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CSF-GM (Leucogen)

✓ Approved

LG Chem Ltd. · CSF2RA · Recombinant Proteins

What is CSF-GM?

CSF-GM is a recombinant proteins developed by LG Chem Ltd.. It is approved for therapeutic indications via injectable (others).

Drug Profile

Brand NamesLeucogen
CompanyLG Chem Ltd.
Drug ClassRecombinant Proteins
Molecular TargetCSF2RA
RouteInjectable (Others)
StatusApproved
Sources: ClinicalTrials.gov, LG Chem Ltd.

Mechanism of Action

Molecular Targets

CSF-GM acts on 1 molecular target:

CSF2RAcolony stimulating factor 2 receptor subunit alpha (CD116, CSF2RX)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

CSF-GM is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Leukaemia✓ Approved
Blood and lymphatic system disordersMyelosuppression✓ Approved

Related Research Articles

PubMedJournal of microbiological methods2026-08-30

Development of an A7G variant of recombinant human G-CSF for improved fibroblast-mediated wound healing.

Thota Sujani S, Myneni Praveen P, Venkateswarulu T C TC

Recombinant human granulocyte colony-stimulating factor (rh-G-CSF) is useful in tissue regeneration due to its angiogenic and anti-inflammatory actions. The current study focused on the downstream process of A7G mutant rh-G-CSF (m-rh-G-CSF) and the effects of m-rh-G-CSF on human fibroblasts. The m-rh-G-CSF was purified and had 97.24% purity, a final protein concentration of 0.814 g/L and a molecular weight of 18,784 Da. The addition of m-rh-G-CSF significantly elevated the ATP level in the treated cells in a concentration-dependent manner. The maximal ATP level was achieved at a concentration of 2.5 μg/mL and was 89% higher than in the control cells and 13% higher than in reference rh-G-CSF. In the scratch-wound assay, 92.67% and 98.69% wound closure were observed at 24 and 48 h after the addition of m-rh-G-CSF, respectively, compared with 49.93% in control cells at 48 h. These findings support the potential of m-rh-G-CSF as a therapeutic candidate for fibroblast-mediated wound healing.

PMID 42669396
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PubMedPakistan journal of medical sciences2026-08-30

Ureaplasma parvum meningitis in neonates: A retrospective case study and literature review.

Yan Fang F, Lin Meifang M, Fu Qinqin Q, Gao Yi Y et al.

To investigate the clinical characteristics and advances in diagnosis and treatment of neonatal Ureaplasma parvum (U. parvum) meningitis. Clinical manifestations, diagnosis, treatment, and follow-up data of a neonate with persistent fever, normal blood routine, but persistently abnormal cerebrospinal fluid (CSF) results due to U. parvum meningitis were retrospectively analyzed. A literature review was conducted to identify relevant studies reporting on neonatal U. parvum meningitis published until May 2025. A male infant born at 35+2 weeks of gestation with eight hours of premature rupture of membranes (PROM) was admitted at 17 days of age with persistent fever. The routine blood test was normal, while the CSF suggested purulent meningitis. Empirical treatment was ineffective, and metagenomic next-generation sequencing (mNGS) of CSF confirmed U. parvum meningitis. The infant recovered after three weeks of azithromycin treatment, but a language delay was found at two-year follow-up. The literature review identified 16 previously reported cases of U. parvum meningitis, which were combined with the current case, totaling 17 cases. Main manifestations included fever and convulsions, or initial circulatory and respiratory symptoms. CSF in the included studies showed leukocytosis, decreased glucose, and elevated protein. Diagnosis was mainly based on mNGS, and the predominant treatment consisted of macrolides, sometimes combined with quinolones, for 3-10 weeks. Two patients relapsed after drug withdrawal, and one had elevated liver enzymes. Major neurological complications included lateral ventricular dilatation and hydrocephalus, cerebral hemorrhage, infarction, malacia, and herniation. Most cases had a favorable prognosis, with rare developmental delay. Clinical manifestations of neonatal U. parvum meningitis are nonspecific. Some patients present with normal blood routine but purulent CSF. U. parvum meningitis should be suspected in patients with poor response to empirical antibiotics and confirmed by CSF mNGS. Macrolides are biologically rational and commonly used for neonatal U. parvum meningitis; however, the optimal regimen and duration remain unclear due to limited and heterogeneous case-based evidence.

PMID 42668932
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PubMedJapanese journal of infectious diseases2026-08-30

Emergence of Human Parechovirus Type 5 Meningitis in Japan, 2025.

Yamamoto Yushi Y, Iwata Aya A, Matsubara Kousaku K, Hamahata Keigo K et al.

Human parechovirus type 5 (HPeV-5) is rarely reported, and, thus, its clinical and virological features remain unclear. This study describes the first cluster of HPeV-5 meningitis in Japan and characterizes its clinical, laboratory, and molecular features. Six infants aged 13-42 days were identified at three municipal hospitals in Kobe, Japan, during a six-week period in summer 2025. Symptoms included fever (6/6), mottled skin (4/6), poor feeding (3/6), and rash (2/6). None developed thrombocytopenia, liver dysfunction, or cerebrospinal fluid (CSF) pleocytosis; one had leukopenia. Two infants who were tested had hyperferritinemia that persisted after defervescence. Fever resolved within three days in all infants, and all were discharged without sequelae. A polymerase chain reaction detected HPeV-5 in the CSF of all infants. A phylogenetic analysis demonstrated high VP1 nucleotide identity (>97%) with strains in Sapporo, Japan (2018), Australia (2019), and USA (2024), suggesting the circulation of a nearly identical lineage across multiple regions. HPeV-5 was also detected in 14 additional non-meningitis cases during the same period, indicating concurrent circulation in the community. These results indicate that HPeV-5 causes meningitis in young infants, even without CSF pleocytosis, and was associated with favorable outcomes in this case series. Continued molecular epidemiological surveillance is warranted.

PMID 42669541
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PubMedThe Journal of craniofacial surgery2026-08-30

Bipedicled Laterally Based Pericranial Flap for Anterior Skull Base Reconstruction.

Ando Taku T, Fujisawa Kou K, Kurita Daichi D, Kitagawa Yosuke Y et al.

Frontal sinus fractures with posterior-wall disruption, dural injury, and cerebrospinal fluid (CSF) leakage require durable separation of the sinonasal cavity from the intracranial space. An anteriorly based pericranial flap is commonly used for this purpose, but its supraorbital and supratrochlear pedicles may be unreliable after frontal soft-tissue trauma or orbital rim fractures. A 67-year-old man sustained complex craniofacial trauma after a fall, including fractures of the anterior and posterior walls of the frontal sinus, a forehead laceration reaching the bone, CSF rhinorrhea, and midfacial fractures. Open reduction and internal fixation of the facial fractures, cranialization of the frontal sinus, dural repair with fascia lata, and anterior skull base reconstruction were performed. Because the anterior pericranial pedicles were suspected to be compromised, a muscle-sparing, bipedicled, laterally based pericranial flap was elevated through a bicoronal approach on the bilateral superficial temporal vascular systems. Intraoperative indocyanine-green angiography confirmed perfusion throughout the flap, which was inset without tension to separate the nasal cavity from the intracranial space. Contrast-enhanced computed tomography at 1 month confirmed enhancement of the transferred flap. At 6 months, there was no recurrent CSF leak, meningitis, or temporal hollowing. A muscle-sparing, bipedicled, laterally based pericranial flap can provide a simple, vascularized, and locally available reconstructive option when the anterior pericranial pedicles are unavailable.

PMID 42669452
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PubMedBrain & development2026-08-30

Cytokine profiles in children with PCR-confirmed HHV-6 infection according to seizure occurrence.

Yeom Jung Sook JS, Kim Young-Soo YS, Park Ji Sook JS, Park Eun Sil ES et al.

Although cytokines are contributors to febrile seizures, previous studies have largely involved pathogen-heterogeneous populations. Human herpesvirus 6 (HHV-6) is a common cause of febrile seizures and is useful for studying pathogen-specific inflammatory responses. This retrospective study included children with polymerase chain reaction-confirmed HHV-6 infection using stored plasma samples obtained within 72 h of hospital presentation, classified according to seizure status. Plasma cytokine levels were measured using a multiplex immunoassay. Multivariable linear regression was used to identify the cytokines associated with seizures, with Benjamini-Hochberg false discovery rate (FDR) correction across 15 cytokines. Correlations between cytokine levels and hematologic parameters were evaluated. Cerebrospinal fluid (CSF)-to-plasma cytokine ratios were analyzed. Sixty patients were included (37, without seizures; 23, seizures), with no significant differences in baseline characteristics between the groups. Plasma interleukin-8 (IL-8) showed an association with seizures (adjusted fold change 1.84, p = 0.03), but this association did not remain statistically significant after FDR correction (q = 0.45). Inverse correlations between IL-8 (and to a lesser extent macrophage inflammatory protein-1 alpha) and neutrophil and platelet counts were observed in the non-seizure group only. In the paired analyses (n = 8), the CSF-to-plasma ratios of IL-8 and monocyte chemoattractant protein-1 exceeded 1.0, with a trend toward higher IL-8 ratios in the seizure group after adjusting for age. Although exploratory, findings from this pathogen-homogeneous cohort suggest that IL-8 is a candidate cytokine associated with both seizure occurrence and an altered relationship with neutrophil and platelet counts, warranting further study.

PMID 42669234
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PubMedCritical reviews in oncology/hematology2026-08-30

Molecular Mechanisms of Exosome-Mediated Drug Resistance in Central Nervous System Tumours.

Mamala Mateusz M, Marczuk Karolina K, Rembiałkowska Nina N

Exosomes are 30-150nm extracellular vesicles released via fusion of multivesicular bodies with the plasma membrane and enriched in selectively sorted proteins, lipids and nucleic acids that reflect both donor-cell state and regulated packaging pathways. In central nervous system (CNS) tumours, exosome-mediated communication is increasingly recognised as a scalable mechanism by which malignant cells coordinate adaptation to therapy across cellular and anatomical barriers, including the blood-brain barrier. This review synthesises current evidence linking exosome biogenesis and cargo selection (ESCRT-associated factors, tetraspanins, Rab GTPases, RNA-binding proteins) with key resistance phenotypes in glioblastoma and other CNS tumour entities. We outline four convergent routes by which exosomes blunt therapeutic efficacy: horizontal transfer of resistance determinants, rapid activation of pro-survival signalling hubs, tumour-microenvironment remodeling, vesicle-enabled "drug scavenging", where cytotoxic agents and/or efflux machinery are sequestered and exported, lowering effective intracellular drug exposure. Finally, we discuss translational opportunities and constraints, highlighting exosome-based liquid biopsy strategies in CSF and blood and therapeutic concepts targeting vesicle biogenesis, release or uptake, while emphasizing the need for rigorous EV characterization and reporting standards to accelerate clinical implementation.

PMID 42669321
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