An Antibody Engineering Service against tumor necrosis factor-alpha (TNF-α), like infliximab, is an attractive therapeutic approach to treat ocular surface diseases. TNF-α is a pleiotropic cytokine with an essential contribution to the pathogenesis of inflammation angiogenesis and collagenolysis.
An individual intraperitoneal dose of Anti-TNF Alpha Antibody in mouse infliction with alkali corneal burns significantly reduced corneal inflammation and inhibited retinal ganglion cell layer apoptosis as been differentiated with isotope IgG treatment control.
The evaluation of infliximab was done to test the stability and release of infliximab using a commercially available sandwich enzyme-linked immunoassay. The assay protocol is modified to include a 60 minutes incubation to permit antigen-antibody binding between a known quality of TNF-α and the infliximab eluted from the DDS TNF-α bound by infliximab through antibody-antigen interaction.
Which is unable to bind to the capture antibody coating of the ELISA well and hence washed away during the subsequent steps of the assay. The remaining TNF-α in the solution which is not bound by the anti-TNF-α antibody is then measured using the standard steps of the assay.
The procedures were performed under general anesthesia using intraperitoneal ketamine and xylazine formerly described. Postoperative analgesia is provided by subcutaneous buprenorphine hydrochloride. To preliminarily access vivo safety, the sections of gamma irradiation DDS were surgically implanted in the dorsal fat pad’s subcutaneous space in two male mice. Two sham DDS without anti-TNF alpha antibody implanted as polymer controls in two male mice. The DDAS and surrounding tissues were sectioned and stained with hematoxylin-eosin and Masson trichrome.
The releases of biologically active anti-TNF alpha antibody from the DDS in the first 3 hours of soaking significantly. The TNF-α inhibition was complete and exceeded the lower detection limit of the assay. At 24 hours, the release of infliximab with inhibition of TNF alpha remained high corresponding to other releases of infliximab. The lower level of drug releases occurred at zero-order kinetics for the following 30 days.
During this period average TNF-α inhibition was 24 percent and corresponding to infliximab release of 1.22 days. In contrast, freshly prepared DDS only exhibited a level of TNF-α inhibition over the first 24 hr. The delivery of the therapeutic proteins says anti-TNF alpha antibody have additional challenges including drug instability, immunogenicity, and shorter half-lives.
The Anti-TNF Alpha Antibody DDS is made of polymers prepared and sterilized by gamma irradiation. The initial burst of biologically active antibodies is followed by zero order release which constitutes a low amount of antibodies for about a month in vitro method. There are future investigations targeting the TNF alpha antibody and research demonstrating their biological stability and in vivo tolerability.
GeNext Genomics, an emerging science research organization, takes pride in serving life science customers by being a ‘One Stop Solution for All Protein Needs’. We have a team of professionals and skilled scientists, who put their efforts to develop high-quality targeted biologics and provide the Antibody Engineering Service that is required by the industry.
The anti-TNF alpha antibody is a component surging demand in the industry and academic research, and we provide them to you without any compromises.