This product is an unconjugated, non-therapeutic research-grade biosimilar of cobolimab (also known as TSR-022 / GSK4069889), an anti-TIM-3 monoclonal antibody built around the HAVCR2 target. It reproduces the human IgG4-kappa framework of the originator molecule and is intended purely as a research tool, not for clinical or diagnostic use. Cobolimab was developed as an immune checkpoint inhibitor and has been studied in oncology, most notably in combination with the anti-PD-1 antibody dostarlimab in advanced solid tumours and non-small cell lung cancer. As a research-grade biosimilar it is supplied unconjugated for functional and in-vitro work such as target-binding characterisation, blockade and neutralisation assays, and use as a reference or comparator standard. It is manufactured to low-endotoxin research specifications and is available at bulk scale, making it suitable for assay development and comparability studies where a consistent, well-characterised anti-TIM-3 reagent is required. Because the intended target is human TIM-3, this analog is oriented toward human-system in-vitro applications rather than routine mouse in-vivo dosing. Guidance provided here is for ichor.bio to review.
HAVCR2 (hepatitis A virus cellular receptor 2), better known as TIM-3 or CD366, is an inhibitory immune checkpoint receptor of the TIM family. It is expressed on activated CD4 and CD8 T cells, regulatory T cells, NK cells, and antigen-presenting cells such as dendritic cells and macrophages. TIM-3 engages a broad set of ligands, including galectin-9, phosphatidylserine, CEACAM1, and HMGB1, and signalling through these interactions negatively regulates T cell responses, promoting tolerance, T cell exhaustion, and immune evasion. In chronic antigen settings such as cancer and persistent viral infection, terminally exhausted T cells characteristically co-express TIM-3 with PD-1. Because it marks and enforces this dysfunctional state, TIM-3 is an actively pursued target for checkpoint-blockade immunotherapy, frequently in combination with PD-1/PD-L1 axis inhibition.