Through in-house research and partnership programs with pharmaceutical companies and academic groups, we are continuously expanding our extensive portfolio of state-of-the-art biomarkers and antibodies. These qualified antibodies are exclusively available to our partners and collaborators.
Robust and reliable assays for cerebrospinal fluid (CSF) and blood can be developed with these antibodies to detect neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease and traumatic brain injury.
Discover our portfolio below. Request a test-sample to verify the unique performance of our materials or let us know how we can help you.
Amyloid-beta is a useful biomarker for the detection of the Alzheimer pathology, even in an early stage. Decreased amyloid-beta 42/40 ratio in CSF and plasma correlates highly with the presence of amyloid plaques in Alzheimer brains.
| ADx101 | Mouse monoclonal antibody against human β Amyloid 1-x | 1 specific |
| ADx102 | Mouse monoclonal antibody against human β Amyloid x-42 | 42 specific |
| ADx103 | Mouse monoclonal antibody against human β Amyloid x-40 | 40 specific |
| ADx104 | Mouse monoclonal antibody against human β Amyloid x-38 | 38 specific |
| ADx401 | Mouse monoclonal antibody against human BACE-1 | |
| ADx402 | Mouse monoclonal antibody against human BACE-1 |
Sutphen et al, JAMA Neurol 2015;72:1029.
Janelidze et al, Ann Clin Transl Neurol 2016;3:154.
Total tau and P-tau are good indicators of neuronal damage. P-tau specifically measures damage caused by Alzheimer’s disease. In contrast, total tau is a general marker, which can also be used to determine severe concussion.
| ADx201 | Mouse monoclonal antibody against human total tau | Mid tau |
| ADx202 | Mouse monoclonal antibody against human total tau | Mid tau |
| ADx215 | Mouse monoclonal antibody against human total tau | N-terminal tau |
| ADx203 | Mouse monoclonal antibody against human total tau | Mid tau |
| ADx204 | Mouse monoclonal antibody against human total tau | N-terminal tau |
| ADx205 | Mouse monoclonal antibody against human total tau | Mid tau |
| ADx252 | Mouse monoclonal antibody against human P-tau181 | Phosphorylated Threonine 181 specific |
| ADx253 | Mouse monoclonal antibody against human P-tau231 | Phosphorylated Threonine 231 specific |
Sutphen et al, JAMA Neurol 2015;72:1029.
Rosseels et al, J Biol Chem 2015;290:4059.
Neurons are interconnected by multiple synapses. In Alzheimer’s disease, synapses show gradual degeneration. Neurogranin, BACE-1 and Neuronal Pentraxin 2 (NPTX2) in CSF are good biomarkers for synapse integrity. They will help predict the progression of the disease.
| ADx401 | Mouse monoclonal antibody against human BACE-1 | |
| ADx402 | Mouse monoclonal antibody against human BACE-1 | |
| ADx403 | Mouse monoclonal antibody against human neurogranin | N-terminal |
| ADx451 | Mouse monoclonal antibody against human truncated neurogranin | Specific for C-terminal truncation at P75 |
De Vos et al, J Alzheimers Dis 2016;53:1523
Willemse et al, Clin Chem 2018;64:927.
The concentration of α-synuclein in CSF is linked to the presence of Lewy bodies in the brain, which are typically found in the brains of Parkinson’s disease patients. Other α-synuclein forms are in development.
| ADx301 | Rabbit monoclonal antibody against human α-synuclein | |
| ADx302 | Rabbit monoclonal antibody against human α-synuclein |
Mollenhauer et al, Mov Disord 2017;32:1117.
Schmitz et al, Mol Neurobiol 2019;56:3476.
Some of the ADx markers were developed and commercialized in collaboration with our partners. The new generation of Alzheimer’s diagnostics, using Ab 1-40, Ab 1-42, P-tau, total tau, neurogranin and synuclein is now available through our partner Euroimmun, a Perkin Elmer company.
For the development of highly sensitive blood tests, we are collaborating with IVD enterprise Quanterix.
ADx antibodies are adaptable to any technology. We are currently exploring additional partnerships with several diagnostic companies.
Find out more on our partner’s websites or get in touch to request more information.
