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Based on 1 Customer Validation
REGN7999 is a monoclonal antibody that inhibits TMPRSS6. REGN7999 inhibits TMPRSS6 activity, preventing Hemojuvelin (HJV) lysis, thereby enhancing BMP6-HJV signaling and increasing serum hepcidin. REGN7999 ameliorates iron overload and impaired erythropoiesis in a β-thalassemia mouse model by inhibiting TMPRSS6 activity. REGN7999 is indicated for research in β-thalassemia.
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- Pureté : 98.00%
- CAS No.: 2996101-49-4
- Masse moléculaire:145.66 kDa
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
Isotype
Human IgG4 kappa
Recommend Isotype Controls
Species Reactivity
Human
IC50 & Target
TMPRSS6
In Vitro
REGN7999 blocks human and mouse TMPRSS6 activity, with IC50s of 0.68, 16 nM, and prevents HJV cleavage in overexpressing HJV and TMPRSS6 HEK293 cells[2].
REGN7999 bounds TMPRSS6 and inhibits TMPRSS6 activity across species, reduces proteolytic activity of human reference and variant TMPRSS6, cynomolgus monkey TMPRSS6, and mouse TMPRSS6[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
REGN7999 (5 mg/kg, s.c., once) increases serum hepcidin and decreases in serum iron in C57BL/6 mice model[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Hbbth3/+ mice model[1][2]
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Dosage:10 mg/kg
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Administration:s.c., once a week, 12 weeks
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Result:Reduced liver iron (~50% reduction compared to the isotype-treated group), improved RBC health as determined by reduced annexin V staining and RBC turnover, extend the RBC life span.
Elevated serum hepcidin and hepatic HAMP1 expression, did not increase markers of liver damage.
Reduced spleen weights to WT levels, displayed normalized reticulocyte numbers, blunted the increase in oxidative stress in blood and spleens, reduced bilirubin levels and lower expression levels of hepatic Hmox1, improved anaerobic capacity, increased bone mineral density.
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Animal Model:C57BL/6 mice model[2]
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Dosage:5 mg/kg
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Administration:s.c., once
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Result:Increased serum hepcidin, and decreased in serum iron, led to a significant drop of transferrin saturation and serum iron in the first 24 hours.
Essai clinique
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Gene ID
Accession
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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Human IgG4 kappa
Application
ELISA, FACS, Functional assay
Chemical Information
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CAS No. 2996101-49-4
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Appearance Liquid
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Masse moléculaire 145.66 kDa
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Color Colorless to light yellow
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SMILES
N/A
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Synonyms
REGN7999
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Livraison
Shipping with dry ice.
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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Perls' Prussian Blue Iron Staining
Perls' Prussian blue staining is a histochemical method used to detect non-heme ferric iron (Fe3+) in biological tissues by exploiting an acid-mediated release of loosely bound iron from storage complexes such as ferritin or hemosiderin, followed by its reaction with potassium ferrocyanide to form an insoluble blue ferric ferrocyanide (Prussian blue) precipitate that marks iron localization under light microscopy. The reaction is classically performed under acidic conditions, which liberate Fe3+ ions that subsequently bind ferrocyanide to generate the visible chromogen, enabling spatial visualization of iron deposits in tissues such as brain, liver, and spleen. Histochemical interpretations are limited to a reactive iron pool rather than total iron content, reflecting only histologically accessible iron species rather than tightly protein-bound iron.
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How to Choose the Right Model Animal
Choosing the right model animal is a validity-driven decision in which the species, strain, sex, age, genetic background, disease-induction method, outcome measures, and welfare burden must match the scientific question rather than laboratory tradition or convenience. A model should be selected by judging face validity, construct validity, and predictive validity: whether it resembles the human phenotype, whether it reproduces relevant mechanisms, and whether results are likely to predict human biology or treatment response. Animal studies often fail to translate because of species differences, weak disease resemblance, poor experimental design, inadequate reporting, publication bias, and underuse of randomization, blinding, and sample-size justification. Unresolved questions include how to rank competing models objectively, how much human-disease complexity must be reproduced for a given objective, and when non-animal systems such as organoids, ex vivo tissue, or computational models
Pureté et documentation
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Fiche technique (281 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Inhibitory Antibodies User Guide (603 KB)
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)