PD-1 Antibodies for in vivo use

ichorbio supplies a range of antibodies targeting PD-1 including low endotoxin antibodies and biosimilar antibodies. 

Anti-mouse PD-1 antibodies

ichorbio sells two clones that detect PD-1 – 29F.1A12 and RMP1-14. We have provided these in low endotoxin, azide and BSA free formats for in vivo research. These clones are available in bulk quantities from 5mg – 100mg.


Mouse anti-mouse PD-1 Antibody

ichorbio has created a mouse anti-mouse version of the anti-PD-1 antibody clone RMP1-14. So you get all of the benefits of using RMP1-14 for your in vivo research, with none of the drawbacks from it being a rat isotype.


Fc Silenced anti-mouse PD-1 Antibody


Anti-PD-1 Biosimilars

ichorbio supplies seven biosimilars which target PD-1 listed below.

Our biosimilar antibodies are strictly for research use only; they are not medicinal grade and therefore are not for therapeutic purposes. They are however provided in a low endotoxin format so can be used in vivo.

PD-1 Background

Inhibitory receptor on antigen activated T-cells that plays a critical role in induction and maintenance of immune tolerance to self. Delivers inhibitory signals upon binding to ligands CD274/PD-L1 and CD273/PD-L2. Following T-cell receptor (TCR) engagement, PD-1 associates with CD3-TCR in the immunological synapse and directly inhibits T-cell activation (By similarity). Suppresses T-cell activation through the recruitment of PTPN11/SHP-2: following ligand-binding, PD-1 is phosphorylated within the ITSM motif, leading to the recruitment of the protein tyrosine phosphatase PTPN11/SHP-2 that mediates dephosphorylation of key TCR proximal signaling molecules, such as ZAP70, PRKCQ/PKCtheta and CD247/CD3zeta (By similarity).

The PD-1-mediated inhibitory pathway is exploited by tumors to attenuate anti-tumor immunity and escape destruction by the immune system, thereby facilitating tumor survival. The interaction with CD274/PD-L1 inhibits cytotoxic T lymphocytes (CTLs) effector function. The blockage of the PD-1-mediated pathway results in the reversal of the exhausted T-cell phenotype and the normalization of the anti-tumor response, providing a rationale for cancer immunotherapy.