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Immune checkpoint antibody panels

Related

  • Immuno-oncology resources
    • PD-L1 clone comparison
      • PD-L1 protocols for automated IHC
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              • Immunochemotherapy: The future of cancer treatment webinar

                Increase your chances of success and do more with your screening​.

                ​Immune checkpoints are critical molecules that modulate the T-cell-stimulatory signals of the immune response1. 

                ​Our immune checkpoint panels are designed to take the legwork out of assay development. With easy access to the best selection of clones on the market for your target in a single kit, you can skip pre-screening and progress your research faster with greater confidence of high-quality outcomes. 

                Multiple clones. Multiple opportunities. One purchase. ​  

                Immune checkpoint studies provide a wealth of information for the development of novel therapeutic strategies that can dramatically improve cancer management. 

                We’re here to take care of the antibody screening and selection that this crucial work demands. To save you time, our team of immuno-oncology experts has hand-picked high-performing checkpoint antibodies from our extensive catalog and assembled them into convenient panels. 

                Each of our immune checkpoint panels contains a selection of extensively validated recombinant monoclonal antibodies that detect the same target protein so that you can maximize your chances of finding the most-suitable IHC-optimized clone for your assay - with just one purchase. 


                Select your target


                We work in close partnership with our network of experts to continually expand our range of immune checkpoint panels to include new and emerging targets in key research areas. 



                280x200-CMS-PDL1-4.png​

                PD-L1

                The PD-1/PD-L1 pathway plays a key role in physiological immune homeostasis and provide a means through which cancer can evade the immune system. The development and application of immune checkpoint inhibitors that block PD-1/PD-L1 interaction result in very durable responses in a wide range of cancers and prolong survival in a subset of patients2.

                Our PD-L1 antibody panel contains four recombinant monoclonal antibodies to human PD-L1 including highly cited and best-in-class clones 28-8, SP142, and 73-10. 

                280x200-CMS-PDL1-5.png

                PD-1

                PD-1 is the receptor to transmembrane ligand PD-L1 and is expressed on the surface of T-cells. Cancer cells may exploit the PD-1/PD-L1 interaction to evade and suppress the immune response. Inhibition of the PD-1 pathway is increasingly being adopted as a therapeutic approach to treat cancers3.

                Our PD-1 antibody panel contains five monoclonal antibodies to human PD-1 including the top-cited NAT105 clone. 

                ​​280x200-CMS-Image-TIM-3.png​​

                TIM-3

                Recent studies have highlighted that TIM-3 has an important role to play in T-cell exhaustion and correlates with the outcome of anti-PD-1 therapy. Findings like these have heightened interest in TIM-3 as a target for cancer immunotherapy​4.

                Our TIM-3 antibody panel contains three recombinant monoclonal antibodies against human TIM-3. 


                280x200-CMS-Image-LAG-3.png​​

                LAG-3

                LAG-3 ensures immune homeostasis through suppressing T-cell activation and cytokine secretion. Right now, immunotherapies targeting LAG-3 are moving forward into clinical trials. Meanwhile, combination immunotherapy of anti-LAG-3 and anti-PD-1 is showing promising efficacy in overcoming resistance to PD-1 immunotherapy​5.

                Our LAG-3 antibody panel contains six recombinant monoclonal antibodies to human LAG-3. 


                280x200-CMS-GITR (003).png​

                GITR

                GITR is a co-stimulatory cell surface receptor expressed by T-cells and natural killer cells. In preclinical models, GITR modulation has shown promising antitumor activity by stimulating effector T-cells and suppressing regulatory T-cells​6.

                Our GITR antibody panel contains three recombinant monoclonal antibodies to human GITR. 

                ​​

                Ongoing support


                If you can’t find the target you’re looking for, we’d be happy to work with you to develop a custom solution or custom IHC panel.  

                Once you’ve established the best clone for your assay, our team of friendly experts is here to support you with everything you need for your checkpoint-blocking antibodies–from flexible formats and scale-up options to custom conjugations and personalized clone recommendations based on your specific research needs or technologies of interest.  

                View our full range of antibody panels.

                Speak to one of our specialists today.

                References

                1. Zhao, X. and Subramanian, S. Intrinsic Resistance of Solid Tumors to Immune Checkpoint Blockade Therapy​. Cancer Research. (2017). 

                2. Akinleye, A., Rasool, Z. Immune checkpoint inhibitors of PD-L1 as cancer therapeutics. J Hematol Oncol 12, 92 (2019). 

                3. Rizvi, Naiyer A et al. “Activity and safety of nivolumab, an anti-PD-1 immune checkpoint inhibitor, for patients with advanced, refractory squamous non-small-cell lung cancer (CheckMate 063): a phase 2, single-arm trial.” The Lancet. Oncology vol. 16,3 (2015): 257-65. 

                4. He, Yayi et al. TIM-3, a promising target for cancer immunotherapy. OncoTargets and therapy vol. 11 7005-7009. (2018). 

                5. Long L, Zhang X, Chen F, et al. The promising immune checkpoint LAG-3: from tumor microenvironment to cancer immunotherapy. Genes Cancer. 2018;9(5-6):176–189.  

                6. Marin-Acevedo JA, Dholaria B, Soyano AE, Knutson KL, Chumsri S, Lou Y. Next generation of immune checkpoint therapy in cancer: new developments and challenges. J Hematol Oncol. 2018;11(1):39.  






                ​​




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