VEGFA Antibodies

AND VEGFA ELISA kits, VEGFA Proteins

Many biological assays use antibodies to detect VEGFA, such as Western Blot (WB), ELISA, Flow Cytometry, Immunocytochemistry (IHC). These antibodies can be polyclonal or monoclonal, and react with VEGFA in Human, Mouse, Rat, and many other animal samples. Boster Bio use mainly mouse and rabbit to develop VEGFA antibodies...

We validate the specificity of these antibodies to VEGFA by testing them on tissues known to express VEGFA positively and negatively. Browse below to find the VEGFA antibody that suites your experiment. We have 32 of these antibodies and many publications and validation images.

If you cannot find antibodies that fit your needs, contact us for making custom antibodies. We have a full suite of custom antibody services covering from research to diagnostic and therapeutic applications.

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VEGFA Infographic by Boster Bio

VEGFA Biomarker Overview

A comprehensive evaluation of Vascular Endothelial Growth Factor A (VEGFA) and VEGFR2 as prognostic biomarkers in bladder cancer, covering testing protocols and clinical integration strategies.

Combined Biomarker Strategies
Standardizing Testing Protocols

Integrating Biomarkers with Clinical Profiles
Frequently Asked Questions

Understanding VEGFA in Bladder Cancer

Vascular endothelial growth factor A (VEGFA) is a key driver of tumor angiogenesis and has emerged as a clinically significant biomarker for stratifying patient prognosis and guiding therapeutic decisions in bladder cancer.

Utilizing VEGFA as a Prognostic Biomarker in Bladder Cancer

VEGFA expression levels correlate with tumor grade, stage, and patient survival outcomes

Bladder cancer is among the most prevalent urological malignancies worldwide, with urothelial carcinoma accounting for the majority of cases. The ability to accurately predict disease progression and patient outcomes remains a central challenge in urological oncology. VEGFA, a potent pro-angiogenic cytokine, has attracted significant research interest as a tissue-based prognostic biomarker due to its central role in regulating tumor blood vessel formation.

Elevated VEGFA expression in tumor tissue, as detected by immunohistochemistry (IHC), has been consistently associated with higher tumor grade, advanced pathological stage, lymphovascular invasion, and diminished overall survival in bladder cancer cohorts. Studies have demonstrated that patients with high VEGFA expression exhibit significantly shorter disease-free survival intervals compared to those with low or negative expression, underscoring the protein's utility as an independent prognostic indicator.

Beyond tissue-based IHC, serum and urine VEGFA concentrations have also been investigated as non-invasive prognostic indicators. Elevated circulating VEGFA levels have been linked to more aggressive disease phenotypes and poorer therapeutic responses, positioning VEGFA as a candidate biomarker across multiple biological compartments. The consistency of these findings across diverse patient populations strengthens the argument for its clinical adoption.

VEGFA Expression Level	Tumor Stage Association	Prognostic Implication
Low / Negative	Superficial (Ta, T1)	Favorable overall survival
Moderate	Muscle-invasive (T2)	Intermediate prognosis
High / Overexpressed	Advanced (T3-T4, N+, M+)	Poor prognosis, high recurrence risk

Critically, the prognostic value of VEGFA appears to extend beyond simple staging. In multivariate analyses controlling for established clinicopathological variables such as age, tumor size, and lymph node status, VEGFA expression has retained independent prognostic significance. This highlights its potential to refine risk stratification beyond what conventional staging systems alone can provide.

Key VEGFA Research Findings

Evidence from clinical studies highlights several consistent findings regarding VEGFA expression patterns in bladder cancer.

Tumor Angiogenesis Promotion

VEGFA drives tumor angiogenesis by binding to endothelial receptors, stimulating new blood vessel formation that supplies oxygen and nutrients to the growing tumor mass, enabling invasion and metastasis.

Independent Prognostic Value

Multivariate studies confirm VEGFA expression retains independent prognostic significance even after controlling for stage, grade, and lymph node status, providing additional risk stratification beyond standard clinicopathological parameters.

Therapeutic Target Potential

As a measurable biomarker and therapeutic target, VEGFA expression data can guide the selection of anti-angiogenic agents such as bevacizumab and sunitinib, aligning treatment choice with the molecular profile of the individual tumor.

Implementation of VEGFR2 Receptor Analysis for Prognostic Evaluation

VEGFR2 is the primary signaling receptor mediating VEGFA-driven angiogenesis and tumor progression

While VEGFA represents the ligand in the VEGF signaling axis, its biological effects are primarily mediated through binding to Vascular Endothelial Growth Factor Receptor 2 (VEGFR2, also known as KDR/Flk-1). Assessing VEGFR2 expression in bladder tumor tissue provides a complementary and mechanistically relevant layer of prognostic information beyond VEGFA expression alone.

VEGFR2 is expressed not only on tumor-associated endothelial cells but has also been detected on bladder carcinoma cells themselves, indicating potential autocrine signaling loops that may confer additional growth advantages. Overexpression of VEGFR2 in tumor specimens has been correlated with enhanced microvessel density (MVD), a histological surrogate of angiogenic activity, and has been associated with shorter recurrence-free survival in bladder cancer patients.

IHC-based VEGFR2 analysis on formalin-fixed paraffin-embedded (FFPE) tissue sections is the most widely employed method for receptor quantification in clinical research settings. Standardized antibody panels targeting the extracellular and intracellular domains of VEGFR2 allow for reproducible semi-quantitative scoring. Phosphorylated VEGFR2 (pVEGFR2), which reflects active receptor signaling, has been identified as a particularly informative biomarker because it indicates not merely receptor presence but functional ligand-receptor engagement within the tumor microenvironment.

Analytical considerations for VEGFR2 assessment:

Validated anti-VEGFR2 antibody selection
Positive and negative tissue controls
Standardized antigen retrieval protocols

Semi-quantitative H-score methodology
Blinded dual pathologist scoring
pVEGFR2 phospho-specific antibodies

Tumor vs. stromal compartment distinction
Microvessel density co-assessment
Correlation with clinical endpoints

VEGFR2 Scoring Reference

VEGFR2 expression is commonly scored using the H-score system, calculated as:

H-score = (% cells with weak staining x 1) + (% cells with moderate staining x 2) + (% cells with strong staining x 3)

Scores range from 0 to 300. A threshold of H-score greater than 100 is frequently used to classify tumors as VEGFR2-high in published bladder cancer cohorts, though cut-offs should be validated within each institutional dataset.

Expression of phosphorylated VEGFR2 (pVEGFR2 Y1175) correlates most closely with downstream ERK and AKT pathway activation and is the most functionally relevant readout for anti-angiogenic therapy selection.

Advanced Biomarker Strategies

Leveraging both VEGFA and VEGFR2 in concert, while anchoring findings within standardized protocols and individualized clinical data, maximizes the prognostic precision achievable in bladder cancer management.

Combining VEGFA and VEGFR2 Biomarkers for Enhanced Prognostic Accuracy

Dual biomarker analysis captures both ligand availability and receptor-mediated signaling activity

Assessing VEGFA and VEGFR2 independently provides valuable prognostic information, but the greatest discriminatory power is achieved when both biomarkers are evaluated in combination. A co-expression analysis approach acknowledges that tumor aggressiveness is not solely a function of ligand overproduction or receptor overexpression, but rather the product of active ligand-receptor signaling within the tumor microenvironment.

Research on bladder cancer cohorts has demonstrated that patients with concurrent high VEGFA and high VEGFR2 expression exhibit the poorest prognosis across multiple endpoints including overall survival, progression-free survival, and recurrence-free survival. Conversely, tumors with low expression of both markers are associated with the most favorable outcomes. Intermediate groups, those with high expression of one marker but not the other, display prognoses that fall between these extremes, reinforcing the additive value of the dual assessment strategy.

From a mechanistic standpoint, the co-expression phenotype reflects a fully activated VEGF signaling axis: abundant ligand, engaged receptor, and downstream pathway activation driving tumor angiogenesis and potentially direct tumor cell growth. This phenotype is also most likely to respond to VEGF pathway-targeted therapies, making the combined biomarker profile directly actionable from a therapeutic standpoint.

VEGFA Status	VEGFR2 Status	Prognostic Category	Clinical Implication
High	High	Worst prognosis group	Anti-angiogenic therapy candidate; intensive follow-up
High	Low	Intermediate prognosis	Evaluate alternative pathway activation
Low	High	Intermediate prognosis	Monitor receptor expression dynamics
Low	Low	Favorable prognosis group	Standard surveillance; lower recurrence risk

Statistically, combined biomarker models show improved C-statistics (a measure of discrimination) compared to models incorporating either marker alone or conventional staging variables in isolation. The incorporation of VEGFA and VEGFR2 co-expression into nomogram-based prognostic tools represents a practical pathway toward clinical translation of this dual biomarker approach.

Standardizing Biomarker Testing Protocols in Bladder Cancer

Reliable prognostic biomarker data requires rigorous, reproducible analytical protocols. The following steps outline the key stages of a standardized VEGFA and VEGFR2 testing workflow for bladder cancer tissue specimens.

Step 1: Tissue Specimen Acquisition and Processing

Bladder tumor tissue is collected at the time of transurethral resection of bladder tumor (TURBT) or radical cystectomy. Specimens must be promptly fixed in 10% neutral buffered formalin for a defined duration (typically 6 to 24 hours) to ensure optimal antigen preservation. Formalin-fixed paraffin-embedded (FFPE) blocks are prepared according to standardized histopathology procedures, and representative tumor-containing sections are selected by a qualified pathologist.
Step 2: Antibody Validation and Panel Selection

Antibodies targeting VEGFA and VEGFR2 (including pVEGFR2 where applicable) must be validated on positive control tissues such as placental tissue for VEGFA or renal cell carcinoma for VEGFR2 before application to study samples. Specificity, sensitivity, and optimal dilution parameters should be established within each laboratory. Use of commercially validated, research-grade antibodies with published validation data in bladder cancer contexts is strongly recommended to ensure inter-laboratory comparability.
Step 3: Immunohistochemical Staining Protocol

Deparaffinized and rehydrated 4-micron tissue sections undergo antigen retrieval (heat-induced epitope retrieval using citrate buffer pH 6.0 or EDTA buffer pH 9.0, depending on target epitope requirements). Endogenous peroxidase activity is blocked, and sections are incubated with primary antibody under optimized time and temperature conditions. Detection is performed using a validated secondary antibody and chromogenic substrate system (typically DAB), followed by hematoxylin counterstaining.
Step 4: Scoring and Quantification

Stained slides are evaluated by two independent pathologists blinded to patient clinical data. VEGFA and VEGFR2 expression are scored using a standardized semi-quantitative system that accounts for staining intensity (0 = none, 1 = weak, 2 = moderate, 3 = strong) and the percentage of positive tumor cells. H-score or composite scoring methods should be specified in advance. Inter-observer concordance is assessed using kappa statistics; discordant cases are resolved through consensus review at a multiheaded microscope.
Step 5: Data Recording and Threshold Application

Scored biomarker data are recorded in a structured database alongside corresponding clinicopathological variables. Expression cut-offs distinguishing high from low expression groups should be pre-specified based on published literature, receiver operating characteristic (ROC) curve analysis, or median expression values within the study cohort. Cut-off selection methodology must be reported transparently to allow comparison across studies and to enable external validation in independent cohorts.

Integrating Biomarker Data with Patient Clinical Profiles

Translating VEGFA and VEGFR2 data into actionable clinical decision-making frameworks

Biomarker data, however informative in isolation, reaches its greatest clinical utility when systematically integrated with the full landscape of a patient's clinical profile. For bladder cancer patients, this includes pathological staging and grading, surgical margin status, lymphovascular invasion, lymph node involvement, performance status, comorbidity burden, prior treatment history, and patient preferences regarding treatment intensity.

A structured biomarker-clinical integration workflow begins with molecular profiling of the tumor specimen at the time of definitive surgical intervention or initial diagnostic workup. VEGFA and VEGFR2 expression scores are entered alongside conventional staging data into a unified patient record or multidisciplinary tumor board database. Prognostic nomograms that incorporate both molecular and clinical variables can then generate individualized risk estimates that inform surveillance intensity, adjuvant treatment decisions, and candidacy for clinical trials targeting the VEGF pathway.

In practice, patients identified as high-risk based on combined high VEGFA/VEGFR2 expression may be prioritized for early initiation of adjuvant systemic therapy, more frequent cystoscopic surveillance, or enrolment in trials evaluating VEGF-targeted regimens such as ramucirumab or cabozantinib. Low-risk molecular profiles may support de-escalation strategies that reduce treatment burden and associated toxicity without compromising oncological outcomes.

Key clinical variables for integration:

Clinical Variable	Relevance to VEGFA/VEGFR2 Context
Pathological Stage (T category)	Higher T stage correlates with elevated VEGFA expression frequency
Tumor Grade	High-grade tumors show significantly greater VEGFR2 overexpression rates
Lymphovascular Invasion (LVI)	LVI presence amplifies prognostic impact of high dual biomarker status
Nodal Status (N category)	Node-positive disease combined with high VEGFA defines the highest-risk subgroup
Prior Intravesical Therapy	BCG-refractory status may correlate with upregulated VEGF signaling

Frequently Asked Questions

Common questions regarding the clinical and research application of VEGFA and VEGFR2 biomarkers in bladder cancer.

Q1. What makes VEGFA a useful prognostic biomarker specifically in bladder cancer?

VEGFA is particularly relevant in bladder cancer because the urothelial tumor microenvironment is heavily dependent on angiogenesis for growth and invasion. High VEGFA expression has been reproducibly linked to advanced tumor stage, higher histological grade, increased risk of lymphovascular invasion, and significantly shorter patient survival in multiple independent cohorts. Its measurability by standard IHC on routine FFPE tissue sections, combined with its retention of independent prognostic significance in multivariate analyses, makes VEGFA one of the most rigorously supported candidate biomarkers for clinical integration in this disease.

Q2. Why should VEGFR2 be assessed in addition to VEGFA when evaluating bladder cancer prognosis?

VEGFA exerts its biological effects primarily through binding to VEGFR2, and receptor expression determines whether the pro-angiogenic signal is actually transduced within the tumor. A tumor with high VEGFA but absent VEGFR2 may have a different biological behavior than one with co-expression of both. Assessing VEGFR2 adds mechanistic depth: it captures not just ligand availability but receptor-mediated signaling capacity. The dual assessment identifies the fully activated VEGF signaling axis, which represents the highest-risk tumor phenotype and the subgroup most likely to respond to anti-angiogenic therapies targeting this pathway.

Q3. What is the recommended tissue source and fixation method for VEGFA and VEGFR2 testing?

Formalin-fixed paraffin-embedded (FFPE) tissue obtained from TURBT or radical cystectomy specimens is the standard source material for IHC-based VEGFA and VEGFR2 analysis. Optimal fixation duration is 6 to 24 hours in 10% neutral buffered formalin. Under-fixation compromises antigen preservation, while over-fixation can impede antibody penetration during IHC. Cold ischemia time (the interval between surgical excision and formalin immersion) should be minimized and standardized across specimens. Fresh-frozen tissue, while suitable for research applications, is not routinely available in clinical practice and requires specialized handling infrastructure.

Q4. How are expression cut-offs determined for classifying patients as VEGFA-high versus VEGFA-low?

Expression cut-offs can be determined using several methodological approaches. The most statistically rigorous approach uses receiver operating characteristic (ROC) curve analysis to identify the threshold that maximizes sensitivity and specificity for predicting a defined clinical outcome, such as five-year overall survival. Alternatively, the median expression value within the study cohort is frequently used as a practical cut-off. Some studies employ pre-specified cut-offs derived from prior published literature to enable direct comparison across studies. Critically, the chosen methodology must be declared in advance as a pre-specified analysis, as post-hoc optimization of cut-offs can introduce significant bias and inflate prognostic estimates. External validation of cut-offs in independent cohorts is essential before clinical translation.

Q5. Can VEGFA or VEGFR2 levels in blood or urine be used instead of tissue-based testing?

Circulating VEGFA levels in serum or plasma, as well as urinary VEGFA concentrations, have been studied as non-invasive prognostic biomarkers in bladder cancer. Several studies have reported associations between elevated circulating VEGFA and more advanced disease or poorer treatment outcomes. However, serum and urine VEGFA measurements are subject to significant pre-analytical variability related to sample handling, hemolysis, and platelet activation, and they reflect systemic rather than tumor-local VEGF biology. At present, tissue-based IHC remains the more validated and clinically utilized approach. Liquid biopsy-based VEGF assays are an active area of research but have not yet been established as routine clinical tools for bladder cancer prognostication.

Q6. How does VEGFA and VEGFR2 biomarker status influence treatment decisions in bladder cancer?

In current clinical practice, VEGFA and VEGFR2 testing is not yet mandated by major oncology guidelines for routine bladder cancer management, but the biomarker profiles are increasingly relevant in the context of anti-angiogenic and targeted therapy trials. Patients with high dual VEGFA/VEGFR2 expression represent the population most biologically likely to benefit from VEGFR2-targeted agents such as ramucirumab or multi-kinase inhibitors including cabozantinib. At the institutional level, biomarker-stratified enrollment in clinical trials represents the most structured avenue for incorporating this information. As evidence accumulates and validation matures, integration into standard-of-care risk stratification frameworks alongside established molecular classifiers is anticipated.

Explore VEGFA and VEGFR2 Research Tools

Access validated antibodies, ELISA kits, and IHC reagents for VEGFA and VEGFR2 research in bladder cancer and other oncology applications.

Browse VEGFA Products View VEGFR2 Antibodies

All VEGFA Products

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Human VEGF ELISA Kit PicoKine®

195 Citations 20 Q&As

Human

ELISA

$399
Cat # EK0539
96 wells/kit, with removable strips.

Rat VEGF ELISA Kit PicoKine®

83 Citations 18 Q&As

Rat VEGF PicoKine ELISA Kit standard curve

Rat

ELISA

$499
Cat # EK0540
96 wells/kit, with removable strips.

Mouse VEGF ELISA Kit PicoKine®

75 Citations 4 Q&As

Mouse

ELISA

$499
Cat # EK0541
96 wells/kit, with removable strips.

Anti-VEGF/VEGFA Antibody Picoband®

191 Citations 18 Q&As

Western blot analysis of VEGFA using anti-VEGFA antibody (PA1080)

IHC analysis of VEGFA using anti-VEGFA antibody (PA1080)

+30

Human, Mouse, Rat

IHC, WB

$370
Cat # PA1080
100 μg/vial

Anti-VEGF/VEGFA Antibody Picoband®

51 Citations 5 Q&As

Lentivirus-mediated PLCγ1 shRNA could suppress migration in human gastric adenocarcinoma BGC-823 cells

Depletion of PLCγ1 suppresses growth and metastasis of gastric adenocarcinoma in a nude mouse tumor xenograft model

Western blot analysis of VEGF/VEGFA using anti-VEGF/VEGFA antibody (PB9071)

Human, Mouse, Rat

Flow Cytometry, IHC, WB

$370
Cat # PB9071
100 μg/vial

Anti-VEGF/Vegfa Antibody Picoband®

11 Citations 15 Q&As

Western blot analysis of VEGF using anti-VEGF antibody (A00045)

Mouse, Rat

$370
Cat # A00045
100 μg/vial

Anti-VEGF VEGFA Rabbit Monoclonal Antibody

17 Citations 17 Q&As

IHC analysis of VEGFA using anti-VEGFA antibody (M00045-1)

+13

Human, Mouse

Flow Cytometry, IF, IHC, ICC

$370
Cat # M00045-1
100 μl

Anti-VEGF/Vegfa/VEGF164 Antibody Picoband®

4 Citations 16 Q&As

Western blot analysis of VEGF/VEGF164 using anti-VEGF/VEGF164 antibody (A00045-1)

Mouse, Rat

ELISA, WB

$370
Cat # A00045-1
100 μg/vial

Mouse VEGF-A Recombinant Protein

1 Citations

Cell Culture

$364
Cat # R00045-4
5 µg/vial

Rat VEGF-A Recombinant Protein

Cell Culture

$364
Cat # R00045-7
5 µg/vial

Mouse VEGF PicoKine® Quick ELISA Kit

5 Citations

Mouse

ELISA

$499
Cat # FEK0541
96 wells/kit, with removable strips.

Anti-VEGF/Vegfa Picoband® Antibody

8 Citations

Western blot analysis of Vegfa using anti-Vegfa antibody (A00045-2)

Mouse, Rat

ELISA, WB

$370
Cat # A00045-2
100 μg/vial

Anti-VEGF Antibody

ICC staining VEGF in MCF-7 cells (green)

Human, Mouse, Rat

Flow Cytometry, IF, IHC, ICC

$405
Cat # A00045-4
100ul

Human VEGF 165 Recombinant Protein

2 Citations

SDS-PAGE

$281
Cat # PROTP15692
Starting from 10ug

Rat VEGFA Recombinant Protein

SDS-PAGE

$250
Cat # PROTP16612
Starting from 4ug

Human VEGF PicoKine® Quick ELISA Kit

18 Citations

Human

ELISA

$499
Cat # FEK0539
96 wells/kit, with removable strips.

Rat VEGF PicoKine® Quick ELISA Kit

9 Citations

Rat

ELISA

$499
Cat # FEK0540
96 wells/kit, with removable strips.

VEGFA (NM_001025366) Human Over-expression Lysate

VEGFA Human Over-expression Lysates NM_001025366

Human

$628
Cat # LS007422
20 µg, 100 µg

Human VEGF ELISA Kit EZ-Set™ (DIY Antibody Pairs)

1 Citations

Human

ELISA

$500
Cat # EZ0539
For 5 plates, 96 wells each, reagents only, plates are not included

Human recombinant VEGF121 (Vascular endothelial growth factor 121) protein, AF

Human

Cell Culture

$77
Cat # PROTP15692-17
5ug,20ug,100ug

Human recombinant VEGF165 (Vascular endothelial growth factor 165) protein, AF

Human

Cell Culture

$77
Cat # PROTP15692-18
5ug,20ug,100ug

Mouse recombinant VEGF121 (Vascular endothelial growth factor 121) protein, AF

Mouse

Cell Culture

$77
Cat # PROTQ00731-6
5ug,20ug,100ug

Mouse recombinant VEGF165 (Vascular endothelial growth factor 165) protein, AF

Mouse

Cell Culture

$77
Cat # PROTQ00731-7
5ug,20ug,100ug

Swine recombinant VEGF (Vascular endothelial growth factor) protein, AF

Swine

Cell Culture

$154
Cat # PROTP49151
5ug,20ug

Anti-VEGF Reference Antibody (BioMab patent anti-VEGF)