific antibody
directed against the immunosuppressive ligand and immune checkpoint inhibitor programmed
cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and the T-cell
surface antigen CD3, with potential oncolytic, immunostimulating and antineoplastic
activities. Upon administration, oncolytic HSV-2 expressing anti-PD-L1/CD3 bispecific
antibody BS-006 selectively infects and replicates in tumor cells, thereby inducing
tumor cell lysis. In addition, BS-006 promotes the secretion of anti-PD-L1/CD3 bispecific
antibody by the infected tumor cells. The bispecific antibody targets and binds to
both the CD3 on T-cells and the PD-L1 expressed on tumor cells. This results in the
cross-linking of T-cells and tumor cells and may induce a cytotoxic T-lymphocyte (CTL)-mediated
immune response against PD-L1-expressing tumor cells. At the same time, BS-006 prevents
PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1;
PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific
T-lymphocytes and enhances CTL-mediated tumor cell lysis, which may further lead to
a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the
expansion and survival of CD8-positive T-cells, suppresses the immune system and results
in immune evasion. Deletion of the gene encoding for ICP34.5 provides tumor selectivity
and prevents replication in healthy cells. As ICP47 blocks antigen presentation in
HSV-infected cells, deletion of this gene may induce a more potent antitumor immune
response in the tumor cells. Deletion of ICP47 also leads to an increased expression
of the HSV US11 gene and allows US11 to be expressed as an immediate early and not
a late gene. This further enhances the degree of viral replication and the oncolysis
of tumor cells.;
Molecule name : BS-006; BS 006;
NCI Metathesaurus CUI : CL1792787;
Origin ID : C188176;
UMLS CUI : C5706458;
Semantic type(s)
- concept_is_in_subset
