Products
Parsatuzumab Biosimilar Monoclonal Antibody (EGFL7) for Research
Pre-Made Parsatuzumab biosimilar, Whole mAb, Anti-EGFL7 Antibody: Anti-NEU1/VE-STATIN/ZNEU1 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.
Parsatuzumab (INN) is a humanized monoclonal antibody designed for the treatment of cancer. It acts as an immunomodulator and binds to EGFL7.
Order Information
| Catalog No. | Package | List Price(In USD) | Discount off | Discount Price |
|---|---|---|---|---|
| GMP-Bios-ab-428-1mg | 1mg | 3090 |
Size： 1mg | 10mg | 100mg
Product Details
| Products Name (INN Index) | Pre-Made Parsatuzumab biosimilar, Whole mAb, Anti-EGFL7 Antibody: Anti-NEU1/VE-STATIN/ZNEU1 therapeutic antibody |
| INN Name | Parsatuzumab |
| Target | EGFL7 |
| Format | Whole mAb |
| Derivation | Humanized |
| Species Reactivity | Human |
| CH1 Isotype | IgG1 |
| 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 | 2012 |
| Year Recommended | 2013 |
| Companies | Chugai Pharmaceutical;Genentech |
| Conditions Approved | na |
| Conditions Active | na |
| Conditions Discontinued | Colorectal cancer;Non-small cell lung cancer;Solid tumours |
| Development Tech | na |
About target - EGFL7
1. Protein Epidermal growth factor-like protein 7
2. Gene EGFL7
3. Organism Homo sapiens (Human)
Function
Regulates vascular tubulogenesis in vivo. Inhibits platelet-derived growth factor (PDGF)-BB-induced smooth muscle cell migration and promotes endothelial cell adhesion to the extracellular matrix and angiogenesis.
Miscellaneous
Endothelial cells depleted in EGFL7 by siRNAs display dramatic alterations in adhesion, morphology, and sprouting. The defects are in part due to diminished RhoA expression and impaired focal adhesion localization.
