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CSF-GM (Leucogen)

✓ Approved

LG Chem Ltd. · CSF2RA · 重组蛋白

什么是 CSF-GM？

CSF-GM 是一种重组蛋白，由LG Chem Ltd.研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)。

药物档案

商品名Leucogen
公司LG Chem Ltd.
药物类别重组蛋白
分子靶点CSF2RA
给药途径Injectable (Others)
状态Approved
来源： ClinicalTrials.gov, LG Chem Ltd.

作用机制

分子靶点

CSF-GM 作用于 1 个分子靶点：

CSF2RAcolony stimulating factor 2 receptor subunit alpha (CD116, CSF2RX)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

CSF-GM 针对 2 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Leukaemia✓ Approved
Blood and lymphatic system disordersMyelosuppression✓ Approved

相关研究文献

PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-08-06

GM-CSF Promotes Neutrophil PD-L1 Expression Through the VEGFR-2/STAT6/CSF2 Signaling Axis in Oral Squamous Cell Carcinoma.

Zhu Fangxing F, You Yuanhe Y, Zhang Yiyi Y, Dai Yibin Y et al.

Oral squamous cell carcinoma (OSCC) remains a highly aggressive malignancy with limited responsiveness to anti-PD-1 immunotherapy. Recent neoadjuvant studies combining VEGFR-2 inhibition (VEGFR2i) with anti-PD-1 (aPD-1) have yielded markedly improved pathological responses, suggesting a VEGFR-2-dependent immunoregulatory mechanism. Here, we identify a PD-L1-expressing CD66b+ neutrophil-enriched tumor-associated population as a critical immunosuppressive population enriched in VEGFR-2-high OSCC tumors and associated with increased metastatic propensity and inferior patient outcomes. Using multiplex immunohistochemistry, scRNA-seq, and flow cytometry, we demonstrate that VEGFR-2-overexpressing OSCC cells drive robust GM-CSF secretion, which in turn induces PD-L1 upregulation in neutrophils. Mechanistically, VEGFR-2 activation promotes STAT6 phosphorylation and nuclear translocation, enabling direct transcriptional activation of CSF2. GM-CSF subsequently activates STAT5 and mTOR/S6K signaling in neutrophils, thereby enhancing PD-L1 protein synthesis. Functionally, these PD-L1+ TANs suppress CD8+ T-cell proliferation, augment T-cell exhaustion, and diminish cytotoxicity. Importantly, VEGFR-2 inhibition or GM-CSF neutralization restored CD8+ T-cell function and improved responsiveness to anti-PD-1 therapy in vivo, whereas exogenous GM-CSF impaired VEGFR2i/aPD-1 efficacy. Collectively, our findings reveal a previously unrecognized VEGFR-2/STAT6/CSF2 axis that licenses neutrophil-mediated immune suppression in OSCC. These data provide mechanistic rationale and preclinical support for targeting the VEGFR-2/GM-CSF-neutrophil axis to improve the efficacy of PD-1 blockade in OSCC.

PMID 42559673
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PubMedFrontiers in microbiology2026-08-06

Interpreting combined BALF-galactomannan and next-generation sequencing in pulmonary aspergillosis and mucormycosis: a two-center clinical decision framework.

Yang Lan L, Zhang Xiaoqi X, Su Nan N, Li Lijuan L

To identify which patients with pulmonary aspergillosis or mucormycosis (PAM) derive the greatest incremental diagnostic benefit from next-generation sequencing (NGS) beyond conventional microbiology, and to derive a GM × NGS interpretive framework that identifies the patient subgroup in which NGS adds the most information, based on routinely available bedside variables. Secondary objectives were to characterize the pathogen spectrum detected by NGS, quantify pairwise concordance with BALF galactomannan and culture, and assess the relationship between quantitative Aspergillus reads and BALF-GM intensity. Two-center retrospective case-cohort study of 595 adults with NGS-tested pulmonary aspergillosis or mucormycosis (PAM; proven, probable, or possible per EORTC/MSGERC and ECMM-MSGERC criteria). Primary method-comparison analysis was restricted to the strict subset with NGS, BALF-galactomannan (GM), and culture all available (n = 434). Total Aspergillus reads were defined as the per-case sum of species-level Aspergillus reads parsed from free-text NGS reports, with Mucorales reads excluded. Multivariable logistic regression identified predictors of GM-negative status among NGS-positive cases (n = 353; complete-case n = 342). The prospective component was registered at the Chinese Clinical Trial Registry (ChiCTR2500099900). In the strict 434-case subset, NGS fungal-signal positivity was 81.3%, BALF-GM (≥0.8) 58.1%, and culture 43.1%; pairwise overlap was substantial but incomplete. The GM-negative/NGS-positive subgroup (n = 150) showed a milder phenotype than GM-positive/NGS-positive cases (severe pneumonia 28.7% (43/150) vs. 52.7% (107/203); mortality 6.7% (10/150) vs. 19.7% (40/203); both p < 0.001). Severe pneumonia was independently inversely associated with GM-negative status (adjusted OR 0.44, 95% CI 0.26-0.75, p = 0.002), while immunocompromise was independently positively associated (adjusted OR 2.01, 95% CI 1.17-3.47, p = 0.012). NGS Aspergillus positivity was essentially flat across BALF-GM intensity bands (79-82%); read counts correlated only weakly with BALF-GM titer [Spearman ρ = 0.185 (mNGS-only, n = 246)]. When BALF-GM and NGS are co-ordered on the same lavage in routine PAM workup, the four GM × NGS quadrants define distinct clinical phenotypes with concrete management implications: NGS positivity in GM-negative cases (34.6%) carries the highest incremental yield and a milder phenotype; conversely, a negative NGS in GM-positive cases must not be used to rule out severe PAM. Across quadrants, NGS adds species- and co-pathogen-level information that changes therapy.

PMID 42559192
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PubMedFrontiers in nutrition2026-08-06

Dietary index for gut microbiota score is inversely associated with carotid calcified plaque score in ischemic stroke patients.

Guan Yichao Y, Chang Dujuan D

Diet influences gut microbiota-derived metabolites, which may affect vascular inflammation and calcification. The Dietary Index for Gut Microbiota (DI-GM) captures dietary patterns hypothesized to support favorable microbial metabolite profiles. In this study, we examined whether higher DI-GM scores are associated with lower carotid calcification burden in ischemic stroke patients and whether trimethylamine N-oxide (TMAO) is statistically associated with this relationship, without implying causality. In this cross-sectional study of 788 ischemic stroke patients from Central Hospital Affiliated to Shandong First Medical University, we calculated DI-GM scores from validated food frequency questionnaires and quantified carotid calcification using the Agatston method via computed tomography angiography. Plasma TMAO levels were measured by enzyme-linked immunosorbent assay (ELISA) ELISA. Our findings revealed that participants in the highest DI-GM tertile had significantly lower calcification scores (76.07 ± 14.55) compared to the lowest tertile (316.00 ± 75.33, p < 0.001). Higher DI-GM scores correlated with lower TMAO, and decreased inflammatory markers (all p < 0.001). Each one-unit increase in DI-GM was independently associated with lower calcification odds (adjusted OR = 0.60, p = 0.02). Mediation analysis confirmed that TMAO significantly mediated these associations, accounting for substantial proportions of the total effects of DI-GM score on inflammatory markers, plaque thickness, and calcification score. Higher DI-GM score is cross-sectionally associated with lower carotid calcification and TMAO-mediated pathways, but causality remains unproven without longitudinal and microbiome-sequencing data.

PMID 42558262
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PubMedNeurobiology of disease2026-08-06

Bi-compartmental CSF-serum analysis of NfL and GFAP differentiates central and peripheral pathology in neuroinfectious diseases: A monocentric real-world cohort study.

Erhart Deborah K DK, Fazeli Badrieh B, Bachhuber Franziska F, Soylu Önder Ö et al.

Neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP), established biomarkers of neuroaxonal injury and astroglial pathology, are frequently only assessed in blood, which limits conclusions regarding their origin. Bi-compartmental analyses of CSF and serum may help differentiate central or peripheral origin of biomarker elevation. Moreover, studies on NfL and GFAP in distinct neuroinfectious disease (NID) phenotypes, particularly those based on real-world cohorts, are limited. This retrospective monocentric study analyzed CSF and serum from patients with (meningo-)encephalitis/myelitis (TI+; n = 48), meningitis (TI-; n = 80), (cranial) nerve palsies/polyradiculitis (PND; n = 61), and 113 non-neuroinflammatory/non-neurodegenerative controls. A bi-compartmental model using scatter plots and simple linear regression was applied to assess the origin of blood biomarker levels and discriminate between central and peripheral pathology. CSF and serum NfL and GFAP z-scores were significantly higher in TI+ compared with TI- (CSF-GFAP p < 0.001/sGFAP p = 0.0083; CSF-NfL p = 0.003/sNfL p = 0.0004). TI+ and PND differed only in GFAP levels, which were higher in TI+ (CSF-GFAP p = 0.0049/sGFAP p = 0.003). The overall group effect (p ≤ 0.003) and principal findings remained significant after adjustment for age, sex, QAlb, and time since (symptom) onset to LP. Bi-compartmental analysis revealed simultaneous elevation of CSF and serum NfL in TI+, indicating predominantly central origin, whereas PND demonstrated a shift toward higher sNfL levels suggesting peripheral origin. Higher clinical severity (modified Rankin Scale 3-5) was associated with elevated serum and CSF GFAP and NfL (sGFAP p = 0.012/sNfL p = 0.002; CSF-GFAP p < 0.0001/CSF-NfL p = 0.0001), which also predicted unfavorable outcome at discharge (sGFAP p = 0.006/sNfL p = 0.004; CSF-GFAP p = 0.003/CSF-NfL p = 0.012). NfL and GFAP were associated with brain/myelon involvement in NID, predominantly reflecting central pathology. Despite strong CSF-serum correlations, bi-compartmental approaches provide additional insight into biomarker origin and disease compartment.

PMID 42556654
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PubMedBrain research bulletin2026-08-06

White and gray matter microstructural alterations in subjective cognitive decline: An exploratory study using TBSS and GBSS.

Lin Shuai S, Xue Ming M, Xu Chang C, Sheng Chenjun C et al.

Subjective cognitive decline (SCD), which may represent the preclinical stage of Alzheimer's disease (AD) in a subset of individuals, lacks objective biomarkers, thus hindering the implementation of early intervention for AD. This study tentatively explored the potential value of neurite orientation dispersion and density imaging (NODDI) in assessing the microstructural integrity of gray matter (GM) and white matter (WM) in SCD. We enrolled 47 SCD subjects and 30 healthy controls (HCs). Through the TBSS and GBSS analysis based on NODDI, the neurite density index (NDI) and orientation dispersion index (ODI) were used to evaluate the microstructural integrity of GM and WM. NODDI parameters were extracted from multiple brain regions to assess their diagnostic utility in distinguishing SCD from HCs. In WM microstructure, NDI of the genu of corpus callosum was decreased, and the ODI of the left posterior thalamic radiation and posterior corona radiata were decreased. In GM microstructure, the NDI of the left hippocampus, amygdala and parahippocampal gyrus were decreased, whereas the ODI of the rolandic operculum, opercular part of inferior frontal gyrus, and precentral gyrus were increased. Logistic regression analysis results showed that the NDI value of GM, the ODI value of GM and the ODI value of WM were independent predictors and the combination of the three parameters had the best classification effect. This exploratory study suggests that NODDI may detect microstructural differences in GM and WM associated with SCD. These preliminary findings provide hypothesis-generating clues for future research into potential imaging markers for identifying SCD individuals. Additional studies are necessary to confirm these preliminary results.

PMID 42551762
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PubMedMolecular neurobiology2026-08-06

Hematopoietic Growth Factors Induce More Extensive Transcriptomic Remodeling in Cerebral Monocytes/Macrophages than in Microglia During the Chronic Phase of Traumatic Brain Injury.

Gaire Sushil S, Gardner Robert S RS, Kyle Michele M, Qiu Xuecheng X et al.

Previous studies show that combined treatment with stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) enhances brain repair and functional recovery during the chronic phase of severe traumatic brain injury (TBI), but the underlying mechanisms remain unclear. Here, we investigated whether SCF + G-CSF modulates brain immune cell states during chronic TBI. In a controlled cortical impact mouse model, SCF + G-CSF was administered subcutaneously for 5 consecutive days beginning 8 months post-injury. CD11b⁺ brain immune cells, including microglia and monocytes/macrophages (Mo/Mac), were isolated one day after the final injection and analyzed by single-cell RNA sequencing. Integrated analyses revealed more extensive transcriptomic changes in Mo/Mac than in microglia following SCF + G-CSF treatment. Flow cytometry confirmed a significant increase in the CD11b+/CD45high Mo/Mac population following treatment. In microglia, SCF + G-CSF modestly upregulated genes such as S100a8, S100a9, Mir682, and Rpl37rt. In contrast, Mo/Mac showed robust upregulation of genes including Wfdc17, Ifitm1/2/3, Tspo, Lrg1, and Igfbp6, consistent with transcriptomic signatures associated with antiviral defense, anti-inflammatory regulation, and acquisition of reparative phenotypes. Volcano plot analysis demonstrated more extensive transcriptomic remodeling in infiltrating peripheral immune cells than in resident microglia. Pathway analysis identified interleukin-17 signaling as a candidate pathway associated with SCF + G-CSF treatment, along with enrichment of programs related to protein synthesis, detoxification, and glial development. Together, these findings demonstrate that the transcriptomic response to SCF + G-CSF treatment is more pronounced in cerebral monocyte/macrophage populations than in microglia, providing insight into candidate immunomodulatory mechanisms associated with brain repair in chronic TBI.

PMID 42557490
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