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CUA-Gym: Scaling Verifiable Training Environments and Tasks for Computer-Use Agents

arXiv:2605.25624v1 Announce Type: new Abstract: Reinforcement learning with verifiable rewards (RLVR) has driven breakthroughs in domains such as math, tool-use, and software engineering, yet its extension to computer-use agents (CUAs) has been bottlenecked by the scarcity of scalable training data with deterministic rewards. Constructing such data for CUAs requires consistent task instruction, executable environment, and verifiable reward. However, hand-curated benchmarks achieve high reward fidelity but cover few applications and LLM-as-judge-based datasets scale broadly but lack reliable verification. We present CUA-Gym, a scalable pipeline that co-generates task instructions, environment states, and reward functions. Concretely, a Generator agent constructs the initial and golden environment states, and a separate Discriminator agent writes the reward function from the task specification. An orchestrator agent drives the two through iterative rounds upon execution. Generated tuples then pass a final filter combining LLM majority voting and agent rollouts, ensuring quality beyond the per-task adversarial loop. To address the scarcity of training environments, we further synthesize CUA-Gym-Hub, a broad suite of high-fidelity mock web applications grounded in real-world software-use distributions, expanding the scale of CUA RLVR data by magnitude. Using this pipeline, we construct CUA-Gym, a dataset of 32,112 verified RLVR training tuples grounded in 110 environments. Trained with GSPO on CUA-Gym, our CUA-Gym-A3B and CUA-Gym-A17B achieve 62.1% and 72.6% on OSWorld-Verified, outperforming prior open-source CUAs at comparable scales, with performance scaling smoothly in both data volume and environment diversity. The same checkpoints also improve on the held-out WebArena benchmark, indicating transfer beyond the training environments. We will open-source the full synthesis pipeline, dataset, CUA-Gym-Hub environments, and models.

Integrated Network Toxicology and Metabolomics Elucidate Mechanisms of Carbosulfan-Induced Respiratory Toxicity in Rats

Int J Mol Sci. 2026 Feb 25;27(5):2170. doi: 10.3390/ijms27052170.

ABSTRACT

Carbosulfan is a widely used carbamate insecticide, yet its mechanisms of respiratory toxicity remain poorly understood. This study integrated network toxicology, untargeted metabolomics, and molecular docking to systematically investigate the potential mechanisms of carbosulfan-induced respiratory toxicity in male Sprague Dawley rats. Rats were administered a single oral dose of carbosulfan (125 or 250 mg/kg) and assessed after 12 h. Exposure resulted in significant pathological lung damage, characterized by disrupted alveolar architecture, inflammatory cell infiltration, and increased serum levels of the pro-inflammatory cytokines IL-6, IL-1β, and TNF-α. Network toxicology analysis identified 51 potential targets associated with respiratory toxicity, with core targets including SRC, EGFR, PTGS2, CXCL8, CYP3A4, and NR3C1. Enriched pathways were primarily related to neuroactive ligand-receptor interaction, VEGF signaling, and arachidonic acid metabolism. Untargeted metabolomics revealed significant metabolic perturbations in pathways central to antioxidant defense and energy homeostasis, including glutathione metabolism, the tricarboxylic acid cycle, and arginine biosynthesis. Molecular docking confirmed stable in silico binding affinities between carbosulfan and the predicted core targets. Integrative analysis suggests that carbosulfan exposure is associated with respiratory damage, potentially through interconnected mechanisms involving oxidative stress, inflammation, and disruption of cell signaling and metabolic enzyme systems. However, given the acute high-dose nature of the model and the interpretative integration of multi-omics data, these findings should be considered hypothesis-generating. This study provides a novel system-level perspective on carbosulfan-induced respiratory toxicity and highlights key pathways and targets for future validation in chronic exposure models.

PMID:41828400 | PMC:PMC12984169 | DOI:10.3390/ijms27052170

Integrated Network Toxicology and Metabolomics Elucidate Mechanisms of Carbosulfan-Induced Respiratory Toxicity in Rats

Int J Mol Sci. 2026 Feb 25;27(5):2170. doi: 10.3390/ijms27052170.

ABSTRACT

Carbosulfan is a widely used carbamate insecticide, yet its mechanisms of respiratory toxicity remain poorly understood. This study integrated network toxicology, untargeted metabolomics, and molecular docking to systematically investigate the potential mechanisms of carbosulfan-induced respiratory toxicity in male Sprague Dawley rats. Rats were administered a single oral dose of carbosulfan (125 or 250 mg/kg) and assessed after 12 h. Exposure resulted in significant pathological lung damage, characterized by disrupted alveolar architecture, inflammatory cell infiltration, and increased serum levels of the pro-inflammatory cytokines IL-6, IL-1β, and TNF-α. Network toxicology analysis identified 51 potential targets associated with respiratory toxicity, with core targets including SRC, EGFR, PTGS2, CXCL8, CYP3A4, and NR3C1. Enriched pathways were primarily related to neuroactive ligand-receptor interaction, VEGF signaling, and arachidonic acid metabolism. Untargeted metabolomics revealed significant metabolic perturbations in pathways central to antioxidant defense and energy homeostasis, including glutathione metabolism, the tricarboxylic acid cycle, and arginine biosynthesis. Molecular docking confirmed stable in silico binding affinities between carbosulfan and the predicted core targets. Integrative analysis suggests that carbosulfan exposure is associated with respiratory damage, potentially through interconnected mechanisms involving oxidative stress, inflammation, and disruption of cell signaling and metabolic enzyme systems. However, given the acute high-dose nature of the model and the interpretative integration of multi-omics data, these findings should be considered hypothesis-generating. This study provides a novel system-level perspective on carbosulfan-induced respiratory toxicity and highlights key pathways and targets for future validation in chronic exposure models.

PMID:41828400 | PMC:PMC12984169 | DOI:10.3390/ijms27052170

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