Products
Abituzumab Biosimilar Monoclonal Antibody (Integrin αV) for Research
Pre-Made Abituzumab biosimilar, Whole mAb, Anti-ITGAV Antibody: Anti-CD51/MSK8/VNRA/VTNR 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.
Abituzumab is a humanized IgG2 monoclonal antibody (mAb) targeted at CD51 (an integrin) currently in development by Merck KGaA Darmstadt, Germany in an attempt to prevent bone lesion metastases in castration-resistant prostate cancer.
Order Information
| Catalog No. | Package | List Price(In USD) | Discount off | Discount Price |
|---|---|---|---|---|
| GMP-Bios-ab-003-1mg | 1mg | 3090 |
Size： 1mg | 10mg | 100mg
Product Details
| Products Name (INN Index) | Pre-Made Abituzumab biosimilar, Whole mAb, Anti-ITGAV Antibody: Anti-CD51/MSK8/VNRA/VTNR therapeutic antibody |
| INN Name | Abituzumab |
| Target | ITGAV |
| Format | Whole mAb |
| Derivation | Humanized |
| Species Reactivity | Human |
| CH1 Isotype | IgG2 |
| VD LC | Kappa |
| Highest_Clin_Trial (Jan '20) | Phase-II |
| Est. Status | Active |
| 100% SI Structure | None |
| 99% SI Structure | None |
| 95-98% SI Structure | None |
| Year Proposed | 2013 |
| Year Recommended | 2014 |
| Companies | Merck |
| Conditions Approved | na |
| Conditions Active | Colorectal cancer;Systemic scleroderma |
| Conditions Discontinued | Ovarian cancer;Prostate cancer;Solid tumours |
| Development Tech | na |
About target - ITGAV
1. Protein Integrin alpha-V
2. Gene ITGAV
3. Organism Homo sapiens (Human)
Function
The alpha-V (ITGAV) integrins are receptors for vitronectin, cytotactin, fibronectin, fibrinogen, laminin, matrix metalloproteinase-2, osteopontin, osteomodulin, prothrombin, thrombospondin and vWF. They recognize the sequence R-G-D in a wide array of ligands. ITGAV:ITGB3 binds to fractalkine (CX3CL1) and may act as its coreceptor in CX3CR1-dependent fractalkine signaling (PubMed:23125415).
ITGAV:ITGB3 binds to NRG1 (via EGF domain) and this binding is essential for NRG1-ERBB signaling (PubMed:20682778).
ITGAV:ITGB3 binds to FGF1 and this binding is essential for FGF1 signaling (PubMed:18441324).
ITGAV:ITGB3 binds to FGF2 and this binding is essential for FGF2 signaling (PubMed:28302677).
ITGAV:ITGB3 binds to IGF1 and this binding is essential for IGF1 signaling (PubMed:19578119).
ITGAV:ITGB3 binds to IGF2 and this binding is essential for IGF2 signaling (PubMed:28873464).
ITGAV:ITGB3 binds to IL1B and this binding is essential for IL1B signaling (PubMed:29030430).
ITGAV:ITGB3 binds to PLA2G2A via a site (site 2) which is distinct from the classical ligand-binding site (site 1) and this induces integrin conformational changes and enhanced ligand binding to site 1 (PubMed:18635536, PubMed:25398877).
ITGAV:ITGB3 and ITGAV:ITGB6 act as a receptor for fibrillin-1 (FBN1) and mediate R-G-D-dependent cell adhesion to FBN1 (PubMed:12807887, PubMed:17158881).
Integrin alpha-V/beta-6 or alpha-V/beta-8 (ITGAV:ITGB6 or ITGAV:ITGB8) mediates R-G-D-dependent release of transforming growth factor beta-1 (TGF-beta-1) from regulatory Latency-associated peptide (LAP), thereby playing a key role in TGF-beta-1 activation (PubMed:15184403, PubMed:22278742, PubMed:28117447).
ITGAV:ITGB3 act as a receptor for CD40LG (PubMed:31331973).
(Microbial infection) Integrin ITGAV:ITGB5 acts as a receptor for Adenovirus type C.
(Microbial infection) Integrin ITGAV:ITGB5 and ITGAV:ITGB3 act as receptors for Coxsackievirus A9 and B1.
(Microbial infection) Integrin ITGAV:ITGB3 acts as a receptor for Herpes virus 8/HHV-8.
(Microbial infection) Integrin ITGAV:ITGB6 acts as a receptor for herpes simplex 1/HHV-1.
(Microbial infection) Integrin ITGAV:ITGB3 acts as a receptor for Human parechovirus 1.
(Microbial infection) Integrin ITGAV:ITGB3 acts as a receptor for West nile virus.
(Microbial infection) In case of HIV-1 infection, the interaction with extracellular viral Tat protein seems to enhance angiogenesis in Kaposi's sarcoma lesions.
