Peptide-drug conjugates (PDCs) are emerging as a promising alternative to antibody-drug conjugates (ADCs), offering enhanced tumor penetration and reduced immunogenicity. Carbonic anhydrase IX (CAIX) and epidermal growth factor receptor (EGFR) are both well-validated targets in oncology due to their role in cancer cell survival, invasion and migration.
Mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) is an important factor from a complex downstream of Bruton tyrosine kinase (BTK) in the B-cell receptor (BCR) signaling pathway.
Minerva Biotechnologies Corp. recently released details on their work to develop a treatment for HER2-positive patients who have acquired resistance to Herceptin (trastuzumab) or Enhertu (trastuzumab-deruxtecan).
Acute myeloid leukemia (AML) harboring KMT2A rearrangements (KMT2A-r) represents a highly aggressive disease subtype, characterized by poor therapeutic response and a high risk of relapse.
DNA damage repair enzymes are interesting targets in cancer, since genomic instability and DNA repair defects are important cancer cell hallmarks. Poly (ADP-ribose) glycohydrolase (PARG) is the dominant eliminator of PARylation in the cell, the activity of which prevents excessive accumulation of PARylation, and promotes the dissociation of repair proteins, as well as ensuring the smooth completion of DNA repair process.
Werner syndrome ATP-dependent helicase (WRN) is an enzyme involved in DNA replication and repair and has been identified as a synthetic lethality target in tumors with high microsatellite instability (MSI-H).
CCR8 is highly expressed on immunosuppressive regulatory T cells (Tregs) in various solid tumors, making it a potential target to enhance antitumor immunity and the efficacy of cancer therapies, including checkpoint inhibitors. However, the impact of CCR8 expression on the Treg phenotype and its role in cancer progression remain unclear.
Current anticancer approaches, such as antibody or CAR T-cell therapies, rely on targeting tumor-associated antigens rather than tumor-specific antigens, with the consequent on-target, off-tumor effects.