Human Immune CheckPoint Antibody panel (ICH9001-8abs)

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

The Human Immune Checkpoint Antibody Panel (ICH9001) is a curated set of unconjugated, non-therapeutic research analogs built around the antibody sequences of clinically established immune checkpoint modulators. The standard panel covers the PD-1, PD-L1, CTLA-4, TIGIT, LAG-3 and 4-1BB axes, with TIM-3 and GITR members available as add-ons. Each analog reproduces the target specificity and human isotype framework of its originator (for example an IgG4 kappa PD-1 binder, IgG1 kappa PD-L1 and CTLA-4 binders, IgG4 S228P kappa LAG-3 and TIM-3 binders), enabling side-by-side benchmarking across the most studied checkpoint pathways in a single, format-consistent reagent set. These are supplied as research-use-only analogs for functional and in-vitro work, not as clinical drugs. Like other ichor.bio in-vivo-grade reagents, the antibodies are produced to low-endotoxin research specifications and are available at bulk milligram-to-gram scale, supporting assay standardization, positive/comparator controls, and multiplexed pathway studies where several checkpoints must be interrogated under matched experimental conditions. Immune checkpoints are receptor-ligand systems that tune T-cell activation. PD-1 and its ligand PD-L1 deliver inhibitory signals that dampen effector responses and are co-opted by tumors for immune escape; CTLA-4 competes with CD28 for B7 ligands to restrain early T-cell priming. TIGIT and LAG-3 are additional co-inhibitory receptors that limit T-cell and NK activity, while TIM-3 marks and regulates exhausted or dysfunctional T cells. In contrast, 4-1BB (CD137) and GITR are co-stimulatory TNF-receptor-family members whose engagement amplifies T-cell proliferation, survival and effector function. Together these pathways form the balance between activation and tolerance that checkpoint therapeutics manipulate. This panel spans both inhibitory (blocking) and co-stimulatory (agonist) nodes, allowing researchers to probe how simultaneous or comparative modulation of multiple checkpoints shapes antitumor immunity in controlled experimental systems.