Products
Alacizumab Biosimilar di-Fab Antibody Fragment (VEGFR2) for Research
Pre-Made Alacizumab biosimilar, di-Fab, Anti-KDR Antibody: Anti-FLK1/CD309/VEGFR/VEGFR2 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.
Alacizumab pegol is an antineoplastic agent. Chemically, it is a pegylated F(ab')2 fragment of a monoclonal antibody.
Order Information
| Catalog No. | Package | Price(In USD) |
|---|---|---|
| GMP-Bios-ab-014-1mg | 1mg | |
| GMP-Bios-ab-014-10mg | 10mg | |
| GMP-Bios-ab-014-100mg | 100mg | |
| GMP-Bios-ab-014-xmg | ≥100mg |
Product Details
| Products Name (INN Index) | Pre-Made Alacizumab biosimilar, di-Fab, Anti-KDR Antibody: Anti-FLK1/CD309/VEGFR/VEGFR2 therapeutic antibody |
| INN Name | Alacizumab |
| Target | KDR |
| Format | di-Fab |
| Derivation | |
| Species Reactivity | Human |
| CH1 Isotype | na |
| VD LC | Kappa |
| Highest_Clin_Trial (Jan '20) | Phase-II |
| Est. Status | Discontinued |
| 100% SI Structure | None |
| 99% SI Structure | None |
| 95-98% SI Structure | None |
| Year Proposed | 2007 |
| Year Recommended | 2008 |
| Companies | UCB |
| Conditions Approved | na |
| Conditions Active | na |
| Conditions Discontinued | Non-small cell lung cancer |
| Development Tech | na |
About target - KDR
1. Protein Vascular endothelial growth factor receptor 2
2. Gene KDR
3. Organism Homo sapiens (Human)
Function
Tyrosine-protein kinase that acts as a cell-surface receptor for VEGFA, VEGFC and VEGFD. Plays an essential role in the regulation of angiogenesis, vascular development, vascular permeability, and embryonic hematopoiesis. Promotes proliferation, survival, migration and differentiation of endothelial cells. Promotes reorganization of the actin cytoskeleton. Isoforms lacking a transmembrane domain, such as isoform 2 and isoform 3, may function as decoy receptors for VEGFA, VEGFC and/or VEGFD. Isoform 2 plays an important role as negative regulator of VEGFA- and VEGFC-mediated lymphangiogenesis by limiting the amount of free VEGFA and/or VEGFC and preventing their binding to FLT4. Modulates FLT1 and FLT4 signaling by forming heterodimers. Binding of vascular growth factors to isoform 1 leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate and the activation of protein kinase C. Mediates activation of MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway. Mediates phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase, reorganization of the actin cytoskeleton and activation of PTK2/FAK1. Required for VEGFA-mediated induction of NOS2 and NOS3, leading to the production of the signaling molecule nitric oxide (NO) by endothelial cells. Phosphorylates PLCG1. Promotes phosphorylation of FYN, NCK1, NOS3, PIK3R1, PTK2/FAK1 and SRC.
Catalytic activityi
ATP + L-tyrosyl-[protein] = ADP + H+ + O-phospho-L-tyrosyl-[protein]
EC:2.7.10.1
Activity regulationi
Present in an inactive conformation in the absence of bound ligand. Binding of VEGFA, VEGFC or VEGFD leads to dimerization and activation by autophosphorylation on tyrosine residues. Inhibited by the small molecule PTK inhibitor SU5614 ((3Z)-5-Chloro-3-[(3,5-dimethyl-1H-pyrrol-2-yl)methylene]-1,3-dihydro-2H-indol-2-one). May be regulated by hydrogen sulfide (H2S) levels via a H2S-sensitive intracellular disulfide bond.
