3 Results for "

hinge region residues

" in MedChemExpress (MCE) Product Catalog:
Products (3)

3 Results for "hinge region residues" in MCE Product Catalog:

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Cat. No.: HY-P11905
CAS No.: 874909-17-8
Research Areas:  

Others

FcIII peptide is a 13-amino-acid peptide that competitively binds the hinge region of IgG Fc fragment with high affinity. FcIII peptide has an inhibition constant Ki of 25 nM when competing with Protein A for binding sites. FcIII peptide displays high selectivity toward human IgG subtypes yet weak binding affinity for murine IgG1. FcIII peptide anchors IgG Fc through hydrophobic interactions formed by tryptophan and valine residues, alongside multiple hydrogen bonds and salt bridges. FcIII peptide alters the local microenvironment of conjugated fluorescein after binding IgG Fc, which triggers enhanced fluorescent signals. FcIII peptide can be applied to researches related to monoclonal antibody production. .
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Cat. No.: HY-187340
Target:  

c-Kit c-Fms

CSF1R/c-Kit-IN-1 is a CSF-1R and c-Kit inhibitor, with an IC50 of 5.88 nM against human CSF-1R and an IC50 of 1.47 nM against human c-Kit. CSF1R/c-Kit-IN-1 binds to the ATP-binding pocket of CSF-1R, forming a hinge interaction with Cys666 via the oxazole nitrogen atom and adjacent amino group, and binds to residues in the hydrophobic binding pocket. CSF1R/c-Kit-IN-1 binds to the ATP-binding pocket of c-Kit, maintains a hinge interaction through its 2-amino-oxazole core, and binds to a broader hydrophobic surface near the solvent-exposed region via its morpholine substituent. CSF1R/c-Kit-IN-1 inhibits CSF-1-induced phosphorylation of ERK, which is a downstream readout of the CSF-1R signaling pathway. CSF1R/c-Kit-IN-1 can be used in the research of neuroinflammation-related neurodegenerative diseases .
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Cat. No.: HY-182281
Target:  

FLT3 STAT Akt ERK Apoptosis

Research Areas:  

Cancer

FLT3-IN-41 is a highly potent FLT3 inhibitor. The IC50 values of FLT3-IN-41 against human FLT3-ITD and FLT3-WT are 3.16 nM and 294.7 nM, respectively. By binding to the ATP-binding pockets of FLT3-ITD and FLT3-WT and forming hydrogen bonds with hinge region residues and Phe830, FLT3-IN-41 inhibits the STAT5, Akt and Erk signaling pathways. FLT3-IN-41 induces G2/M phase arrest and promotes apoptosis in FLT3-ITD-positive acute myeloid leukemia cells, exhibiting significant antiproliferative activity. FLT3-IN-41 serves as a valuable tool for the study of acute myeloid leukemia .
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