The FDA has cleared Cullinan Oncology Inc.'s IND application for CLN-978, a CD19/CD3 T-cell engaging antibody construct with a human serum albumin (HSA) binding domain to increase serum half-life.

Carina Biotech Pty Ltd. has received FDA...

Induction of immunogenic cell death (ICD) in cancer has been proposed as a promising strategy to elicit potent adaptive immune responses against tumor-associated antigens, potentially overcoming the limited efficacy of immunotherapy in some patients and tumor types. Since type I interferon (IFN) is a key modulator of ICD in antitumor responses, researchers at the University of California, San Diego are investigating how to expand the IFN effect to promote ICD responses in cancer cells.

While immune checkpoint inhibitors have revolutionized oncology, still only 20-30% of patients respond to PD-1/PD-L1 antibody monotherapy. This can be due to a failure of T cells to recognize “cold” tumors (low T-cell infiltrates).

Natural killer (NK) cells are key players in antitumor immunity and can directly eliminate tumor cells without prior sensitization.

TANK-binding kinase 1 (TBK1) is a multifunctional serine/threonine kinase with an established role coordinating innate immune responses, and it has been previously identified as a candidate immune evasion gene. Additionally, disrupting TBK1 signaling has shown potential for enhancing response to immunotherapy with immune checkpoint blockade (ICB) in murine tumor models.

Immunotherapy, a treatment that increases the survival of cancer patients to the point of remission of the disease, can also have the opposite effect. In some patients, immune checkpoint blockade accelerates cancer. Now, researchers at the University of Michigan Medical School have discovered that the answer to this hyperprogressive disease (HPD) lies in the interconnection of the molecular pathways of interferon signaling (IFNγ), fibroblast growth factor 2 (FGF2) and the β-catenin protein.