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

PubMedRespiratory investigation2026-07-17

Inhaled granulocyte-macrophage colony-stimulating for autoimmune pulmonary alveolar proteinosis: From pathogenesis to clinical practice.

Tazawa Ryushi R

Autoimmune pulmonary alveolar proteinosis (aPAP) is a rare, diffuse lung disease characterized by surfactant accumulation in the alveoli, leading to impaired gas exchange and progressive respiratory insufficiency. It is caused by neutralizing autoantibodies against granulocyte-macrophage colony-stimulating factor (GM-CSF), which disrupts the GM-CSF signaling required for alveolar macrophage maturation and surfactant clearance. Whole-lung lavage (WLL), the standard treatment for aPAP, improves oxygenation by removing accumulated surfactants, but is invasive and often must be repeated. An improved understanding of disease pathogenesis has shifted therapy toward restoring GM-CSF signaling, rather than simply removing alveolar material. Thus, inhaled recombinant human GM-CSF is a promising disease-directed therapeutic agent for aPAP. Direct delivery to the alveolar compartment is intended to restore GM-CSF signaling, while minimizing systemic exposure. Randomized controlled trials have demonstrated improvements in oxygenation, pulmonary function, and radiographic findings. Despite these advances, important questions remain unresolved because aPAP is rare and clinical studies have been limited, including the optimal dose, treatment duration, maintenance strategy, and the role of device-dependent drug delivery to the distal lung. This review summarizes the pathogenesis of aPAP, biological rationale for GM-CSF replacement, available formulations and aerosol delivery strategies, and clinical evidence supporting inhaled GM-CSF therapy. This review also discusses unresolved issues and future directions, including the potential contributions of quantitative models of aerosol deposition and pharmacokinetics to optimize treatment.

PMID 42462405
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PubMedXi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology2026-07-17

[Research progress on the trans-organ regulation of renal fibrosis by type 3 innate lymphoid cells].

Wang Qianyu Q, Guo Zhaoan Z

Type 3 innate lymphoid cells (ILC3s) are a subset of innate immune cells regulated by the transcription factor retinoic acid receptor-related orphan receptor γt (RORγt). They are primarily distributed in the intestinal mucosa and lymphoid tissues, where they secrete cytokines such as interleukin 17(IL-17), IL-22, and granulocyte-macrophage colony-stimulating factor (GM-CSF), playing a crucial role in maintaining intestinal mucosal homeostasis, defending against pathogen invasion, and modulating immune responses. Renal fibrosis (RF) is a pathological process triggered by pathogenic factors such as trauma, infection, inflammation, or metabolic abnormalities. It is characterized by damage to renal parenchymal cells, abnormal deposition of extracellular matrix (ECM), and progressive fibrosis of renal tissue, ultimately leading to irreversible loss of kidney function. Recent studies have revealed that ILC3s not only contribute to intestinal homeostasis but are also involved in the progression of RF. Therefore, this review summarizes the research advances in the mechanisms of ILC3-mediated cross-organ regulation in RF, aiming to provide new perspectives for the prevention and treatment of RF.

PMID 42463315
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PubMedAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2026-07-17

Recipient interleukin-1β production is critical for lung allograft acceptance.

Bery Amit I AI, Yokoyama Yuhei Y, Nunna Venkatrao V, Amrute Junedh M JM et al.

Proinflammatory cytokines, including IL-1β, TNF-α, and IL-6 have been linked to graft rejection and protocols have been developed to target these in solid organ transplant recipients. Pathways regulating rejection and tolerance differ across organs and remain poorly understood in lungs. Here, we used a mouse lung transplantation model to examine the role of inflammatory cytokines in graft acceptance. We found that recipient IL-1β drove systemic granulocyte colony-stimulating factor (G-CSF) release early after transplantation and promoted allograft infiltration with neutrophils that express immunosuppressive gene signatures. IL-1β promoted inducible nitric oxide synthase (iNOS) expression in neutrophils and accumulation of nitric oxide (NO) in allografts, a pathway that is critical for the acceptance of transplanted lungs. We observed that human and mouse neutrophils from lung transplant recipients suppress T cell responses in an NO-dependent fashion. Finally, recipients deficient in Il1b, but not Tnfa or Il6, acutely rejected lung allografts despite receiving immunosuppression that results in tolerance when administered to wildtype hosts. Thus, contrary to the widely held notion that proinflammatory cytokines promote deleterious outcomes after transplantation, our findings uncovered a previously unknown role for recipient IL-1β as a critical mediator of pulmonary allograft acceptance. Our findings inform future studies developing lung-specific immunosuppressive strategies.

PMID 42462852
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PubMedExpert opinion on biological therapy2026-07-17

Targeting autoimmune pulmonary alveolar proteinosis with GM-CSF: insights from clinical trials and emerging therapies.

Higgins Margaret M, Boyle Niamh N, McCarthy Cormac C

Pulmonary alveolar proteinosis (PAP) is a rare lung disease caused by impaired surfactant clearance resulting in lipoproteinaceous material accumulation in the alveoli often causing progressive dyspnea and respiratory failure. Autoimmune PAP (aPAP), accounting for ~90% of cases with a prevalence of 6.7-6.9 per million, disrupts granulocyte-macrophage colony-stimulating factor (GM-CSF) signaling via neutralizing autoantibodies. This article explores the role of GM-CSF in the pathogenesis and treatment of PAP. GM-CSF autoantibodies block signaling essential for alveolar macrophage function. Therapeutic whole lung lavage (WLL) remains the gold standard of treatment for PAP. While WLL is an effective and safe treatment, and can indeed complement GM-CSF therapy, it is labor intensive and often requires repeated procedures. GM-CSF augmentation represents a new era of therapeutic advancement targeting the pathogenesis of PAP to ensure sustained, efficacious results. Inhaled GM-CSF shows superior efficacy over subcutaneous treatment. Trials through recent decades including IMPALA-2 show improvements in symptoms physiology, radiology with a favorable safety profile. These studies have helped inform the much-needed European Respiratory Society guidelines for the diagnosis and management of PAP in 2024. Despite our greater understanding of this ultra-rare disease, further studies are required to explore the mechanistic and logistical aspects of treatment with GM-CSF. We explore some of these aspects in our expert opinion section.

PMID 42466621
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PubMedInternational journal of cancer2026-07-17

Survival Outcomes Associated With Short-Acting Versus Long-Acting G-CSF Use During First-Line Chemoimmunotherapy for Advanced Lung Cancer: A Retrospective Study.

Xiong Yanjuan Y, Guo Wenjing W, Ma Chenxi C, Ren Xiubao X et al.

While granulocyte colony-stimulating factor (G-CSF) is used to prevent and treat chemotherapy-induced neutropenia, it also regulates key immune cells and may therefore affect the efficacy of immunotherapy. Short-acting and long-acting G-CSF have similar efficacy in managing neutropenia, but they differ in effects on immune cells. However, the overall impact of G-CSF and its different formulations on survival in advanced lung cancer patients receiving chemoimmunotherapy remains unclear. This retrospective study enrolled patients with advanced primary lung cancer receiving first-line chemoimmunotherapy at Tianjin Medical University Cancer Institute and Hospital. The primary outcome was overall survival (OS). Inverse probability of treatment weighting (IPTW) was used to balance heterogeneity between groups. Kaplan Meier and Cox models were used to estimate OS and progression-free survival (PFS). Among 606 patients, 308 developed neutropenia and received G-CSF support (pegylated recombinant human G-CSF [PEG-rhG-CSF]: 183; recombinant human G-CSF [rhG-CSF]: 125); 298 without neutropenia received no G-CSF. After IPTW, no significant differences in PFS and OS were observed between G-CSF group and non-G-CSF group. Patients receiving rhG-CSF had significantly improved OS (42.6 vs. 28.2 months, p = 0.041) and PFS (15.4 vs. 9.4 months, p < 0.001) than those receiving PEG-rhG-CSF. Multivariable analysis confirmed rhG-CSF as a favorable independent prognostic factor for both PFS and OS. Among patients with advanced primary lung cancer receiving first-line chemoimmunotherapy, G-CSF support effectively abrogates the adverse survival impact of chemotherapy-induced neutropenia. Moreover, rhG-CSF was associated with improved clinical outcomes versus PEG-rhG-CSF. Prospective randomized trials are required to validate these findings and guide clinical practice.

PMID 42463467
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PubMedStem cell research & therapy2026-07-17

Patient-derived decidual organoids reveal rhG-CSF-associated protective responses involving JAK2/STAT3 signaling in recurrent spontaneous abortion.

Wei Changqiang C, Tan Xuemei X, Wei Yiyun Y, Cheng Jinlian J et al.

Recurrent spontaneous abortion (RSA) is a complex reproductive disorder frequently lacks effective therapeutic interventions. Recombinant human granulocyte colony-stimulating factor (rhG-CSF) has shown promise in improving pregnancy outcomes in RSA, but its underlying mechanisms remain unclear. Organoid technology offers new opportunities for disease modeling and mechanistic research in reproductive medicine. Decidual tissue samples from RSA patients were utilized to establish decidual organoids using three-dimensional (3D) culture techniques. These organoids were characterized via morphological observation, hematoxylin and eosin (H&E) and Periodic Acid-Schiff (PAS) staining, immunofluorescence, and immunohistochemistry to validate key marker expression and hormone responsiveness. The effects of rhG-CSF on organoid viability were evaluated using luminescence assays. Transcriptomic sequencing and bioinformatics analyses were performed to identify differentially expressed genes and pathways following rhG-CSF stimulation. Protein expression and signaling pathway activation were further assessed via Western blot analysis. Decidual organoids were successfully established and recapitulated the structural and functional features of primary tissue, including hormone responsiveness and marker expression. rhG-CSF significantly promoted organoid proliferation, enhanced anti-apoptotic and angiogenic capacity, and induced inflammatory responses. Transcriptomic and pathway analyses indicated an enrichment and activation of the JAK2/STAT3 signaling pathway following rhG-CSF treatment. Western blot indicated increased phosphorylation of JAK2 and STAT3, upregulation of PCNA, VEGFA, IL-1β, IL-6, and Bcl-2, and downregulation of Bax in response to rhG-CSF. A patient-derived decidual organoid model was established and validated to recapitulate in vivo tissue characteristics. In this in vitro RSA model, rhG-CSF appeared to exert protective effects by promoting proliferation, inhibiting apoptosis, and enhancing angiogenesis-responses that are potentially associated with the activation of JAK2/STAT3 signaling. These findings provide new insights and experimental evidence that may inform future RSA treatment strategies.

PMID 42464318
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