RKER-216
RKER-216 is a human monoclonal IgG antibody inhibitor targeting ALK2 with a KD of 58.7 pM. RKER-216 reduces hepcidin transcription in Hep3B.RKER-216 competes with BMP ligands for binding to the extracellular domain of ALK2, thereby inhibiting BMP-SMAD signal. RKER-216 mobilizes tissue iron effectively in inflammatory conditions. RKER-216 improves microcytic anemia in a dose-dependent manner by inhibiting SMAD signaling to reduce hepcidin and promote iron absorption and utilization in vivo. RKER-216 can be used for research on anemia of inflammation.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
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Biologische Aktivität
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Chemical Information
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Biologische Aktivität
Beschreibung
Species Reactivity
Human
IC50 & Target
[1]|
ACVR1 58.7 pM (Kd) |
In Vitro
RKER-216 (0.02-1 μg/mL, 6 h) binds to ALK2 with a KD of 58.7 pM, but does not bind to ALK3 at a concentration 10-fold higher than those necessary to bind ALK2[1].
RKER-216 achieves potential interactions between ALK2 with a robust peptide coverage of 92.2% in ACVR1 knockout in HepG2 and Huh7 cells[1].
RKER-216 (0.02-30 μg/mL,6 h) inhibits alk2-mediated hepcidin transcription in Hep3B cells (0.02-1 μg/mL), HepG2 (ACVR1 knockout (KO)) (1-30 μg/mL) and Huh7 cell (ACVR1 knockout (KO)) (1-30 μg/mL) [1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Hep3B, HepG2 (ACVR1 knockout (KO)), and Huh7 cell (ACVR1 knockout (KO)) cell lines
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Concentration:0.02, 0.2 and 1 μg/mL and 0, 1, 10 and 30 μg/mL
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Incubation Time:6 h
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Result:Resulted HAMP mRNA a dose dependent decrease (0.02, 0.2 and 1 μg/mL) in Hep3B cells.
Exhibited the greatest suppression in BMP6-stimulated hepcidin expression, followed by BMP2/6 and BMP2 in Hep3B cells at 0-1 μg/mL.
Did not decreased HAMP mRNA at 1-30 μg/mL in HepG2 (ACVR1 knockout (KO)) and Huh7 (ACVR1 knockout (KO)) cell lines.
In Vivo
RKER-216 (compound m216) (1-3 mg/kg, s.c., once, persisted for 6, 24 or 96 h) inhibited SMAD signaling to lower serum hepcidin, allowing more iron absorption to increase TSAT in TMPRSS6 KO mice[2].
RKER-216 (1 mg/kg, s.c., twice daily for 9 days) regulates iron metabolism through a unique mechanism that differs from intravenous iron in TMPRSS6 KO mice[2].
RKER-216 (1-3 mg/kg, s.c., twice daily for 3 weeks) g a dose proportional mitigation in improving microcytic anemia in TMPRSS6 KO mice[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:B6N male mice (7 weeks)[1]
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Dosage:3 mg/kg
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Administration:s.c. once followed by LPS (1 mg/kg, i.p.)
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Result:Induced Liver Il6 mRNA and decreased serum IL-6.
Resulted a greater fold-change ((11.7-fold for Hamp mRNA and 3.2-fold for serum hepcidin).
Inhibited SMAD1/5/9 phosphorylation regardless of inflammatory status.
Failed to impair LPS-mediated STAT3 phosphorylation, and the same LPS-induced effect was seen in isotype control groups in immunoblot analyses.
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Animal Model:TMPRSS6 KO mice (8-11 weeks) [2]
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Dosage:1 or 3 mg/kg
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Administration:s.c., once, persisted for 6, 24 or 96 h
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Result:Decreased liver smAD1/5/9 phosphorylation, hepcidin (Hamp) mRNA, and serum hepcidin levels dosed with 1 or 3 mg/kg for 6 h.
Decreased serum hepcidin by 88% and increased TSAT by 4-fold at 1 or 3 mg/kg for 24 h.
Had sustained effects by 96 h at 3 mg/kg.
Gene ID
Accession
Conjugated
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Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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Product Image
Anwendung
ELISA, FACS, Functional assay
Chemical Information
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Reinheit & Dokumentation
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Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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