Innocare Pharma Ltd. has obtained IND approval from China’s National Medical Products Administration (NMPA) to initiate a clinical trial of the B7-H3 targeted antibody-drug conjugate.

Brightpath Biotherapeutics Co. Ltd.’s iPS cell-derived BCMA CAR-natural killer T cell therapy candidate has been awarded orphan drug designation by the FDA for the treatment of multiple myeloma.

A recent study published in the Journal for Immunotherapy of Cancer has revealed a promising new approach for the treatment of glioblastoma (GBM), an aggressive and incurable form of primary brain cancer.

A newly developed oncolytic virus, SKV-012, has demonstrated promising results in preclinical studies and a phase I clinical trial for the treatment of advanced solid tumors.

Boehringer Ingelheim Pharma GmbH & Co KG has selected a third oncology drug candidate to advance into IND-enabling studies under its ongoing collaboration with Oxford Biotherapeutics Ltd.

Aussie researchers have used CRISPR gene editing tools to “armor” chimeric antigen receptor (CAR) T cells to activate additional cancer-fighting proteins at the tumor site, enabling them to target cancer cells in solid tumors.

In a study published recently in Cancer Immunology, Immunotherapy journal, researchers from Jiangsu Province Hospital and colleagues investigated the impact of targeting the TP53-induced glycolysis and apoptosis regulator (TIGAR) on T-cell function and antitumor immunity in acute myeloid leukemia.

Researchers at Caedo Oncology AS and collaborators have recently developed a new chimeric bifunctional anti-CD47 (IgG4) fusion protein, CO-001, and its optimized variant CO-005, a bivalent humanized single-chain fragment variable-fragment crystallizable fusion protein, which exhibited potent anti-cancer activity through a dual mechanism of action.

Taiwan’s Hanchorbio Inc. is out-licensing its breakthrough checkpoint inhibitor, HCB-101, to Shanghai Henlius Biotech Inc. in a deal worth more than $200 million.

NKG2A is an inhibitory immune checkpoint receptor expressed on cytotoxic T cells and natural killer (NK) cells. Its upregulation in the tumor microenvironment (TME) contributes to the functional exhaustion of T cells, enabling tumor cells to evade immune surveillance. Therapeutic targeting of NKG2A represents a promising strategy to restore T-cell activity and enhance antitumor immunity.