| Species Reactivity | Human |
| Clone | Mavrilimumab |
| Source/Isotype | Human IgG4, Lambda2 |
| Application | Bioactivity-ELISA |
| Target | Detects GM-CSFRA |
| Gene | GM-CSFRA |
| Other Names | GM-CSF R alpha, CSF2RA, CSF2R, CSF2RY, CDw116, CD116 |
| Gene ID | 1438 (Human) |
| Background | The core research value of anti-GM-CSFRA lies in precisely intervening in the GM-CSF inflammatory axis, positioning it as a critical therapeutic node connecting chronic inflammation and tumor immunity. In the realm of autoimmune diseases, anti-GM-CSFRA can precisely inhibit macrophage activation and the release of inflammatory cytokines by blocking GM-CSF signaling. This approach has demonstrated significant progress in Phase III clinical trials for rheumatoid arthritis. |
| In oncology, this strategy exhibits a dual potential of "direct cytotoxicity" and "immune modulation". On one hand, CAR-T therapies targeting CSF2RA are under clinical investigation for CD116-positive acute myeloid leukemia (AML) and juvenile myelomonocytic leukemia. On the other hand, blocking this pathway can remodel the tumor microenvironment; for instance, in gastric cancer, high CSF2RA expression activates the JAK2/STAT3 pathway to drive progression, making it a promising precision target. Furthermore, anti-GM-CSFRA interventions can control excessive immune responses, showing therapeutic promise in cytokine storms triggered by COVID-19 and offering novel gene therapy approaches for hereditary pulmonary alveolar proteinosis caused by CSF2RA mutations. | |
| Storage | Store at 2-8℃ short term (1-2 weeks). Store at ≤ -20℃ long term. Avoid repeated freeze-thaw. |
| Formulation | Supplied as a 0.2 μm filtered solution of PBS, pH7.2-7.4. |
| Endotoxin | < 1 EU/mg, determined by LAL gel clotting assay |
| Species Reactivity | Human |
| Clone | Mavrilimumab |
| Source/Isotype | Human IgG4, Lambda2 |
| Application | Bioactivity-ELISA |
| Target | Detects GM-CSFRA |
| Gene | GM-CSFRA |
| Other Names | GM-CSF R alpha, CSF2RA, CSF2R, CSF2RY, CDw116, CD116 |
| Gene ID | 1438 (Human) |
| Background | The core research value of anti-GM-CSFRA lies in precisely intervening in the GM-CSF inflammatory axis, positioning it as a critical therapeutic node connecting chronic inflammation and tumor immunity. In the realm of autoimmune diseases, anti-GM-CSFRA can precisely inhibit macrophage activation and the release of inflammatory cytokines by blocking GM-CSF signaling. This approach has demonstrated significant progress in Phase III clinical trials for rheumatoid arthritis. |
| In oncology, this strategy exhibits a dual potential of "direct cytotoxicity" and "immune modulation". On one hand, CAR-T therapies targeting CSF2RA are under clinical investigation for CD116-positive acute myeloid leukemia (AML) and juvenile myelomonocytic leukemia. On the other hand, blocking this pathway can remodel the tumor microenvironment; for instance, in gastric cancer, high CSF2RA expression activates the JAK2/STAT3 pathway to drive progression, making it a promising precision target. Furthermore, anti-GM-CSFRA interventions can control excessive immune responses, showing therapeutic promise in cytokine storms triggered by COVID-19 and offering novel gene therapy approaches for hereditary pulmonary alveolar proteinosis caused by CSF2RA mutations. | |
| Storage | Store at 2-8℃ short term (1-2 weeks). Store at ≤ -20℃ long term. Avoid repeated freeze-thaw. |
| Formulation | Supplied as a 0.2 μm filtered solution of PBS, pH7.2-7.4. |
| Endotoxin | < 1 EU/mg, determined by LAL gel clotting assay |
