Pipeline

Coming soon
Immuno-Oncology IHC marker
CD112R
FOXP3
LAG3
TIGIT - more clones
CD226 - different clones
CD155 - different clones
CD112R

CD112R is preferentially expressed on T-cells and inhibits T-cell receptor mediated signals. Blockade of the CD112R-CD112 interaction enhances T cell response.

FOXP3

FOXP3 (Forkhead box protein P3) is mainly expressed in Regulatory T (Treg) cells, a subset of CD4+ T-cells, that play a suppressive role in the immune system. Treg cells ensure immune homeostasis through their ability to suppress the activation and function of leukocytes. FOXP3 has emerged as a prominent target for the development of new immunotherapies for cancer and autoimmune diseases.

LAG3

LAG3 (Lymphocyte activation gene-3, CD223) plays an important role in modulating T cell expansion and function. Interestingly, LAG-3 bears structural homology to CD4 and functions as a cell surface molecule expressed on activated T cells. Blockade of LAG-3 can augment T cell function. Moreover, several preclinical and clinical studies suggest a role for LAG-3 blocking antibodies in cancer immunotherapy.

TIGIT - more clones

The complexity of the TIGIT axis in immune oncology has increased the demand for different antibody clones targeting different immunogenic motifs.

CD226 - different clones

CD226 and TIGIT share ligands and binding of CD155 and CD112  has different impact on T cell responses. This complexity may be investigated with different antibody clones targeting different immunogenic motifs.

CD155 - different clones

CD155 acts as the ligand for both costimulatory receptor CD226 and coinhibitory receptor TIGIT and CD96 on natural killer and T cells. This complexity may be investigated with different antibody clones targeting different immunogenic motifs.

Available now
Immuno-Oncology IHC marker
TIGIT - clone TG1
CD73 - clone KK3
CD8 - clone TC8
TIGIT - clone TG1

Clone TG1 immunohistochemistry allows the identification of invading TIGIT positive T-cells in routine fixed FFPE human tumor tissues.

CD73 - clone KK3

CD73, together with CD39, plays an important role in promoting immunosuppression through the pathway degrading ATP into adenosine, which has a significant effect on the tumor microenvironment. Theses cell surface enzymes have emerged as novel therapeutic targets to enhance antitumor immune responses across a wide range of tumors.

CD8 - clone TC8

Cytotoxic CD8+ T cells induce apoptosis in cancer cells and contribute to immune response in the tumor microenvironment.

Tumor IHC marker
PSA - clone HAM18
p16 - clone JAP16
more IHC marker antibodies
PSA - clone HAM18

Anti-PSA clone HAM18 has been tested for sensitivity, specificity and prognostic significance on more than 20.000 tissues and stands for being the best validated anti-PSA clone.

p16 - clone JAP16

Clone JAP16 has been validated for detection of p16 INK4 in routine fixed FFPE tissues with focus on gynecological pathology.

more IHC marker antibodies

Find more antibody clones for tumor IHC markers excessively validated in routine fixed FFPE tissues listed in our shop.

Our Cancer Immunology Pipeline

TIGIT - more clones

The expression of TIGIT on T cells in cancer models is highly correlated with the expression of other co-inhibitory molecules, including PD-1. Our mission is to provide multiple clones against different immunogenic epitopes on TIGIT.

CD112R

CD112R is preferentially expressed on T-cells and inhibits T-cell receptor mediated signals. Blockade of the CD112R-CD112 interaction enhances T cell response.

CD112

CD112 is widely expressed on tumor cells and a high affinity ligand for CD112R. Disruption of CD112 ligand binding to its receptor CD112R on T cells has a positive effect on immune response.

CD155

CD155 is frequently overexpressed in human malignant tumors acts as the ligand for both costimulatory receptor CD226 and coinhibitory receptor TIGIT and CD96 on natural killer and T cells.

CD226

CD226 and TIGIT share ligands, CD155 and CD112 and binding has opposite results: Binding of CD226 with CD155 or CD112 enhances T cell activation, the interaction between TIGIT and CD155 or CD112 inhibits T cell responses.

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