Products
Gantenerumab Biosimilar Monoclonal Antibody (Amyloid Beta (Aβ)) for Research
Pre-Made Gantenerumab biosimilar, Whole mAb, Anti-APP Antibody: Anti-AAA/AD1/PN2/ABPP/CVAP/ABETA/PN-II/preA4/CTFgamma therapeutic antibody is a biosimilar expressed by mammalian cell line as a benchmark reference therapeutic antibody for biological drug disovery items including cell culture, assay development, animal model development, PK/PD model development (Pharmacokinetics & Pharmacodynamic) and mechanism of action (MOA) research.
Gantenerumab is a monoclonal antibody for the treatment of Alzheimer's disease being developed by Hoffmann-La Roche pharmaceuticals.
Order Information
| Catalog No. | Package | List Price(In USD) | Discount off | Discount Price |
|---|---|---|---|---|
| GMP-Bios-ab-232-1mg | 1mg | 3090 |
Size： 1mg | 10mg | 100mg
Product Details
| Products Name (INN Index) | Pre-Made Gantenerumab biosimilar, Whole mAb, Anti-APP Antibody: Anti-AAA/AD1/PN2/ABPP/CVAP/ABETA/PN-II/preA4/CTFgamma therapeutic antibody |
| INN Name | Gantenerumab |
| Target | APP |
| Format | Whole mAb |
| Derivation | Human |
| Species Reactivity | Human |
| CH1 Isotype | IgG1 |
| VD LC | Kappa |
| Highest_Clin_Trial (Jan '20) | Phase-III |
| Est. Status | Active |
| 100% SI Structure | 5csz:HL:AB |
| 99% SI Structure | None |
| 95-98% SI Structure | None |
| Year Proposed | 2012 |
| Year Recommended | 2008 |
| Companies | MorphoSys;Chugai Pharmaceutical;Roche |
| Conditions Approved | na |
| Conditions Active | Alzheimer's disease |
| Conditions Discontinued | na |
| Development Tech | na |
About target - APP
1. Protein Amyloid-beta precursor protein
2. Gene APP
3. Organism Homo sapiens (Human)
Function
Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Interaction between APP molecules on neighboring cells promotes synaptogenesis (PubMed:25122912).
Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibits Notch signaling through interaction with Numb. Couples to apoptosis-inducing pathways such as those mediated by G(O) and JIP. Inhibits G(o) alpha ATPase activity (By similarity).
Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1 (By similarity).
By acting as a kinesin I membrane receptor, plays a role in axonal anterograde transport of cargo towards synapes in axons (PubMed:17062754, PubMed:23011729).
Involved in copper homeostasis/oxidative stress through copper ion reduction. In vitro, copper-metallated APP induces neuronal death directly or is potentiated through Cu2+-mediated low-density lipoprotein oxidation. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV. The splice isoforms that contain the BPTI domain possess protease inhibitor activity. Induces a AGER-dependent pathway that involves activation of p38 MAPK, resulting in internalization of amyloid-beta peptide and leading to mitochondrial dysfunction in cultured cortical neurons. Provides Cu2+ ions for GPC1 which are required for release of nitric oxide (NO) and subsequent degradation of the heparan sulfate chains on GPC1.
Amyloid-beta peptides are lipophilic metal chelators with metal-reducing activity. Bind transient metals such as copper, zinc and iron. In vitro, can reduce Cu2+ and Fe3+ to Cu+ and Fe2+, respectively. Amyloid-beta protein 42 is a more effective reductant than amyloid-beta protein 40. Amyloid-beta peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. APP42-beta may activate mononuclear phagocytes in the brain and elicit inflammatory responses. Promotes both tau aggregation and TPK II-mediated phosphorylation. Interaction with overexpressed HADH2 leads to oxidative stress and neurotoxicity. Also binds GPC1 in lipid rafts.
Appicans elicit adhesion of neural cells to the extracellular matrix and may regulate neurite outgrowth in the brain.
The gamma-CTF peptides as well as the caspase-cleaved peptides, including C31, are potent enhancers of neuronal apoptosis.
N-APP binds TNFRSF21 triggering caspase activation and degeneration of both neuronal cell bodies (via caspase-3) and axons (via caspase-6).
Miscellaneous
Chelation of metal ions, notably copper, iron and zinc, can induce histidine-bridging between amyloid-beta molecules resulting in amyloid-beta-metal aggregates. The affinity for copper is much higher than for other transient metals and is increased under acidic conditions. Extracellular zinc-binding increases binding of heparin to APP and inhibits collagen-binding.
