TMB-365
Exhibitor: TAIMED BIOLOGICS INC.
Booth No: M104
Characteristic
The TMB-365 is an ibalizumab (TMB-355) based, IgG1-scaffold, anti-CD4 recombinant humanized monoclonal antibody used against HIV infections. The major medication or medicament of TMB-365 is mainly focused upon treatment and prevention against HIV infections (including opportunistic infections), said therapeutic and prophylactic usages or medical application. The TMB-365-relevant technology platforms of TMB-365 are licensed from Arron Diamond AIDS Research Center (ADARC) anchored at Rockefeller University (RU).
During the clinical development of the first generation anti-CD4 humanized, recombinant monoclonal antibody, TMB-355, also ibalizumab and formerly TNX-355, for the treatment against HIV infections, the drug resistance testing showed that there is around or excess 10% of the HIV clinical isolates and strains identified to be the existing ibalizumab drug resistant mutants while ibalizumab demonstrated itself to be the outstanding highly neutralizing antibody against HIV infection in clinical setting.
The existent drug resistance against ibalizumab in clinical investigation was sending a call or signal of message and drawing attentions to well-known HIV research group led by Dr. David Ho, the distinguishing, leading investigator and inventor of the creative and innovative cocktail therapy against HIV, at Arron Diamond AIDS Research Center (ADARC) anchored at Rockefeller University (RU). Through intensive efforts via internal and external collaboration with AIDS research institutions around the globe, the ADARC team decoded that the ibalizumab resistance is elicited from an unusual glycan mutation on the HIV envelop protein gp120 broadly neutralizing antibodies from HIV infected patients. That is, if the absence of the glycan originated on HIV gp120 is existent, the mutant HIV viruses are capable of exerting the “entry” process of intact viral particle into the cell without jeopardizing the viral binding to CD4 receptor and the following process of binding to co-receptor CCR5 or CXCR4, engaging the fusion and engulfment of HIV in to the human host cell like CD4+ T lymphocytes or T cells. In such a scenario, the presence or absence of ibalizumab as the post-attachment blocker against HIV entry will be unable to impose any impact on the HIV mutants successfully to infect the healthy human T cells.
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