Stimulator of interferon genes (STING) is a component of the innate immune response that binds to cyclic dinucleotides (CDNs), which are bacterial second messengers, leading to activation of NF-κB and transcription of immunomodulatory genes, including type I interferon (IFN).1,2,3,4 The C-terminal region of STING binds to CDNs, such as cyclic di-GMP (c-di-GMP; Item No. 17144) in the cytoplasm at a ratio of two STING molecules to one c-di-GMP.4,5 Mutations in the C-terminal region modify the activity of STING in a variety of ways.4 Certain mutations, such as the mutation found in the Goldenticket mouse strain, I199N, prevent STING from binding to CDNs and from inducing an IFN response. However, other mutations in the C-terminal region allow STING to bind c-di-GMP but not induce IFN, hyperinduce IFN without binding c-di-GMP, or induce IFN only when overexpressed and without binding c-di-GMP. STING inhibition has the potential to be beneficial for the treatment of autoimmune diseases that are associated with uncontrolled activation of the STING pathway, while activation of STING can lead to an adaptive immune response that reduces tumor growth in animal models.6,7,8,9 Cayman’s STING (C-Term) Monoclonal Antibody (Clone 1B10) can be used for ELISA, IHC, and WB applications. The antibody recognizes the C-terminal region of STING at 42 kDa from human samples.WARNING This product is not for human or veterinary use.