ArticlemAbs2026
JMB2403, a potential best-in-class PD-1-dependent IL2Rβγ-activating tri-specific antibody for safe and potent immunotherapy.
Article in mAbs, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Article
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PD-1-based immunocytokines, such as interleukin (IL)-2 fused with anti-PD-1, have been designed to increase efficacy, but their use is hampered by dose-limiting toxicity. To overcome this, substantial efforts have focused on engineering attenuated IL-2 variants, albeit with limited success to date. Taking an alternative approach, we screened a naïve alpaca library for weak agonistic nanobodies of IL-2/15Rβ and the common γ chain and attached a potent anti-PD-1 IgG to generate a tri-specific antibody JMB2403. JMB2403 did not bind IL2Rα (CD25), but activated STAT5 phosphorylation in an engineered Jurkat cell reporter assay albeit far less potently compared to wildtype IL-2. This translated to a JMB2403-induced pSTAT5 increase in natural killer (NK) cells, but minimal STAT5 phosphorylation in Treg cells. Notably, JMB2403 retained PD-1 blocking activity and concentration-dependently induced phospho-STAT5 only in activated (PD-1
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