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 >  Protein>GM-CSF >GMF-H4214

Human GM-CSF Protein, premium grade

GMP version GMP-GMFH28 is now available for seamless transition.

分子别名(Synonym)

GM-CSF,CSF2,MGC131935

表达区间及表达系统(Source)

Human GM-CSF, premium grade (GMF-H4214) is expressed from human 293 cells (HEK293). It contains AA Ala 18 - Glu 144 (Accession # NP_000749.2).

Predicted N-terminus: Ala 18

It is produced under our rigorous quality control system that incorporates a comprehensive set of tests including sterility and endotoxin tests. Product performance is carefully validated and tested for compatibility for cell culture use or any other applications in the early preclinical stage.
GMP-GMFH28 is the GMP version of this GMF-H4214. These two proteins display indistinguishable performance profiles, thereby ensuring a seamless transition for end users from early preclinical stag to later clinical phases.

Request for sequence

蛋白结构(Molecular Characterization)

GM-CSF Structure

This protein carries no "tag".

The protein has a calculated MW of 14.5 kDa. The protein migrates as 25 kDa±3 kDa when calibrated against Star Ribbon Pre-stained Protein Marker under reducing (R) condition (SDS-PAGE) due to glycosylation.

内毒素(Endotoxin)

Less than 0.01 EU per μg by the LAL method.

宿主蛋白残留(Host Cell Protein)

<0.5 ng/µg of protein tested by ELISA.

宿主核酸残留(Host Cell DNA)

<0.02 ng/μg of protein tested by qPCR.

无菌(Sterility)

Negative

支原体(Mycoplasma)

Negative.

纯度(Purity)

>95% as determined by SDS-PAGE.

>95% as determined by SEC-MALS.

制剂(Formulation)

Lyophilized from 0.22 μm filtered solution in PBS, pH7.4 with trehalose as protectant.

Contact us for customized product form or formulation.

重构方法(Reconstitution)

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

存储(Storage)

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:

  1. -20°C to -70°C for 24 months in lyophilized state;
  2. -70°C for 3 months under sterile conditions after reconstitution.

质量管理控制体系(QMS)

  1. 质量管理体系(ISO, GMP)
  2. 质量优势
  3. 质控流程
 

电泳(SDS-PAGE)

GM-CSF SDS-PAGE

Human GM-CSF, premium grade on SDS-PAGE under reducing (R) and non-reducing (NR) conditions. The gel was stained with Coomassie Blue. The purity of the protein is greater than 95% (With Star Ribbon Pre-stained Protein Marker).

SEC-MALS

GM-CSF SEC-MALS

The purity of Human GM-CSF, premium grade (Cat. No. GMF-H4214) is more than 95% and the molecular weight of this protein is around 20-30 kDa verified by SEC-MALS.

Report

 

活性(Bioactivity)-CELL BASE

GM-CSF CELL

Human GM-CSF, premium grade (Cat. No. GMF-H4214) stimulates proliferation of TF-1 cells. The specific activity of Human GM-CSF, premium grade is > 5.00ⅹ10^6 IU/mg, which is calibrated against human GM-CSF WHO International Standard (NIBSC code: 88/646) (QC tested).

Protocol

 

活性(Bioactivity)-ELISA

GM-CSF ELISA

Immobilized Human GM-CSF, premium grade (Cat. No. GMF-H4214) at 1 μg/mL (100 μL/well) can bind Human GM-CSF R alpha, Fc Tag (Cat. No. GRA-H5255) with a linear range of 0.2-2.5 ng/mL (QC tested).

Protocol

 

活性(Bioactivity)-BLI

GM-CSF BLI

Loaded Human GM-CSF R alpha, Fc Tag (Cat. No. GRA-H5255) on Protein A Biosensor, can bind Human GM-CSF, premium grade (Cat. No. GMF-H4214) with an affinity constant of 16.8 nM as determined in BLI assay (ForteBio Octet Red96e) (Routinely tested).

Protocol

 

稳定性(Stability)

GM-CSF STABILITY

The Cell based assay shows batch-to-batch consistency between Acro's GMP and PG GM-CSF.

 
评论(16)
  1. 153XXXXXXX5
  2. 4人赞
  3. 使用该产品Mouse SCF / KITLG Protein, His Tag(SCF-M5228-50ug包装),主要出于研究细胞活性实验的目的,应用于诱导人骨髓细胞分化实验,获得了满意的结果,通过诱导4-8周的时间可以得到分化的目的细胞。
  4. 2022-5-21
 
ACRO质量管理体系
 
 

背景(Background)

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is also known as Colony stimulating factor 2 (granulocyte-macrophage), is a cytokine initially characterized by its ability to induce colonies of granulocytes and macrophages from myeloid progenitor cells, and is secreted by macrophages, T cells, mast cells, endothelial cells and fibroblasts. GM-CSF is a cytokine that functions as a white blood cell growth factor. GM-CSF stimulates stem cells to produce granulocytes (neutrophils, eosinophils, and basophils) and monocytes. Monocytes exitthe circulation and migrate into tissue, whereupon they mature into macrophages and dendritic cells. Thus, it is part of the immune/inflammatory cascade, by which activation of a small number of macrophages can rapidly lead to an increase in their numbers, a process crucial for fighting infection. The active form of the protein is found extracellularly as a homodimer. Human GM-CSF glycosylated in its mature form. As a part of the immune/inflammatory cascade, GM-CSF promotes Th1 biased immune response, angiogenesis, allergic inflammation, and the development of autoimmunity, and thus worthy of consideration for therapeutic target. GM-CSF has also recently been evaluated in clinical trials for its potential as a vaccine adjuvant in HIV-infected patients. The preliminary results have been promising. GM-CSF is also used as a medication to stimulate the production of white blood cells following chemotherapy.

文献引用(Citations)

 

前沿进展

The Big Four in the Pathogenesis and Pathophysiology of Prurigo Nodularis: Interplay among Type 2 Inflammation, Epidermal Hyperplasia, Dermal Fibrosis, and Itch from Neuroimmune Dysregulation
Hashimoto, Okuno
Clin Dermatol (2025)
Abstract: Prurigo nodularis (PN) is a distinct inflammatory dermatosis. It is characterized by intensely pruritic, firm nodules, typically 1-2 cm in diameter, which usually develop on the extensor surfaces of the extremities. Histopathologically, the following characteristics are observed in PN lesions: (1) dermal cellular infiltrates composed of type 2 inflammation-associated immune cells with lesional overexpression of type 2 cytokines (including IL-4, IL-13, and IL-31); (2) dermal fibrosis; and (3) epidermal hyperplasia with hyperkeratosis. Additionally, functional and structural alterations of cutaneous sensory nerve fibers profoundly contribute to itch in cooperation with type 2 inflammation. This abnormal interaction is referred to as neuroimmune dysregulation. The scratching behavior induced by itching from neuroimmune dysregulation initiates the development of prurigo nodules. This distinctive pathogenic feature of "itch-first" in PN is distinct from "inflammation-first" in atopic dermatitis, another pruritic skin disease with type 2 inflammation. In atopic dermatitis, the skin initially exhibits type 2 inflammation, which is subsequently followed by itching. The interplay between the four elements, namely type 2 inflammation, epidermal hyperplasia, dermal fibrosis, and itch resulting from neuroimmune dysregulation, appears to be pivotal in the pathogenesis and pathophysiology of PN.Copyright © 2025. Published by Elsevier Inc.
Mechanisms of Itch in Atopic Dermatitis
Kamata, Tominaga, Takamori
Juntendo Med J (2025) 71 (1), 43-50
Abstract: Atopic dermatitis (AD) is a common inflammatory skin disease characterized by recurrent eczematous lesions and intense itch. The pathological mechanism of AD involves a complex interaction between skin barrier dysfunction and a predominantly T helper (Th) 2-skewed immune dysregulation. The dysfunctional skin barrier in AD enhances antigen penetration, exacerbating allergic reactions. Scratching further damages the skin barrier, worsens dryness and increases the release of pro-inflammatory mediators, perpetuating the itch-scratch cycle. Breaking this cycle with appropriate treatments is vital. Th2 cells secrete interleukin (IL)-4, IL-13 and IL-31 which play keys roles in AD pathogenesis. IL-31 directly induces pruritus, while IL-4 and IL-13 enhance itching. An increased density of intraepidermal nerve fibers has been observed in AD lesions in a disease-state-dependent manner. In normal skin, both semaphorin 3A (Sema3A; a nerve repulsion factor) and nerve growth factor (NGF; a nerve elongation factor) are expressed. However, in AD lesions, Sema3A expression decreases while NGF expression increases. These findings suggest that epidermal nerve density is regulated by a fine balance between Sema3A and NGF, with Sema3A playing a key role in itch sensitivity in AD. In healthy skin, Sema3A is produced during the early-stage of differentiation of keratinocytes and moves into the upper epidermis. The levels of Sema3A and the density of epidermal nerve fibers may vary depending on the disease state of AD. Our future research will focus on the regulatory mechanisms of Sema3A in skin, and potential clinical applications.© 2025 The Juntendo Medical Society.
A Case of Erythema Multiforme Following the Administration of Nemolizumab
Mima, Ohtsuka
Cureus (2025) 17 (2), e79070
Abstract: Prurigo nodularis (PN) is a chronic inflammatory skin disorder characterized by intensely pruritic nodules. The pathogenesis of PN involves immune dysregulation, with a predominance of T helper (Th2)-type inflammation, including interleukin (IL)-4, IL-5, IL-13, and IL-31. Nemolizumab, an IL-31 receptor A inhibitor, was newly approved for PN in 2024. We report a case of erythema multiforme (EM) that developed three weeks after the first administration of nemolizumab. Three weeks post-injection, she developed multiple targetoid edematous erythematous patches and plaques on her trunk and limbs, leading to a clinical diagnosis of EM. Since she had no new medications and no recent history of infections, we inferred that the development of EM was likely associated with the administration of nemolizumab. The pathophysiology of EM involves a predominant Th1-driven inflammatory response. Therefore, nemolizumab likely suppressed Th2 inflammation, leading to compensatory Th1 hyperactivation, which may have triggered EM. To our knowledge, this may be the first reported case of EM following nemolizumab treatment for PN. Further research is necessary to investigate its immunomodulatory effects and potential adverse events.Copyright © 2025, Mima et al.
Prurigo Nodularis and Acquired Perforating Dermatosis in Chronic Kidney Disease: Are They the Same Entity?
Mahmoud, Coscarella, Kwak et al
Clin Dermatol (2025)
Abstract: Prurigo nodularis (PN) has been reported in itchy chronic kidney disease (CKD) patients, in particular, in end-stage renal failure. Acquired perforating dermatitis (APD) associated with CKD and diabetes is a group of disorders where dermal materials are eliminated through the epidermis and is characterized by itchy papules and nodules. We focus on the relationship between PN and APD in CKD and provide data to support that both entities share many of the same clinical and histologic features. These cutaneous diseases often go underreported in this patient population, leading to inadequate treatment and suboptimal patient outcomes. Our review of the literature suggests a relationship between PN/APD and CKD, presumably driven by uremic pruritus, changes in the renin-angiotensin-aldosterone system, a predisposing immune dysregulation with increased IL-31 expression, and opioid system imbalances. A variety of pharmacologic therapies may be efficacious. The use of the new targeted biologics for PN and whether they are also helpful for CKD and APD are welcome..Copyright © 2025. Published by Elsevier Inc.
Showing 1-4 of 832 papers.
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GM-CSF靶点信息
英文全称:Macrophage colony stimulating factor 2
中文全称:巨噬细胞集落刺激因子2
种类:Homo sapiens
上市药物数量:0详情
临床药物数量:12详情
最高研发阶段:申请上市
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