Mouse Immune CheckPoint Antibody Panel (ICH9002-7abs)

Please refer to the specific buffer information in the hardcopy of datasheet or the lot-specific COA.

The Mouse Immune Checkpoint Antibody Panel (ICH9002) is a curated collection of in-vivo grade research antibodies assembled for syngeneic mouse tumour immunology and immune-modulation studies. Rather than a single product, it bundles well-characterised clones against the principal checkpoint and costimulatory targets under investigation in cancer immunotherapy research: PD-1, PD-L1, CTLA-4, TIGIT, LAG-3 and 4-1BB as standard, with TIM-3 and GITR available as add-ons. The panel spans two complementary pharmacologies, inhibitory-pathway blockers and costimulatory agonists, allowing researchers to interrogate single agents, combinations and mechanistic controls within one consistent, quality-matched set. Like ichor.bio's other in-vivo antibodies, panel members are supplied at research-grade low endotoxin, purified, and in bulk quantities suitable for repeat dosing across treatment cohorts. Because every antibody is mouse-reactive, the panel is intended for immunocompetent mouse models where an intact immune system is required to read out checkpoint or agonist activity. Supplying clones from a single vendor helps standardise lot quality, formulation and endotoxin specification across a combination study, reducing a common source of inter-reagent variability. The panel targets the core nodes of T-cell regulation. PD-1 (with ligand PD-L1), CTLA-4, TIGIT, LAG-3 and TIM-3 are inhibitory ("checkpoint") receptors that dampen T-cell activation; tumours exploit these axes to evade immune attack, and blocking them can restore anti-tumour T-cell responses. PD-1 and CTLA-4 act at distinct stages, CTLA-4 during priming in lymphoid tissue, PD-1 at the effector phase in tissue, while TIGIT, LAG-3 and TIM-3 mark and enforce deeper T-cell exhaustion, making them combination targets. In contrast, 4-1BB (CD137) and GITR are costimulatory TNF-receptor-superfamily members whose agonism amplifies effector T-cell expansion, survival and, for GITR, modulation of regulatory T cells. Together these targets let researchers dissect both the release of inhibitory brakes and the engagement of activating accelerators that govern productive anti-tumour immunity.