Mouse neutrophil gelatinase-associated lipocalin,NGAL ELISA Kit

SKU:BHE10506355
Overview
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Quantitative ELISA kit for measuring mouse neutrophil gelatinase-associated lipocalin (LCN2) in serum, plasma, tissue homogenates, and urine to support immunology studies. Sensitivity 3.12 pg/mL, detection range 12.5 pg/mL–800 pg/mL, typical assay time 1–5 h.
Target NGAL
Species Mus musculus (Mouse)
Sample Type(s) serum, plasma, tissue homogenates, urine
Assay Type Competitive ELISA (quantitative)
Sensitivity 3.12 pg/mL
Detection Range 12.5 pg/mL-800 pg/mL
Assay Time 1-5h
Options selector
Catalog no. Size
CSB-E09410m-96T 96 T
CSB-E09410m-96TX5 96 T×5
CSB-E09410m-96TX10 96 T×10
Available Options

Select from the available variant options shown for this product. Availability and lead time can vary by option.

  • Options: Size (96 T, 96 T×10, 96 T×5).
  • Lead time: options listed as "In Stock at Manufacturer" typically ship in 5–7 business days; other statuses may take longer.
  • Storage: refer to the product datasheet for storage and handling.
  • Sales terms and conditions: Please review prior to ordering.
Field Specification
Mfr No CSB-E09410m
Alternative Names Lcn2 ELISA Kit; Neutrophil gelatinase-associated lipocalin ELISA Kit; NGAL ELISA Kit; Lipocalin-2 ELISA Kit; Oncogene 24p3 ELISA Kit; 24p3 ELISA Kit; SV-40-induced 24p3 protein ELISA Kit; Siderocalin LCN2 ELISA Kit; p25 ELISA Kit
Assay Time
  • 1-5h
Assay Type
  • Competitive ELISA (quantitative)
Detection Range 12.5 pg/mL-800 pg/mL
Detection Wavelength 450 nm
Product Type
  • ELISA Kits
Reactivity
  • Mouse
Sample Type(s) serum, plasma, tissue homogenates, urine
Sensitivity 3.12 pg/mL
Species Mus musculus (Mouse)
Target NGAL
UniProt # P11672

Background

neutrophil gelatinase-associated lipocalin (LCN2) is a biological molecule commonly studied in immunology research. It is commonly used as a molecular readout in mechanistic and biomarker-focused studies.

UniProt: P11672

Biological context

Researchers often monitor neutrophil gelatinase-associated lipocalin in serum, plasma, tissue homogenates, and urine to better understand themes such as innate and adaptive immune responses, cytokine signaling networks, and host–pathogen interactions. In many model systems, measured levels can shift with physiology, experimental perturbation, or disease-associated changes, making careful biological interpretation important.

Interpreting changes in measured levels

Depending on sample matrix and study design, increases or decreases in neutrophil gelatinase-associated lipocalin may reflect differences in expression, secretion, turnover, or compartmentalization rather than a single mechanism. Interpretation is typically strengthened by evaluating related molecules (for example, cytokines, chemokines, acute-phase proteins, and immune-cell activation markers) and by keeping pre-analytical variables consistent across groups.

Nomenclature

In publications and databases, neutrophil gelatinase-associated lipocalin may also appear under names such as Lcn2 and Neutrophil gelatinase-associated lipocalin. When comparing studies, confirm that the reported analyte refers to the same molecule and species context.

Why ELISA data are widely used

ELISA is a common approach for quantitative measurement of proteins and biomarkers in complex samples, enabling comparisons across experimental groups and time points. When integrating results with other readouts, consider species biology, sample type, and the broader pathway context that neutrophil gelatinase-associated lipocalin participates in.

Can’t Find What You’re Looking For? We can help you source the best match or customize an ELISA solution for your study. Options may include alternative target synonyms, different species reactivity, sample type/matrix compatibility (serum/plasma/lysate/supernatant), assay format (sandwich/competitive), sensitivity/range, detection chemistry (colorimetric/fluorescent/chemiluminescent), plate format (pre-coated/uncoated, strips vs full plate), and bulk or custom packaging. Click Talk to a Scientist to submit a request form, email us at support@biohippo.com, or explore our Research Services for additional support. Our team will be in contact with you shortly.

Lactobacillus johnsonii alleviates experimental colitis by restoring intestinal barrier function and reducing NET-mediated gut-liver inflammation

HY Liu, P Yuan, S Li, KJ Ogamune, X Shi,Communications Biology,2025

NGAL knockdown alleviated CSE-induced cellular senescence and reduced MMP2 and MMP9 expression in alveolar macrophages through the PI3K/Akt pathway

Y Wang, C Jin, Y Zheng,European Journal of Medical Research,2025

Ursodeoxycholic acid protects against sepsis-induced acute kidney injury by activating Nrf2/HO-1 and inhibiting NF-κB pathway

Y Lou, H Shi, N Sha, F Li, X Gu, H Lin,BMC nephrology,2025

CHAC1 Mediates Endoplasmic Reticulum Stress‐Dependent Ferroptosis in Calcium Oxalate Kidney Stone Formation

C Dong, Z He, W Liao, Q Jiang, C Song,Advanced Science,2025

Multi-omics analysis reveals the interaction of gut microbiome and host microRNAs in ulcerative colitis

L Ma,Annals of medicine,2023

Modulation of TLR4/NF-Modulation of TLR4/NF-κB, Nrf2/HO-1 and PI3K/Akt signaling by cilostazol mitigates lipopolysaccharide-induced septic acute kidney injury

AF Mohamed,/,2023

Yi-Shen-Xie-Zhuo formula alleviates cisplatin-induced AKI by regulating inflammation and apoptosis via the cGAS/STING pathway

J Qi,Journal of ethnopharmacology,2023

Trimethylamine N-oxide promotes hyperoxaluria-induced calcium oxalate deposition and kidney injury by activating autophagy

F Dong,Free Radical Biology and Medicine,2021

UCP2 ameliorates mitochondrial dysfunction, inflammation, and oxidative stress in lipopolysaccharide-induced acute kidney injury

Ding Y, et al,International Immunopharmacology,2019

Nephro-toxic effects of intraperitoneally injected EGCG in diabetic mice: involvement of oxidative stress, inflammation and apoptosis

Rasheed NO.et al,Scientific Reports,2017

Telluric Acid Ameliorates Endotoxemic Kidney Injury in Mice: Involvement of TLR4, Nrf2, and PI3K/Akt Signaling Pathways

Mohamed AF.et al,Inflammation,2017

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