FXG1 Antibody
Description
Fc Core Afucosylation
Nonfucosylated IgG1 antibodies (e.g., BMS-986012 ) exhibit:
Fc Engineering for Complement Activation
HexaBody technology (e.g., E345K/E430G mutants) enables:
Pharmacokinetic Enhancements
Mutations like YTE (Tyr-349, Thr-366, Glu-333) or LS (Met428Leu, Asn434Ser) improve:
Research Gaps and Recommendations
Product Specs
Constituents: 50% Glycerol, 0.01M Phosphate Buffered Saline (PBS), pH 7.4
Target Background
Q&A
Here’s a structured collection of FAQs for researchers focusing on FGFR1 antibodies in academic research, synthesized from peer-reviewed studies and technical guidelines:
How do I select and validate FGFR1 antibodies for immunohistochemistry (IHC)?
Methodological Answer:
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Epitope specificity: Prioritize antibodies targeting distinct domains (e.g., extracellular vs. cytoplasmic). For membranous FGFR1 detection, D8E4 (C-terminal) outperforms others in specificity and reproducibility .
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Validation controls: Use FGFR1-amplified cell lines (e.g., MDA-MB-134) as positive controls and FGFR1-knockout models (e.g., MCF7 KO) as negative controls .
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Scoring criteria: Adapt HER2 IHC guidelines: 3+ (strong, complete membranous staining in ≥10% cells), 2+/1+ (weaker/incomplete staining) .
Data Table 1: FGFR1 Antibody Performance in IHC
What techniques complement FGFR1 IHC for biomarker confirmation?
Methodological Answer:
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Fluorescence in situ hybridization (FISH): Use dual probes for FGFR1 and CEP8. Amplification thresholds:
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RNA sequencing: Moderate correlation with protein expression (r=0.58, p<0.0001) . Prioritize FISH for clinical trial enrollment due to higher reproducibility.
How do I resolve discrepancies between FGFR1 protein expression and gene amplification?
Methodological Answer:
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Heterogeneity: 14% of amplified cases show zonal amplification (Figure 2C-D) . Perform multi-region sampling.
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Post-translational modifications: Cytoplasmic/nuclear FGFR1 isoforms (detected via subcellular fractionation) may evade IHC detection .
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Alternative drivers: Co-occurring FGF3/4/19 amplifications may activate FGFR1-independent pathways .
Data Table 2: FGFR1 Amplification vs. Protein Expression
| Cohort (n=209) | Amplified (FISH) | IHC 3+ | Correlation (r) |
|---|---|---|---|
| ER+ Breast Cancer | 10% (21/209) | 4.3% (9/209) | 0.76 (p<0.0001) |
What experimental strategies mitigate off-target effects of FGFR1 antibodies?
Methodological Answer:
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Cross-reactivity screens: Test antibodies against FGFR2-4 and KLB (co-receptor) . For example, BFKB8488A (bispecific FGFR1/KLB antibody) shows <5% binding to FGFR2 .
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Fc engineering: Modify glycosylation at Asn-297 to reduce FcγR binding (e.g., afucosylation enhances ADCC for cancer immunotherapy) .
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Dose-response validation: In primate models, 10 mg/kg FGFR1 agonists induced sustained metabolic effects without thrombocytopenia .
How should persistent FGFR1 antibody responses be analyzed in longitudinal studies?
Methodological Answer:
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Titer thresholds: High IgG (>1,600) or IgM (>3,200) titers predict poor clinical outcomes (GBS disability score >4 at 6 months, p<0.001) .
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Persistence criteria: Define "persistent" as detectable titers at ≥3 months post-baseline .
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Treatment confounders: IVIg + methylprednisolone reduces IgG titers vs. plasma exchange (p=0.027) .
