AG18,

AG18,

AG18,

Min.Order / FOB Price:Get Latest Price

100 Gram

FOB Price: USD 1.0000

  • Min.Order :100 Gram
  • Purity: 98%
  • Payment Terms : L/C

Keywords

AG18, RARECHEM AL BX 0069;RG-50810;TYRPHOSTIN RG 50858;TYRPHOSTIN AG 18;TYRPHOSTIN A23;TYRPHOSTIN 23;ALPHA-CYANO-(3,4-DIHYDROXY)CINNAMONITRILE;AG 18 118409-57-7

Quick Details

  • Appearance:white crystalline solid
  • Application:CAS:118409-57-7; Small molecule inhibitors
  • PackAge:100g,500g,1kg,25kg/drum
  • ProductionCapacity:1000|Gram|Week
  • Storage:Dry seal
  • Transportation:shipping

Superiority:

We are specialized in custom synthesis, chemical/pharmaceutical/ pesticides outsourcing and contract research.
 
 
 
We are committed to provide excellence in researching, manufacturing and drug discovery process.
 
 
 
Our research team of scientists consists of western-trained Ph.D.s with experience and capabilities in drug R&D methodologies and medicinal chemistry.

 

Details:

AG-18(RG-50810; Tyrphostin A23) inhibits EGFR with IC50 of 40 μM.
IC50 Value: 40 uM (inhibition of EGFR autophosphorylation)[1]
Target: EGFR
AG-18 (Tyrphostin A23) are inhibitors of tyrosine kinases and function by binding to the active sites of the enzymes. Molecular modeling of tyrphostin A23 into the tyrosine-binding pocket in mu2 provides a structural explanation for A23 being able to inhibit the interaction between YXXPhi motifs and mu2.
in vitro: A23 inhibited the internalization of (125)I-transferrin in Heb7a cells without having any discernible effect on the morphology of compartments of the endocytic pathway. Control tyrphostins, active as inhibitors of tyrosine kinase activity, but incapable of inhibiting the YXXPhi motif/mu2 interaction, did not inhibit endocytosis [2]. Tyrphostin A23 inhibits Tfn internalization and redistributes most of hTfR to the plasma membrane [3]. TK-inhibiting A23 reversibly increased membrane conductance under conditions designed to minimize Na+, Ca2+, K+, and Na+-K+ pump currents [4].
in vivo: Pretreatment with the tyrosine kinase inhibitor Tyr-23 (50 microM, 10 min) caused a slow 40% increase in baseline [Ca(2+)](i). Tyr-23 attenuated peak and plateau responses to NE, both by approximately 70%. In the absence of extracellular Ca(2+) (0 Ca), Tyr-23 reduced the immediate [Ca(2+)](i) response to NE by approximately 60%, indicative of mobilization of internal stores, and abolished the plateau phase [5].
Clinical trial:
 

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