This antibody is a IgG2a isotype switch variant of the murine parent antibody 14.18. This antibody can direct efficient complement-dependent cytotoxicity against neuroblastoma tumor cells and melanoma cell lines in vitro in the presence of human complement. 14G2a was coupled to the ribosome-inactivating plant toxin gelonin with the heterobifunctional cross-linking reagent N-succinimidyl-3(2-pyridyldithio)propionate. The immunoreactivity and specificity of 14G2a-gelonin immunotoxin determined by ELISA. Assays for complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) revealed that these functional properties of the native 14G2a antibody were also preserved in the 14G2a-gelonin immunotoxin. An immunotoxin prepared by linked 14G2a via the bivalent linker N-succinimidyloxycarbonyl-amethyl-a-(2-piridyldithio)toluene to deglycosylated ricin A chain was shown to inhibit the protein synthesis of neuroblastoma cell lines IMRS and NMB. Treatment with 14G2a mAb (1–4 mg/kg cumulative dose given as five i.v. daily administrations) dramatically reduced the metastatic spread of NB cells and prolonged the long-term survival of treated mice in a dose-dependent manner. This antibody is also reported to be used in the study of interactions between peptides mimicking the GD2 ganglioside using flow ctyometry and ELISA
Citations
Publication ()
Have you cited CABT-L6418 in a publication? Let us know and earn a reward for your research.
My Review for Rabbit Anti-Human GD2 monoclonal antibody, clone 14G2a
Creative Diagnostics products are for RESEARCH USE ONLY, please make sure your review is research based.
Required fields are marked with *
Terms and conditions:
We will select high-quality review customers and offer a $30 coupon for your next purchase.
All product reviews must be submitted in the English language.
Creative Diagnostics will not share any personal information of applicants, and all information will be treated with strict confidentiality and will not be sold or disclosed to a third party.