Human von Willebrand Factor,vWF ELISA Kit

Code CSB-E08437h
Size 96T,5×96T,10×96T
See More Details 24T ELISA kits trial application
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Product Details

Target Name von Willebrand factor
Alternative Names Coagulation factor VIII ELISA Kit; Coagulation factor VIII VWF ELISA Kit; F8VWF ELISA Kit; Factor VIII related antigen ELISA Kit; von Willebrand antigen 2 ELISA Kit; von Willebrand antigen II ELISA Kit; Von Willebrand disease ELISA Kit; Von Willebrand factor precursor ELISA Kit; VWD ELISA Kit; vWF ELISA Kit; VWF_HUMAN ELISA Kit
Abbreviation VWF
Uniprot No. P04275
Species Homo sapiens (Human)
Sample Types
Detection Range
Assay Time 1-5h
Sample Volume 50-100ul
Detection Wavelength 450 nm
Research Area Cardiovascular
Assay Principle quantitative
Measurement Sandwich
Typical Data  
and FAQs
Storage Store at 2-8°C. Please refer to protocol.
Lead Time 3-5 working days

Q&A and Customer Reviews


I want to detect the factor VIII of VWF (von Willebrand factor).
Please confirm that the kit (CSB-E08437h) can measure factor VIII of VWF.
If yes, please provide your reference data for samples, your lab tested.
If not, could you please recommend a suitable kit for my purposes.
Please provide the current manual and the information about kit’s components:
a. Capture antibody or capture antigen.
b. Detection antibody (if applicable).
c. Standard – if recombinant protein, please specify sequence (including species source and accession no. if available) and expression host.

Thanks for your inquiry.
This kit is designed according to:
It detects VWF in human samples.
Capture antibody is mouse monoclonal antibody.
Detection antibody is goat polyclonal antibody.
Standard is NS0-derived recombinant protein.
I will send you the kit manual by email.
We tested serum and plasma samples before and the test value is 25--100ng/ml.
 Customer Reviews

Target Data

Function Important in the maintenance of hemostasis, it promotes adhesion of platelets to the sites of vascular injury by forming a molecular bridge between sub-endothelial collagen matrix and platelet-surface receptor complex GPIb-IX-V. Also acts as a chaperone for coagulation factor VIII, delivering it to the site of injury, stabilizing its heterodimeric structure and protecting it from premature clearance from plasma.
Gene References into Functions
  1. High VWF expression is associated with age-related macular degeneration. PMID: 29367644
  2. The Plasma Levels of ADAMTS-13, von Willebrand Factor, VWFpp, and Fibrin-Related Markers in Patients With Systemic Sclerosis Having Thrombosis. PMID: 29130325
  3. vWF acts as a simple prognostic biomarker in AF and, whilst its addition to current scores statistically improves prediction for some endpoints, absolute changes and impact on clinical decision-making are marginal. PMID: 28134282
  4. The aim of the study was to investigate the role of von Willebrand factor (vWF), the vWF-cleaving protease, ADAMTS13, the composition of thrombus, and patient outcome following mechanical cerebral artery thrombectomy in patients with acute ischemic stroke. PMID: 29887594
  5. High vWF plasma concentrations may discriminate patients with non-valvular atrial fibrillation at greater risk of stroke or all-cause death. PMID: 29685722
  6. Coronary artery disease patients exhibited significantly lower plasma BDNF and higher vWF levels than those of control patients. PMID: 29409455
  7. A discontinuous autoinhibitory module masks the A1 domain of von Willebrand factor, preventing binding to GPIba. PMID: 28692141
  8. VWF, GMP-140, ADAMTS13 and the cerebral vasospasm, delayed cerebral ischemia, tumor diameter and prognosis of aneurysmal subarachnoid hemorrhage patients are closely related PMID: 29077161
  9. von Willebrand Factor is steadily elevated throughout the course of dysrhythmia in NVAF patients treated with warfarin and in those with higher intensity of left atrium blood stasis. PMID: 28952167
  10. The levels of VWF-cleaving protease ADAMTS13 among neonates were higher as compared with healthy adults, despite a significant elevation of VWF antigen (Ag) and Ristocetin cofactor (RiCof) noted in all neonates. PMID: 28087247
  11. The pathogenic effects of candidate VWF gene mutations were explored in this study. Molecular dynamic simulations on p.M771I mutant VWF revealed distinct structural rearrangements including a large deviation in the E' domain, and significant loss of beta-sheet secondary structure. PMID: 27483487
  12. investigated the roles of ADAMTS13 and VWF in thrombotic events of patients with Connective Tissue Diseases PMID: 26759371
  13. vWF had a significant prognostic impact on cardiovascular mortality when OPG levels were low. Low levels of both OPG and act vWF were associated with a 99 % survival rate during the follow-up of five years. PMID: 28726980
  14. Studied the significance of the von Willebrand factor (VWF)/ ADAMTS-13 ratio in advanced non-small-cell lung cancer (NSCLC). Findings suggest that the imbalance between VWF secretion and ADAMTS-13 may play a role in the hypercoagulability state in advanced NSCLC, and increase of the plasma VWF/ADAMTS-13 ratio may serve as an independent predictive factor for mortality in patients with advanced NSCLC. PMID: 28374895
  15. Type 3 von Willebrand disease patients with the Pro2808Leufs*24 have bioavailable platelet-derived VWF that may produce a milder bleeding phenotype than other type 3s PMID: 28453889
  16. vaso-occlusive crisis in sickle cell disease is associated with increased reactivity of VWF, without a pronounced ADAMTS-13 deficiency PMID: 28457019
  17. Overexpression of factor VIII-RA in the endothelial cells of capillary like vessels in the periphery of central and peripheral giant cell granuloma of jaw was prominent. PMID: 28832079
  18. Different patterns of VWF multimer loss were seen in heart failure patients treated with implantation of left ventricular assist device and total artificial heart, which may contribute to bleeding patterns. PMID: 28586149
  19. A high degree of clinical and laboratory variability exists within type 2M von Willebrand disease variants. PMID: 28544236
  20. Complex VWF-ADAMTS13-mediated mechanisms disturb haemostasis in inflammatory bowel disease. PMID: 28765701
  21. PP2B-Aalpha-Munc18c complex supports agonist-induced VWF secretion by HUVECs. PMID: 28294518
  22. Deficiency of the von Willebrand factor-cleaving protease ADAMTS13 is central to the pathophysiology of thrombotic thrombocytopenic purpura. Reviewed is the evidence emerged from epidemiological studies of an inverse relationship between the plasma levels of ADAMTS13 and the risk of acute coronary syndrome. [review] PMID: 28521259
  23. genetic variation of vWF V1565L polymorphism modulates ADAMTS13 activity. PMID: 27536857
  24. Plasma levels of VWF antigen and activity are significantly increased with concomitant reduction in plasma ADAMTS13 activity in patients with subarachnoid haemorrhage. PMID: 28102428
  25. Report a diagnostic algorithm that can reliably identify pathogenic variants of factor 8/9 and von Willebrand factor and diagnose patients with hemophilia A, hemophilia B or von Willebrand disease. PMID: 27734074
  26. analysis of an artificial botrocetin that can inhibit the VWF-GPIb interaction PMID: 28071872
  27. VWF binding to MMRN1 was enhanced by shear exposure and ristocetin, and required VWF A1A2A3 region, specifically the A1 and A3 domains. PMID: 27052467
  28. coronary thrombi in STEMI patients resistant to fibrinolysis are characterised by higher fibrin, P-selectin and VWF content than lysis-sensitive thrombi PMID: 26962963
  29. We compared the classical Sanger sequencing approach and NGS to assess the value-added effect on the analysis of the mutation distribution in different types of VWD. Sixty-two different VWF mutations were identified, 27 of which had not been previously described. NGS detected 26 additional mutations, contributing to a broad overview of the mutant alleles present in each VWD type. PMID: 26988807
  30. These observations support the hypothesis that a significantly reduced ADAMTS13/VWF ratio in the coronary artery flow plays a pathogenic role in acute coronary syndromes (ACS) and suggest that transition from laminar to turbulent flow at sites of coronary stenosis further enhances VWF activation and deposition. PMID: 27034431
  31. the major genetic factors affecting plasma VWF levels, i.e. variants at ABO, VWF and a locus on chromosome 2, operate primarily through their effects on VWF clearance PMID: 27359253
  32. The unique phenotype of VWD2 type IIC-Miami results from dominant impairment of multimer assembly, an aberrant structure of mutant mature VWF and reduced clearance in vivo PMID: 27344059
  33. Low ADAMTS-13 activity is associated with an increased risk of coronary heart disease in the elderly, independently of VWF and established cardiovascular risk factors PMID: 27559008
  34. Very low birth weight preterm neonates have increased numbers of platelets interacting with von Willebrand Factor, and increased GPIbalpha expression on the platelet surface PMID: 27416003
  35. N-linked glycan truncation causes enhanced clearance of plasma-derived von Willebrand factor; variation in VWF glycosylation may be important in the pathophysiology underlying type 1C VWD PMID: 27732771
  36. Data suggest that an aspartate at position 1261 is the most critical residue of VWF N-terminal linker for inhibiting binding of VWF A1 domain to GP1BA on platelets in a model simulating blood flow velocity; network of salt bridges between Asp1261 and rest of VWF A1 domain lock N-terminal linker in place such that binding to GP1BA is reduced. PMID: 28924049
  37. In people with dysglycaemia and other cardiovascular risk factors, basal insulin does not improve the levels of markers of fibrinolysis or von Willebrand factor compared to standard glucose-lowering treatments. PMID: 28403644
  38. low VWF levels can be associated with significant bleeding and are predominantly due to reductions in VWF synthesis and/or constitutive secretion. PMID: 28916584
  39. Refrigeration-induced binding of VWF to platelets facilitates their rapid clearance by inducing GPIbalpha-mediated signaling. PMID: 29097365
  40. Data show that von Willebrand factor (VWF) is first converted from a compact to linear form by flow, and is subsequently activated to bind platelet glycoprotein Ib alpha polypeptide (GPIbalpha) in a tension-dependent manner. PMID: 28831047
  41. The >30 nm macroglycopeptide separating the two domains of GPIbalpha transmits force on the VWF-GPIbalpha bond (whose lifetime is prolonged by leucine-rich repeat domain unfolding) to the juxtamembrane mechanosensitive domain to enhance its unfolding, resulting in unfolding cooperativity at an optimal force. PMID: 27434669
  42. von Willebrand factor processing and function has been summarized using various biophysical techniques. (Review) PMID: 27717713
  43. Soluble VWF was statistically elevated in major depressive disorder. PMID: 27598970
  44. Rare genetic variants in the ADAMTS13 on Willebrand factor-binding domain contribute to pediatric stroke. PMID: 27412500
  45. results indicate that VWF multimer accumulation on endothelium, as occurs in congenital thrombotic thrombocytopenic purpura, promotes the activation of the complement alternative pathway that proceeds until C5 cleavage with the formation of C5a and the terminal C5b-9 complex PMID: 28652401
  46. Findings also identify VWF as a new complement regulator on vascular endothelial cells and suggest that VWF has a protective effect on endothelial cells and complement-mediated injury. PMID: 27236750
  47. LVAD recipients achieved a new hemostatic equilibrium characterized by infrequent major hemorrhagic and thrombotic events, despite a mildly impaired vWF function and a markedly enhanced thrombin formation. PMID: 27485105
  48. These results demonstrate that cancer cells of non-endothelial origin can acquire de novo expression of VWF, which can enhance processes, including endothelial and platelet adhesion and extravasation, that contribute to cancer metastasis. PMID: 28035064
  49. level of vWF-ag in the chronic phase correlated with the amounts of VAT and PAT, but not with subcutaneous adipose tissue PMID: 28570705
  50. both in acute and chronic cerebrovascular disease patients, ADAMTS13 levels were significantly decreased, with the lowest ADAMTS13 levels found in acute stroke patients. This difference was even more distinct when the ratio of VWF:ADAMTS13 was considered. These results demonstrate the potentially important involvement of the VWF/ADAMTS13 axis in ischemic stroke. PMID: 28591212
  51. Erythrocyte retention in venous thrombi is mediated by erythrocyte-VWF or erythrocyte-VWF-fibrin interactions. PMID: 28775074
  52. A novel single-domain antibody against von Willebrand factor A1 domain that interferes with VWF-platelet interactions in vivo. By using this sdAb, show that the A1 domain is pertinent to the participation of VWF in the inflammatory response. PMID: 28642239
  53. Of special importance is the sequential formation of disulfide bonds with different functions in structural support of VWF multimers, which are packaged, stored and further processed after secretion. Here, all these processes are being reviewed in detail including background information on the occurring biochemical reactions. [review] PMID: 28139814
  54. These signaling pathways can trigger several secretion modes including single WPB release and multigranular exocytosis. In this review we will give an overview of the WPB lifecycle from biogenesis to secretion and we will discuss several deficiencies that affect the WPB lifecycle. [review] PMID: 28004844
  55. A subgroup of patients with end-stage heart failure already suffers AvWS preoperatively. In both CF-LVAD groups, AvWS begins immediately after surgery. Intraoperative vWF:ratios <0.7 correlate with higher incidences of pericardial tamponade and re-operation. The presumably dilutive effect of the heart lung machine on vWF vanishes immediately at the end of surgery, possibly as part of an acute-phase response PMID: 28234916
  56. this studies show binding of VWF to C1q and thus a direct interaction between starter molecules of hemostasis and the classical pathway of complement PMID: 27698012
  57. Elevated endothelium-related mediators (vWF, E-selectin and EPCR) appear to participate in the development of pancreatic necrosis and may be a potential indicator of overall prognosis. PMID: 28007459
  58. Plasma vWF levels are associated with tissue fibrosis in patients undergoing cardiac surgery and with post-surgical atrial fibrillation development in ischaemic patients. PMID: 26566941
  59. a new role for AP-1 in the basolateral constitutive secretion of VWF. PMID: 27106123
  60. Low ADAMTS-13 levels correlated with high levels of NTproBNP but had no independent prognostic significance. In conclusion, high VWF:Ag levels, probably representing endothelial dysfunction, are associated with prognosis in patients with AL amyloidosis, independently of other features of the disease or cardiac biomarkers. PMID: 27166361
  61. RNA interference of the type II phosphatidylinositol 4-kinases PI4KIIa and PI4KIIa in primary human endothelial cells leads to formation of an increased proportion of short WPB with perturbed packing of VWF, as exemplified by increased exposure of antibody-binding sites. PMID: 27068535
  62. these novel findings support the hypothesis that conformation of the VWF A domains plays a critical role in modulating macrophage-mediated clearance of VWF in vivo. PMID: 27554083
  63. discuss potential mechanisms through which these intronic SNPs regulate ST3GAL4 biosynthesis and the activity that affects VWF and FVIII PMID: 27584569
  64. the half-life of VWF ( approximately 15 hours) appears to be the limiting factor that has confounded attempts to extend the half-life of rFVIII. PMID: 27587878
  65. This study provides evidence of mutations outside consensus splice sites disrupting splicing and introduces the concept that VWF splicing is affected by shear stress on endothelial cells. PMID: 27317792
  66. results revealed localized vascular expression of FVIII and von Willebrand factor and identified lymphatic endothelial cell as a major cellular source of FVIII in extrahepatic tissues. PMID: 27207787
  67. these results demonstrate that HNPs1-3 may be potent inhibitors of ADAMTS13 activity, likely by binding to the central A2 domain of VWF and physically blocking ADAMTS13 binding. PMID: 27207796
  68. We identified a heterozygous silent mutation, c.7464C>T, in exon 44 of the von Willebrand factor (VWF) gene in a family with type 1 von Willebrand disease. PMID: 27543438
  69. Most associated ABO SNPs are also associated with vWF gene expression; elevated vWF levels are associated with recurrent stroke. PMID: 28495826
  70. Here, evidence is presented from two patients, which confirms that cysteine amino acid substitutions that break the disulfide bond induce a gain-of-function phenotype that manifests in a 1-desamino-8-Darginine vasopressin (DDAVP)-treatment-induced transient thrombocytopenia, which promptly restores to a homeostasis of low von Willebrand Factor and normal platelet counts within hours following treatment. PMID: 28533135
  71. von Willebrand factor A1 domain-collagen binding is independent of gain- or loss-of-function phenotype and under shear stress, platelet translocation pause times on collagen-bound A1A2A3 are either normal or shorter depending on whether A1 is concertedly bound with the A3 domain to collagen. PMID: 27889474
  72. ADAMTS13 activity and VWF:Ag levels are both associated with an increased risk of all-cause and cardiovascular mortality. PMID: 27737864
  73. VWF susceptibility to plasmin proteolysis at K1491-R1492 is modulated by local N-linked glycan expression within A1A2A3, and specifically inhibited by heparin binding to the A1 domain. PMID: 28279966
  74. four mutants (M771I, Y1146C, T1156M, R782Q) cause defective intracellular packaging and markedly reduced VWF secretion PMID: 27533707
  75. These findings support an ADAMTS13 activation model in which VWF D4-CK engages the TSP8-CUB2 domains, inducing the conformational change that disrupts the CUB1-spacer domain interaction and thereby activates ADAMTS13 PMID: 28209710
  76. Low von Willebrand Factor expression is associated with severe aortic stenosis. PMID: 27052664
  77. These results reveal a functional link between VWF and TF under whole blood flow conditions, in which surface-immobilized TF and VWF mutually contribute to mural thrombus formation, which is essential for normal hemostasis. By contrast, TF circulating in blood may be involved in systemic hypercoagulability, as seen in sepsis caused by severe microbial infection, in which neutrophil inflammatory responses may be active. PMID: 27562418
  78. Low serum albumin and high hsCRP and vWF levels, and their correlations with cIMT, indicate that patients could be at risk of developing malnutrition-inflammation-atherosclerosis syndrome PMID: 27619398
  79. Von Willebrand factor deficiency (VWF) deficiency is associated with a decreased prevalence of cardiovascular disease. Subclinical carotid atherosclerosis is not reduced in VWF deficiency. VWF deficiency may prevent cardiovascular events but not affect atherosclerosis. PMID: 27297464
  80. Data indicate that binding of hemoblobin (Hb) to glycoprotein1balpha (GP1balpha) induced platelet activation plays a crucial role in thrombus formation on immobilized von Willebrand factor (VWF) or type I collagen under shear stresses. PMID: 27105433
  81. analysis of the O-glycosylation sites in VWF PMID: 26784534
  82. As a clot grows, shear stresses can become sufficiently extreme in diseased arteries to drive von Willebrand Factor self-association into massive fibers, potentially the final burst of clot growth towards full thrombotic occlusion. PMID: 27207416
  83. Neutrophil proteases in the glomerular basement membrane cleave von Willebrand factor (VWF) and may protect the kidney from microthrombi. PMID: 28139439
  84. results of this study suggest that the assessment of the VWF genetic defect might be helpful to guide therapeutic decision-making in patients with von Willebrand disease type2 PMID: 27353798
  85. Tissue factor stimulated von Willebrand factor secretion by umbilical vein endothelial cells. PMID: 27766025
  86. Significantly lower ADAMTS-13 levels and significantly higher VWF antigen levels were concluded to be the result of a pathological process rather than an etiological factor for Venous thromboembolism. PMID: 26872106
  87. Endothelial cell cycle and vWF expression and secretion affected by chronic lymphocytic leukemia plasma; NF-kappaB plays a role in the process. PMID: 27472040
  88. von Willebrand factor activity and concentration of prekallikrein may both be of importance regarding the evolution of thrombus in abdominal aortic aneurysm and possible biomarkers for aneurysm growth. PMID: 27581227
  89. ADAMTS13 and VWF are co-expressed in microvascular endothelial cells. PMID: 26366828
  90. ADAMTS13-a disintegrin-like metalloproteinase with thrombospondin motif type 1 member 13-regulates a key physiological process of coagulation in the circulation by cleaving VWF multimers into small, inactive fragments. Low levels of ADAMTS13 in the blood may play a role in cardiovascular and hematological disorders, and clarifying its role may help improve disease management. PMID: 27746209
  91. von Willebrand factor binds to the surface of dendritic cells and modulates peptide presentation of factor VIII. PMID: 26635035
  92. von Willebrand factor and ADAMTS-13 are associated with the occurrence of venous thromboembolism in patients with cancer. PMID: 26589836
  93. REVIEW: VWF biosynthesis, maturation, and secretion is a complex process, which mandates tight regulation; significant progress has been made in our understandings of VWF expression and secretion and its association with thrombotic diseases PMID: 26771163
  94. This brief review will highlight knowledge acquired and key problems that remain to be solved to elucidate fully the role of VWF in normal haemostasis and pathological thrombosis. [human] PMID: 25612915
  95. data suggest that increased levels of VWF and reduced levels of ADAMTS13 activity may contribute to the pathogenesis of cerebral infarction. PMID: 25916953
  96. The VWF nets as well as the platelet-VWF conglomerates are controlled by the cleaving protease ADAMTS13 within minutes under high shear flow. PMID: 25983111
  97. ADAMTS13 is the key protease that regulates the multimeric state of VWF. Without ADAMTS13, VWF multimers can grow to pathologically large sizes. This is a risk factor for the life-threatening condition thrombotic thrombocytopenic purpura (TTP) PMID: 26595154
  98. Stroke in human immunodeficiency virus infection is associated with a prothrombotic state, characterized by elevated von Willebrand factor and low ADAMTS13 levels PMID: 26121272
  99. An in vitro model for LVAD associated aVWD demonstrated that ADAMTS-13 and platelets contribute to the depletion of HMWM of VWF. PMID: 26616301
  100. free thiol groups are shown to be involved in VWF binding to both collagen III and platelet GP1b receptor. PMID: 26581637

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Involvement in disease von Willebrand disease 1 (VWD1); von Willebrand disease 2 (VWD2); von Willebrand disease 3 (VWD3)
Subcellular Location Secreted, Secreted, extracellular space, extracellular matrix
Tissue Specificity Plasma.
Database Links

HGNC: 12726

OMIM: 193400

KEGG: hsa:7450

STRING: 9606.ENSP00000261405

UniGene: Hs.440848

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