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Human PCSK9 Protein, Fc Tag

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分子别名(Synonym)

PCSK9,FH3,HCHOLA3,LDLCQ1,NARC1,PC9

表达区间及表达系统(Source)

Human PCSK9, Fc Tag (PC9-H5256) is expressed from human 293 cells (HEK293). It contains AA Gln 31 - Gln 692 (Accession # Q8NBP7-1).

Predicted N-terminus: Gln 31

Request for sequence

蛋白结构(Molecular Characterization)

PCSK9 Structure

This protein carries a human IgG1 Fc tag at the C-terminus. This protein undergoes autocatalytic cleavage to release the pro-peptide and mature chain. The pro-peptide and mature chain are associated through non‑covalent interactions and with a calculated MW of 13.8 kDa and 83.7 kDa respectively. The protein migrates as 16 kDa and 100 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.

内毒素(Endotoxin)

Less than 1.0 EU per μg by the LAL method.

纯度(Purity)

>90% as determined by SDS-PAGE.

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 12 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)

PCSK9 SDS-PAGE

Human PCSK9, Fc Tag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 90%.

 

活性(Bioactivity)-ELISA

PCSK9 ELISA

Immobilized Human VLDL R, His Tag (Cat. No. VLR-H5227) at 5 μg/mL (100 μL/well) can bind Human PCSK9, Fc Tag (Cat. No. PC9-H5256) with a linear range of 1-10 ng/mL (QC tested).

Protocol

PCSK9 ELISA

Immobilized Human PCSK9, Fc Tag (Cat. No. PC9-H5256) at 5 μg/mL (100 μL/well) can bind Biotinylated Human LDL R, His Tag, Avi Tag (Cat. No. LDR-H82E7) with a linear range of 0.04-0.625 μg/mL (Routinely tested).

Protocol

 

活性(Bioactivity)-BLI

PCSK9 BLI

Loaded Human PCSK9, Fc Tag (Cat. No. PC9-H5256) on Protein A Biosensor, can bind Human LDL R, His Tag (Cat. No. LDR-H5224) with an affinity constant of 12.7 nM as determined in BLI assay (ForteBio Octet Red96e) (Routinely tested).

Protocol

 
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背景(Background)

Proprotein convertase subtilisin/kexin type 9 (PCSK9) is also known as NARC1 (neural apoptosis regulated convertase), is a newly identified subtilase belonging to the peptidase S8 subfamily. Mouse PCSK9 is synthesized as a soluble zymogen, and undergoes autocatalytic intramolecular processing in the endoplasmic reticulum, resulting in the cleavage of its propeptide that remains associated with the secreted active enzyme with a broad alkaline pH optimum. This protein plays a major regulatory role in cholesterol homeostasis. PCSK9 binds to the epidermal growth factor-like repeat A (EGF-A) domain of the low-density lipoprotein receptor (LDLR), inducing LDLR degradation. PCSK9 may also have a role in the differentiation of cortical neurons. Mutations in this gene have been associated with a rare form of autosomal dominant familial hypercholesterolemia (HCHOLA3).

 

前沿进展

Effects of PCSK9 inhibitors on cancer, diabetes, and cardiovascular diseases
Nejabat, Hadizadeh, Almahmeed et al
Drug Discov Today (2025)
Abstract: Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) have potential applications in cancer therapy and as cholesterol-lowering treatments. The impact of PCSK9 suppression on both tumor growth and metastasis, as well as the management of diabetes, has been demonstrated. PCSK9i can also enhance outcomes and reduce cardiovascular (CV) events in individuals with a history of such events. In this review, we provide insights into the pharmacology, safety, and impact of PCSK9i. We highlight cutting-edge investigations, the development of innovative PCSK9i-based products, and a more comprehensive understanding of the potential effects of these drugs on cancer, diabetes, and CV and cerebrovascular diseases.Copyright © 2025 Elsevier Ltd. All rights reserved.
A LASSO-derived model for the prediction of nonattainment of target LDL-C reduction with PCSK9 inhibitors in patients with atherosclerotic cardiovascular disease
Duan, Zhang, Sun et al
Lipids Health Dis (2025) 24 (1), 65
Abstract: Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors have demonstrated significant efficacy in lowering low-density lipoprotein cholesterol (LDL-C) levels in patients with atherosclerotic cardiovascular disease (ASCVD), but some fail to achieve the target levels. This study aimed to explore the potential risk factors associated with this nonattainment of target LDL-C reduction (NTR-LDLC) and develop a prediction model.The population was randomly divided into derivation and verification subsets in a 7:3 ratio. Utilizing the Least Absolute Shrinkage and Selection Operator (LASSO) regression, we filtered the variables within the derivation set. Subsequently, we assessed the model's predictive accuracy for the NTR-LDLC in both subsets through the application of decision curve analysis (DCA) and the plotting of receiver operating characteristic (ROC) curves.The study enrolled 748 patients, with 115 individuals experiencing NTR-LDLC. Using LASSO regression, five significant predictive factors associated with NTR-LDLC were identified: statin therapy, diastolic blood pressure (DBP), alanine aminotransferase (ALT), total cholesterol (TC), and LDL-C. Based on these results, a nomogram prediction model was constructed and validated, showing predictive accuracy with the area under the ROC curve (AUC) of 0.718 (95% confidence interval [CI]: 0.657 - 0.779) and 0.703 (95% CI: 0.605 - 0.801) for the derivation and validation sets, respectively.This study presents a LASSO-derived predictive model that can be used to predict the risk of NTR-LDLC with PCSK9 inhibitors in patients with ASCVD.© 2025. The Author(s).
Lipids dysregulation in diseases: core concepts, targets and treatment strategies
Dakal, Xiao, Bhusal et al
Lipids Health Dis (2025) 24 (1), 61
Abstract: Lipid metabolism is a well-regulated process essential for maintaining cellular functions and energy homeostasis. Dysregulation of lipid metabolism is associated with various conditions, including cardiovascular diseases, neurodegenerative disorders, and metabolic syndromes. This review explores the mechanisms underlying lipid metabolism, emphasizing the roles of key lipid species such as triglycerides, phospholipids, sphingolipids, and sterols in cellular physiology and pathophysiology. It also examines the genetic and environmental factors contributing to lipid dysregulation and the challenges of diagnosing and managing lipid-related disorders. Recent advancements in lipid-lowering therapies, including PCSK9 inhibitors, ezetimibe, bempedoic acid, and olpasiran, provide promising treatment options. However, these advancements are accompanied by challenges related to cost, accessibility, and patient adherence. The review highlights the need for personalized medicine approaches to address the interplay between genetics and environmental factors in lipid metabolism. As lipidomics and advanced diagnostic tools continue to progress, a deeper understanding of lipid-related disorders could pave the way for more effective therapeutic strategies.© 2025. The Author(s).
Evolocumab Reduces Oxidative Stress and Lipid Peroxidation in Obese Zucker Rats
Cebova, Bulkova, Pechanova
Pathophysiology (2025) 32 (1)
Abstract: Background/Objectives: Evolocumab inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9) binding to low-density lipoprotein (LDL) receptors, thus allowing more LDL receptors to remove LDL cholesterol from the blood. We aimed to determine the effects of evolocumab on the plasma lipid profile, reactive oxygen species (ROS), and nitric oxide (NO) generation in the heart of adult male obese Zucker rats. Methods: The rats were divided into lean and obese controls and obese rats treated with evolocumab subcutaneously at a dose of 10 mg/kg every two weeks. After 6 weeks, the lipid profile was determined in the plasma, and NO synthase (NOS) activity, thiobarbituric acid reactive substance (TBARS), conjugated diene (CD) concentration, and protein expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, nuclear factor kappaB (NF-κB), endothelial NOS (eNOS), and phosphorylated eNOS (peNOS) were measured in the heart. Results: Evolocumab treatment did not reduce body weight, relative heart weight, or systolic blood pressure in obese Zucker rats. Evolocumab treatment, however, reduced plasma LDL levels, TBARS, and CD concentrations along with decreasing expression of NADPH oxidase and NF-kappaB proteins in the heart. On the other hand, evolocumab had no effect on NOS activity or eNOS and peNOS protein expression. Conclusions: Besides its lipid-lowering effect, evolocumab may exert antioxidant properties and protect cardiomyocytes from lipid peroxidation while not affecting NO production.
Showing 1-4 of 6645 papers.
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PCSK9靶点信息
英文全称:Proprotein convertase subtilisin kexin type 9
中文全称:前蛋白转化酶枯草杆菌蛋白酶Kexin-9
种类:Homo sapiens
上市药物数量:6详情
临床药物数量:28详情
最高研发阶段:批准上市
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