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The 11B11 monoclonal antibody reacts with mouse IL-4 (interleukin-4) a multifunctional 14 kDa cytokine. IL-4 is expressed primarily by activated Th2 cells and NK cells, and at lower levels by mast cells, and basophils. IL-4 signals through the IL-4Rα. Upon receptor binding IL-4 stimulates activated B and T lymphocyte proliferation, and the differentiation of B cells into plasma cells. It also induces B cell class switching to IgE, and up-regulates MHC class II production while decreasing the production of Th1 cells, macrophages, IFNγ, and dendritic cell IL-12. Like other Th2 associated cytokines, IL-4 is involved in the airway inflammation observed in the lungs of patients with allergic asthma. The 11B11 monoclonal antibody has been shown to neutralize the bioactivity of natural or recombinant IL-4.

The XMG1.2 monoclonal antibody reacts with mouse IFNγ (interferon gamma) a 20 kDa soluble pleiotropic cytokine and the sole member of the type II class of interferons. IFNγ is primarily produced by activated lymphocytes including T, B, NK cells, and ILCs. IFNγ exerts immunoregulatory, anti-proliferative, anti-viral, and proinflammatory activities and plays an important role in activation, growth, and differentiation of T and B lymphocytes, macrophages, NK cells and other non-hematopoietic cell types. Additionally, IFNγ induces the production of cytokines, Fc receptor, and adhesion molecules and up-regulates MHC class I and II antigen expression by antigen presenting cells during an immune response. IFNγ has also been shown to modulate macrophage effector functions, influence isotype switching and induce the secretion of immunoglobulins by B cells. IFNγ signals through the IFN gamma receptor which exists as a heterodimer composed of CD119 (IFN gamma receptor 1) and AF-1 (IFN gamma receptor 2). The IFNγ receptor is expressed ubiquitously on almost all cell types with the exception of mature erythrocytes. The XMG1.2 antibody is a neutralizing antibody.

The OX-86 monoclonal antibody reacts with mouse OX-40 also known as CD134. OX-40 is a 50 kDa type I membrane glycoprotein and a member of the TNF receptor superfamily. OX-40 is expressed on activated CD4 and CD8 T cells, but is not found on resting naïve T cells or most resting memory T cells. Although it was originally thought that OX-40 expression was restricted to activated conventional T cells, it has now been visualized on activated regulatory T cells, NKT cells, NK cells, and neutrophils. OX-40 plays a major role in regulating both CD4 and CD8 T cell clonal expansion. It provides a costimulatory signal to an antigen-reacting naive T cells to prolong proliferation, as well as augment the production of several cytokines. This is demonstrated by OX-40 knockout mice which generate fewer primary effector CD4 T cells after immunization. Furthermore, in vivo treatment with an agonist antibody to OX-40 has been shown to strongly enhance the generation of antigen-specific effector T cells and prevent the induction of T cell tolerance. The OX-86 antibody is an agonistic antibody that has been shown to delay tumor growth in vivo.

The UC10-4F10-11 monoclonal antibody reacts with mouse CTLA-4 (cytotoxic T lymphocyte antigen-4) also known as CD152. CTLA-4 is a 33 kDa cell surface receptor encoded by the Ctla4 gene that belongs to the CD28 family of the Ig superfamily. CTLA-4 is expressed on activated T and B lymphocytes. CTLA-4 is structurally similar to the T-cell co-stimulatory protein, CD28, and both molecules bind to the B7 family members B7-1 (CD80) and B7-2 (CD86). Upon ligand binding, CTLA-4 negatively regulates cell-mediated immune responses. CTLA-4 plays roles in induction and/or maintenance of immunological tolerance, thymocyte development, and regulation of protective immunity. The critical role of CTLA-4 in immune down-regulation has been demonstrated in CTLA-4 deficient mice, which succumb at 3-5 weeks of age due to the development of a lymphoproliferative disease. CTLA-4 is among a group of inhibitory receptors being explored as cancer treatment targets through immune checkpoint blockade. The UC10-4F10-11 antibody has been shown to promote T cell co-stimulation by blocking CTLA-4 binding to the B7 co-receptors, allowing for CD28 binding.

The PK136 monoclonal antibody reacts with mouse NK1.1 also known as CD161b/CD161c, KLRB1, NKR-P1A and Ly-55. NK1.1 is a type II integral membrane glycoprotein with a C-type lectin domain and is encoded by the Klrb1c/NKR-P1C gene. NK1.1 plays roles in NK cell activation and differentiation, IFN-γ production, cytotoxic granule release, and is thought to be involved in the generation of Th2 cells. NK1.1 is predominantly expressed as a disulfide-linked homodimer on NK cells however, it is also expressed on NK-T cells, a rare population of T lymphocytes. NK 1.1 is only expressed by C57BL/6, FVB/N, and NZB strains of mice and not AKR, BALB/c, CBA/J, C3H, DBA/1, DBA/2, NOD, SJL, and 129 strains.

The 9H10 monoclonal antibody reacts with mouse CTLA-4 (cytotoxic T lymphocyte antigen-4) also known as CD152. CTLA-4 is a 33 kDa cell surface receptor encoded by the Ctla4 gene that belongs to the CD28 family of the Ig superfamily. CTLA-4 is expressed on activated T and B lymphocytes. CTLA-4 is structurally similar to the T-cell co-stimulatory protein, CD28, and both molecules bind to the B7 family members B7-1 (CD80) and B7-2 (CD86). Upon ligand binding, CTLA-4 negatively regulates cell-mediated immune responses. CTLA-4 plays roles in induction and/or maintenance of immunological tolerance, thymocyte development, and regulation of protective immunity. The critical role of CTLA-4 in immune down-regulation has been demonstrated in CTLA-4 deficient mice, which succumb at 3-5 weeks of age due to the development of a lymphoproliferative disease. CTLA-4 is among a group of inhibitory receptors being explored as cancer treatment targets through immune checkpoint blockade. The 9H10 antibody has been shown to promote T cell co-stimulation by blocking CTLA-4 binding to the B7 co-receptors, allowing for CD28 binding.

The 1A8 monoclonal antibody reacts with mouse Ly6G. Ly6G is a 21-25 kDa member of the Ly-6 superfamily of GPI-anchored cell surface proteins with roles in cell signaling and cell adhesion. Ly6G is expressed differentially during development by cells in the myeloid lineage including monocytes, macrophages, granulocytes, and neutrophils. Monocytes typically express Ly6G transiently during development while mature granulocytes and peripheral neutrophils retain expression making Ly6G a good cell surface marker for these populations. Unlike the RB6-8C5 antibody, the 1A8 antibody reacts specifically with mouse Ly6G with no reported cross reactivity with Ly6C.

The MAR1-5A3 monoclonal antibody reacts with mouse IFNAR-1 (IFN alpha/beta receptor subunit 1). IFNAR-1 is coexpressed with IFNAR-2 on nearly all cell types and together these two subunits make up the heterodimeric Type I IFN Receptor complex. Type I IFNs (IFN-α/β) bind to the Type I IFN Receptor complex to induce cellular responses including induction of anti-viral, anti-microbial, anti-tumor, and autoimmune responses as well as to regulate the activation, proliferation, and differentiation of many cell types. The MAR1-5A3 antibody has been shown to inhibit Type I IFN receptor signaling in vitro and in vivo.

The 9D9 monoclonal antibody reacts with mouse CTLA-4 (cytotoxic T lymphocyte antigen-4) also known as CD152. CTLA-4 is a 33 kDa cell surface receptor encoded by the Ctla4 gene that belongs to the CD28 family of the Ig superfamily. CTLA-4 is expressed on activated T and B lymphocytes. CTLA-4 is structurally similar to the T-cell co-stimulatory protein, CD28, and both molecules bind to the B7 family members B7-1 (CD80) and B7-2 (CD86). Upon ligand binding, CTLA-4 negatively regulates cell-mediated immune responses. CTLA-4 plays roles in induction and/or maintenance of immunological tolerance, thymocyte development, and regulation of protective immunity. The critical role of CTLA-4 in immune down-regulation has been demonstrated in CTLA-4 deficient mice, which succumb at 3-5 weeks of age due to the development of a lymphoproliferative disease. CTLA-4 is among a group of inhibitory receptors being explored as cancer treatment targets through immune checkpoint blockade.

The 10F.9G2™ monoclonal antibody reacts with mouse PD-L1 (programmed death ligand 1) also known as B7-H1 or CD274. PD-L1 is a 40 kDa type I transmembrane protein that belongs to the B7 family of the Ig superfamily. PD-L1 is expressed on T lymphocytes, B lymphocytes, NK cells, dendritic cells, as well as IFNγ stimulated monocytes, epithelial cells and endothelial cells. PD-L1 binds to its receptor, PD-1, found on CD4 and CD8 thymocytes as well as activated T and B lymphocytes and myeloid cells. Engagement of PD-L1 with PD-1 leads to inhibition of TCR-mediated T cell proliferation and cytokine production. PD-L1 is thought to play an important role in tumor immune evasion. Induced PD-L1 expression is common in many tumors and results in increased resistance of tumor cells to CD8 T cell mediated lysis. In mouse models of melanoma, tumor growth can be transiently arrested via treatment with antibodies which block the interaction between PD-L1 and PD-1. The 10F.9G2™ antibody has been shown to block the interaction between PD-L1 and PD-1 and between PD-L1 and B7-1 (CD80).

The 1D11.16.8 monoclonal antibody reacts with mouse, human, rat, monkey, hamster, canine and bovine TGF-β (transforming growth factor beta) isoforms 1, 2 and 3. TGF-β is a multifunctional cytokine that regulates the proliferation of epithelial cells, endothelial cells, fibroblasts, neurons, lymphoid cells including T lymphocytes and NK cells, and other hematopoietic cell types. TGF-β also regulates the activities of activated macrophages and the development of regulatory T cells. Additionally, TGF-β plays roles in immune function, tissue remodeling and wound repair. TGF-β exists as five highly similar isoforms (TGF-β 1-5) with homologies of 70-80%. TGF-β1 is synthesized by the enzymatic cleavage of a long precursor TGF-β1 polypeptide encoded by the TGFB1 gene which yields the mature protein and the Latency Associated Peptide (LAP). The LAP and mature TGF-β1 non-covalently associate during secretion. TGF-β is ubiquitously expressed by many cell types including macrophages and platelets which express high levels of TGF-β. TGF-β signaling has been shown to plays roles in cancer, autoimmune diseases, asthma, heart disease, and diabetes. Its importance is illustrated by TGF-β knockout mice which show defects in hematopoiesis and endothelial differentiation, and die of overwhelming inflammation. The 1D11.16.8 monoclonal antibody is a neutralizing antibody.

The J43 monoclonal antibody reacts with mouse PD-1 (programmed death-1) also known as CD279. PD-1 is a 50-55 kDa cell surface receptor encoded by the Pdcd1 gene that belongs to the CD28 family of the immunoglobulin superfamily. PD-1 is transiently expressed on CD4 and CD8 thymocytes as well as activated T and B lymphocytes and myeloid cells. PD-1 expression declines after successful elimination of antigen. Additionally, Pdcd1 mRNA is expressed in developing B lymphocytes during the pro-B-cell stage. PD-1’s structure includes a ITIM (immunoreceptor tyrosine-based inhibitory motif) suggesting that PD-1 negatively regulates TCR signals. PD-1 signals via binding its two ligands, PD-L1 and PD-L2 both members of the B7 family. Upon ligand binding, PD-1 signaling inhibits T-cell activation, leading to reduced proliferation, cytokine production, and T-cell death. Additionally, PD-1 is known to play key roles in peripheral tolerance and prevention of autoimmune disease in mice as PD-1 knockout animals show dilated cardiomyopathy, splenomegaly, and loss of peripheral tolerance. Induced PD-L1 expression is common in many tumors including squamous cell carcinoma, colon adenocarcinoma, and breast adenocarcinoma. PD-L1 overexpression results in increased resistance of tumor cells to CD8 T cell mediated lysis. In mouse models of melanoma, tumor growth can be transiently arrested via treatment with antibodies which block the interaction between PD-L1 and its receptor PD-1. For these reasons anti-PD-1 mediated immunotherapies are currently being explored as cancer treatments. The J43 antibody has been shown to block the binding of both mouse PD-L1-Ig and mouse PD-L2-Ig to PD-1.

This non-therapeutic biosimilar antibody uses the same variable regions from the therapeutic antibody Rituximab making it ideal for research use. This Rituximab biosimilar reacts with human CD20. CD20 is a B cell-specific 33-37 kDa transmembrane protein which is also known as B-lymphocyte antigen, B1, and Bp35. CD20 plays roles in intracellular calcium regulation and B cell activation and is critical for an optimal B cell immune response against T-independent antigens. CD20 is first expressed after the induction of CD19 together with IgM during the pre-B to immature B cell transition in the bone marrow. It’s expression then increases during maturation with almost all mature B cells expressing some level of CD20. However, CD20 is not expressed by plasma blasts or plasma cells. CD20 is expressed by most B cell neoplasms, and is useful in diagnosing B cell lymphomas and leukemia’s. Many anti-CD20 monoclonal antibodies are currently being used to successfully treat leukemia’s, lymphomas, and various autoimmune diseases. Rituximab has depleting activity and mediates ADCC and CDC of CD20+ cells. This results in the elimination of B cells from the body.

This non-therapeutic biosimilar antibody uses the same variable regions from the therapeutic antibody Ipilimumab making it ideal for research use. This Ipilimumab biosimilar reacts with human CTLA-4 (cytotoxic T lymphocyte antigen-4) also known as CD152. CTLA-4 is a 33 kDa cell surface receptor encoded by the Ctla4 gene that belongs to the CD28 family of the Ig superfamily. CTLA-4 is expressed on activated T and B lymphocytes. CTLA-4 is structurally similar to the T-cell co-stimulatory protein, CD28, and both molecules bind to the B7 family members B7-1 (CD80) and B7-2 (CD86). Upon ligand binding, CTLA-4 negatively regulates cell-mediated immune responses. CTLA-4 plays roles in induction and/or maintenance of immunological tolerance, thymocyte development, and regulation of protective immunity. CTLA-4 is among a group of inhibitory receptors being used as cancer treatment targets through immune checkpoint blockade. Ipilimumab binds to CTLA-4, blocking the inhibitory signal, which allows the cytotoxic T cells to kill cancer cells.

The RMP1-14 monoclonal antibody reacts with mouse PD-1 (programmed death-1) also known as CD279. PD-1 is a 50-55 kDa cell surface receptor encoded by the Pdcd1 gene that belongs to the CD28 family of the Ig superfamily. PD-1 is transiently expressed on CD4 and CD8 thymocytes as well as activated T and B lymphocytes and myeloid cells. PD-1 expression declines after successful elimination of antigen. Additionally, Pdcd1 mRNA is expressed in developing B lymphocytes during the pro-B-cell stage. PD-1’s structure includes a ITIM (immunoreceptor tyrosine-based inhibitory motif) suggesting that PD-1 negatively regulates TCR signals. PD-1 signals via binding its two ligands, PD-L1 and PD-L2 both members of the B7 family. Upon ligand binding, PD-1 signaling inhibits T-cell activation, leading to reduced proliferation, cytokine production, and T-cell death. Additionally, PD-1 is known to play key roles in peripheral tolerance and prevention of autoimmune disease in mice as PD-1 knockout animals show dilated cardiomyopathy, splenomegaly, and loss of peripheral tolerance. Induced PD-L1 expression is common in many tumors including squamous cell carcinoma, colon adenocarcinoma, and breast adenocarcinoma. PD-L1 overexpression results in increased resistance of tumor cells to CD8 T cell mediated lysis. In mouse models of melanoma, tumor growth can be transiently arrested via treatment with antibodies which block the interaction between PD-L1 and its receptor PD-1. For these reasons anti-PD-1 mediated immunotherapies are currently being explored as cancer treatments. Like the J43 antibody the RMP1-14 antibody has been shown to block the binding of both mouse PD-L1-Ig and mouse PD-L2-Ig to PD-1.