Drug Database
GR

granulocyte colony stimulating factor (Hebervital)

✓ Approved

Heber Biotec · CSF3 · Recombinant Proteins

What is granulocyte colony stimulating factor?

granulocyte colony stimulating factor is a recombinant proteins developed by Heber Biotec. It is approved for therapeutic indications via injectable (others).

Drug Profile

Brand NamesHebervital
CompanyHeber Biotec
Drug ClassRecombinant Proteins
Molecular TargetCSF3
RouteInjectable (Others)
StatusApproved
Sources: ClinicalTrials.gov, Heber Biotec

Mechanism of Action

Molecular Targets

granulocyte colony stimulating factor acts on 1 molecular target:

CSF3colony stimulating factor 3 (GCSF, CSF3OS)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

granulocyte colony stimulating factor is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Blood and lymphatic system disordersNeutropenia✓ Approved
Blood and lymphatic system disordersBone marrow disorder✓ Approved

Related Research Articles

PubMedBioresource technology2026-07-25

Systematic engineering of Pichia pastoris for high-level production of recombinant human granulocyte-macrophage colony-stimulating factor.

Cheng Zhenzhen Z, Gong Keyu K, Song Yuchao Y, Guo Zhenchang Z et al.

Human granulocyte-macrophage colony-stimulating factor (hCSF2) is a clinically important therapeutic glycoprotein with growing market demand, underscoring the need for efficient recombinant production platforms. To enable high-level production of recombinant hCSF2 (rhCSF2), the Pichia pastoris GS115 strain was systematically engineered through multi-copy integration of the expression cassette, screening for suitable secretory signal peptides, and enhancement of protein folding and transport pathways. The combination of multi-copy integration at multiple genomic loci with the combinatorial use of endogenous and exogenous signal peptides proved critical for improving rhCSF2 titers, while reinforcement of the folding and transport machinery further alleviated the bottleneck of protein throughput. Following high-density fermentation in a 3‑L bioreactor, the optimally engineered strain achieved an rhCSF2 titer of 3.4 g/L-markedly exceeding the highest titer previously reported in yeast hosts by an order of magnitude. Importantly, this engineering strategy was successfully extended to a glycoengineered strain SuperMan5, where it enabled production of rhCSF2 with more homogeneous and humanized N‑glycans and a titer of 4.3 g/L under high‑density fermentation condition. Our work demonstrates that the high-yield production of recombinant human therapeutic glycoproteins bearing homogeneous, humanized N-glycans in engineered yeast offers promising prospects.

PMID 42498019
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PubMedImmunotherapy advances2026-07-25

Growth factor supportive care for chemotherapy-induced neutropenia suppresses antitumour immunity in checkpoint blockade-responsive pancreatic cancer.

Parent Brendan D BD, Kelly Anthony E AE, Hoffman Megan T MT, Dougan Michael M et al.

Growth factors, including granulocyte colony-stimulating factor (G-CSF; pegfilgrastim, filgrastim), are used for prophylaxis or treatment of chemotherapy-induced neutropenia, yet their effects on antitumour immunity remain incompletely understood. We previously found that serum from patients with pancreatic ductal adenocarcinoma (PDAC) treated with multiagent chemotherapy plus G-CSF drove differentiation of T cell-suppressive monocytes in vitro, suggesting that supportive care interventions may shape immune responses in this disease. We evaluated the immunologic and therapeutic impact of G-CSF in two murine PDAC models that differ in their baseline frequencies of infiltrating T cells and in their responsiveness to checkpoint blockade immunotherapy. In poorly immunogenic, T-cell-low tumours, use of G-CSF did not affect tumour growth or response to chemo- or immunotherapy, although neutrophil recovery was improved in mice receiving FOLFIRINOX and G-CSF compared to chemotherapy alone. In immunogenic tumours with a robust endogenous T-cell response, combination anti-PD1 and anti-CTLA-4 therapy resulted in durable tumour clearance. Combination with G-CSF diminished the effectiveness of checkpoint blockade and resulted in significantly fewer cured mice. G-CSF, commonly used for supportive care with FOLFIRINOX and other chemotherapy regimens, induces systemic immune suppression that can reduce the efficacy of T-cell-targeting immunotherapies.

PMID 42500327
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PubMedJournal of immunology (Baltimore, Md. : 1950)2026-07-25

Donor cell GATA3 is critical for gut pathogenic T cell effector function and intestinal eosinophilia after hematopoietic cell transplantation.

Yeo Franklin J FJ, Wang Mengbo M, Park Sungtae S, Rodriguez J Alejandra JA et al.

Hematopoietic cell transplantation (HCT) is a curative immunotherapy for hematologic malignancies such as acute myeloid leukemia, primarily through graft-versus-tumor (GVT) effects mediated by donor T cells. However, up to 60% of recipients develop graft-versus-host disease (GVHD), with intestinal involvement being a major contributor to morbidity and mortality. While CD8 T cells drive GVT, CD4 T helper (Th) cells are largely the key mediators of intestinal GVHD. Although IFN-γ-producing Th1 cells have been implicated in this process, recent evidence suggests a more complex role for Th cell subtypes. In our study, we identify the transcription factor GATA3, often associated with Th2 function, as a key regulator of Th cell proliferation, gut persistence, and cytokine production. Specifically, donor cell GATA3 was required for the early production of gut‑damaging granzyme A by intestinal Th cells and sustained granulocyte-macrophage colony-stimulating factor (GM‑CSF) production at later phases of the intestinal GVHD response. GATA3‑mediated maintenance of GM‑CSF expression during these later stages of disease was associated with increased intestinal eosinophil recruitment and activation, features that have been linked to GVHD severity in humans. Collectively, our findings demonstrate that GATA3‑expressing Th cells contribute to intestinal GVHD pathogenesis by sustaining GM-CSF-driven inflammatory circuits and promoting chronic eosinophilia. Targeting GATA3, or its downstream effector pathways, may therefore represent a novel therapeutic strategy to attenuate intestinal GVHD while preserving the overall efficacy of HCT.

PMID 42498264
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PubMedOncology research2026-07-25

Real-World Experience with Venetoclax Therapeutic Drug Monitoring in Acute Myeloid Leukemia: Role of Posaconazole, Correlation with Safety and Efficacy.

Sani Beatrice B, Cignetti Alessandro A, Leporati Marta M, Sommariva Sara S et al.

Objectives: Venetoclax (VEN) is approved for acute myeloid leukemia (AML) in association with azacitidine, in a 28-day schedule at a fixed dosage, which requires reduction if azoles are co-administered. The present study aims to evaluate VEN therapeutic drug monitoring (TDM) in a real-word setting, where the VEN schedule is frequently reduced, investigating: (i) the posaconazole impact, and (ii) whether VEN exposure correlates with safety and efficacy. Methods: We analyzed data from 43 AML patients treated with different VEN-containing regimens, for whom a near-trough VEN plasma concentration (Cmin) was determined at different timepoints (days 5-8-11-15-22-29) across different cycles (163 cycles, 290 determinations). The posaconazole impact was explored in the whole study population, while safety and efficacy were investigated only in patients treated with azacitidine-VEN, respectively in the safety (35 patients) and in the efficacy subset (29 patients at their first cycle). VEN exposure was expressed through multiple parameters, taking into account both VEN concentrations and the days of VEN administration. Results: Posaconazole was used in 40.5% of cycles and, despite dose adjustment, was associated with: (i) greater interpatient variability, (ii) higher VEN concentrations, (iii) delayed elimination, (iv) accumulation along the cycle, and (v) the need for VEN-dosage change. In the safety subset, VEN exposure correlated with neutropenia and its duration, Granulocyte Colony-Stimulating Factor requirement, platelet transfusions, cycle duration, and infections. Finally, no correlation was found between VEN exposure and response in the efficacy subset. Conclusion: VEN TDM appears valuable in clinical practice to reduce toxicity, especially in patients receiving posaconazole, where VEN exposure remains highly unpredictable.

PMID 42500589
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PubMedBrain communications2026-07-25

The ILLUMINATE natural history study in colony-stimulating factor 1 receptor-related adult-onset leukoencephalopathy with axonal spheroids and pigmented glia.

Lynch David S DS, Wade Charles C, Schöls Ludger L, Hayer Stefanie N SN et al.

Colony-stimulating factor 1 receptor-related adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (CSF1R-ALSP) is a rare, fatal, autosomal-dominant neurodegenerative disorder caused by pathogenic CSF1R variants and characterized by progressive cognitive, neuropsychiatric, and motor dysfunction, white matter lesions on brain imaging, and white matter demyelination, swollen axons, and pigmented glial cells on pathology. Limited data regarding clinical, biofluid or radiological biomarkers of disease severity are available, and no clinical trial endpoints have yet been validated. The objectives of this first-of-its-kind, prospective, observational natural history study were to characterize the clinical trajectory of CSF1R-ALSP and to identify and evaluate key biomarkers and clinical endpoints indicative of disease severity and progression. ILLUMINATE (NCT05020743) was a multicentre, noninterventional natural history study of adults with CSF1R-ALSP and prodromal carriers of CSF1R variants. Participants were followed for up to 36 months, with clinical assessments, fluid biomarkers and volumetric MRI assessments of brain atrophy collected at screening and every 6 months. This study was terminated early (4 June 2025). The analyses reported here include data collected through 19 February 2025. Of 53 participants, 19 were prodromal and 34 were symptomatic (11 of whom had a history of haematopoietic stem cell transplant and 23 who did not). Mean participant age was 47.8 (standard deviation, 4.5) years, and 36.4% were female. Prodromal participants remained relatively stable over 36 months, with little change in neurological function, neurodegeneration biomarkers or radiological disease burden. Impaired neurological function, MRI characteristics of CSF1R-ALSP, and elevated NfL (neurofilament light chain; neurodegeneration biomarker) and GFAP (glial fibrillary acidic protein; astrogliosis biomarker) levels were more pronounced at baseline and often showed progression over time among symptomatic participants who had not previously received haematopoietic stem cell transplant compared with participants who had previously received haematopoietic stem cell transplant. Significant correlations were observed at baseline and longitudinally between MRI measures of brain atrophy and clinical outcome measures. Based on the fluid biomarkers, MRI measures, and clinical outcome assessments evaluated here, active neurodegeneration, widespread changes visualized on brain MRI, and impaired cognitive and motor function were observed in symptomatic patients with CSF1R-ALSP. The neurological impairment can be assessed using the Montreal Cognitive Assessment and Cortical Basal ganglia Functional Scale. Our data suggest that quantification of brain atrophy using MRI volumetry is a potential biomarker of disease severity and progression in CSF1R-ALSP. It is hoped that this report will contribute to the understanding of disease progression in CSF1R-ALSP and inform future drug development.

PMID 42500553
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PubMedClinics and research in hepatology and gastroenterology2026-07-25

Real world experience with granulocyte and monocyte adsorptive apheresis (ADACOLUMN®) in patients with refractory inflammatory bowel disease: a retrospective observational multicenter cohort study.

Hupé Marianne M, Bouguen Guillaume G, Buisson Anthony A, Landman Cecilia C et al.

The exact positioning of granulocyte and monocyte adsorptive apheresis (GMA) using the ADACOLUMN® system (JIMRO, Takasaki, Japan) remains unclear in the era of advanced therapy. We conducted a retrospective multi-centre cohort study which included all patients with active Crohn's disease (CD) or ulcerative colitis (UC) who were treated with GMA alone or in combination with advanced therapy at 15 French tertiary care centres between 2007 and 2024. A total of 129 patients with IBD (median age: 40.9 years; IQR: 29.3-58.1; 79% with UC; IBD duration: 7.0 [2.9-13.1] years; 97 (75%) had been previously exposed to advanced therapies) were included. In patients with UC, the rates of clinical remission, steroid-free clinical remission, and response at week 14 were 33.3%, 27.5%, and 52.0%, respectively. In patients with CD, the corresponding rates were 33.3%, 29.6% and 66.7%, respectively. At week 54, 33 patients (26%) were still receiving maintenance GMA therapy, including 12 with CD and 21 with UC. Among these patients, the rates of steroid-free clinical remission were 71.4% for those with UC and 41.7% for those with CD. A total of 26 adverse events were reported, 16 of which were an exacerbation of IBD activity. In this real-world cohort of patients with refractory IBD, GMA induced steroid-free clinical remission in one-third of patients with CD and UC by week 14. A significant proportion of patients who continued GMA therapy beyond week 14 experienced ongoing clinical benefits.

PMID 42498026
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