Plonmarlimab

Plonmarlimab (TJ003234) is a humanized monoclonal antibody and a specific neutralizing antibody against granulocyte-macrophage colony-stimulating factor (GM-CSF/CSF2). Plonmarlimab binds to and neutralizes GM-CSF with high affinity, blocking its binding to receptor complexes. This inhibits the activation of the downstream JAK2-STAT5 pathway, reduces the recruitment of various inflammatory cells and the release of pro-inflammatory factors, thereby alleviating tissue inflammation and damage. In a mouse model of macrophage activation syndrome (MAS), Plonmarlimab significantly improved disease progression, including weight loss and anemia. Plonmarlimab can be used in research on immune diseases and antiviral studies.

Methods: The GM-CSF-dependent human erythroleukemia cell line TF-1 was used. Plonmarlimab (0.001, 0.01, 0.1, 1, 10, 100, 1000 ng/mL) and recombinant human GM-CSF (1 ng/mL) were added, and the cells were incubated for 72 hours. Cell viability was assessed using the CellTiter-Glo assay.
Results: Plonmarlimab dose-dependently inhibited GM-CSF-induced proliferation of TF-1 cells, with an IC₅₀ of 2.6 ng/mL.[1]

Methods: A MAS model was established in NOG-EXL mice by transplanting human umbilical cord blood (UCB) cells following 1 Gy irradiation; starting on day 7, the mice were treated with plonmarlimab (10 mg/kg, twice weekly for a total of 15 weeks); body weight, complete blood count, and serum ferritin levels were monitored, and histopathological examination assessed hemophagocytosis, lymphocyte depletion, and inflammatory infiltration.
Results: Plonmarlimab significantly mitigated weight loss (final weight loss of only 1.1% vs. 14.1% in the control group); corrected anemia and neutropenia; reduced serum ferritin by 56%; and reduced hemophagocytosis in the bone marrow and spleen, lymphocyte depletion in the spleen and lymph nodes, and inflammatory infiltration in the liver and meninges. [1]
Methods: Rhesus monkeys received intravenous injections of plonmarlimab (30, 150 mg/kg, once weekly for a total of 27 doses); clinical symptoms, hematology, biochemistry, T-cell-dependent antibody response (TDAR), and pulmonary surfactant accumulation were monitored.
Results: Good tolerability at the 150 mg/kg dose with no adverse reactions; no suppression of anti-KLH antibody response and no immunosuppression; no pathological changes indicative of pulmonary alveolar proteinosis (PAP); half-life of approximately 5 days, with dose-dependent drug exposure.[1]

Virus

Monoclonal

Unconjugated