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Dual-targeting CD33 CD123 NANOBODY T-cell engager with potent anti-AML . . . CD33 CD123 NANOBODY TCE kills single and double-positive cells, outperforming single-targeting TCE in a subset of AML samples CD33 CD123-TCE efficiently kills AML cells in a mouse model and targets cells in nonhuman primates without signs of cytokine release
The CD33xCD123xCD70 Multispecific CD3-Engaging DARPin MP0533 Induces . . . We designed MP0533, a multispecific CD3-engaging designed ankyrin repeat protein (DARPin) that can simultaneously bind to three antigens on AML cells (CD33, CD123, and CD70), aiming to enable avidity-driven T cell–mediated killing of AML cells coexpressing at least two of the antigens
1080 A bispecific pan-γδ T cell engager with IL-15 fusion that . . . The addition of the IL-15 domain further boosted the ability of the engager to promote the activation and proliferation of γδ T cells In humanized AML cell xenograft models, the CD123 bispecific pan γδ T cell engager effectively recruited γδ T cells to control AML tumor growth
Targeting CD123 in AML: The Latest Therapeutic Advancements One is CD3 for the T-cell; the other is CD123 for the leukemic cell, and when the bi-specific antibody engages it, it brings the CD123-expressing AML cell in proximity to the CD3-expressing immune T-cell, resulting in T-cell-mediated killing of the acute myeloid leukemia cell
Targeting cancer stem cells with CAR-based immunotherapy: biology . . . A study compared various dual-CAR T-cell designs—compound, split, tandem, and pooled approaches—and found that split CAR T-cells targeting TIM3 and CD33 were the most precise, effectively targeting AML cells with both markers while avoiding healthy cells, indicating their potential use without stem cell transplants [42]
Transgenic Expression of IL15 Retains CD123-Redirected T Cells in a . . . In vivo, CD123-ENG IL15 T-cells exhibited superior antigen-specific anti-AML activity and T-cell persistence in both peripheral blood and tissues (BM, spleens, and livers), resulting in a significant survival advantage in one AML xenograft model and two autologous AML PDX models