Model NO.: Azd9291
Trademark: XXJLHGH
Transport Package: Silver Foil Bag
Specification: 1kg
Origin: China
HS Code: 3913900000
Model NO.: Azd9291
Trademark: XXJLHGH
Transport Package: Silver Foil Bag
Specification: 1kg
Origin: China
HS Code: 3913900000
99.8% Purity Pharmaceutical Raw Osimertinib Powder Azd9291 Mesylate for Lung Cancer 1421373-66-1

1. AZD-9291 Details:
Name:AZD-9291
Synonyms:N(2{[2(diMethylaMino)ethyl](Methyl)aMino}4Methoxy5{[4(1Methyl1Hindol3yl)pyriMidin2yl]aMino}phenyl)prop2enaMide;
N-[2-[[2-(Dimethylamino)ethyl]methylamino]-4-methoxy-5-[[4-(1-methyl-1H-indol-3-yl)-2-pyrimidinyl]amino]phenyl]-2-propenamide;AZD9291;
CAS:1421373-65-0 
MF:C28H33N7O2 
MW:499.61 
Feature:Orally bioavailable mutant-selective EGFR inhibitor that has been tested in Phase III clinical trials for treatment of Non-Small Cell Lung Cancer.

2. AZD-9291 Usage:
Cell lines.
Human lung cancer cells with EGFR-mutations or wild type EGFR stable expression

Preparation method
The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.
 
3. AZD-9291 Application:
AZD9291 administered once daily orally at 5 mg/kg caused profound regression of tumours across EGFRm+ (PC9; 178% growth inhibition) and EGFRm+/T790M (H1975; 119% growth inhibition) tumour models in vivo,after 14 days dosing. Furthermore 5 mg/kg AZD9291 was sufficient to cause significant shrinkage of EGFRm+ and EGFRm+/T790M transgenic mouse lung tumours. Tumour growth inhibition was associated with profound inhibition of EGFR phosphorylation and key downstream signaling pathways such as AKT and ERK. Chronic long-term treatment of PC9 and H1975 xenograft tumours with AZD9291 led to a complete and sustained macroscopic response, with no visible tumours after 40 days dosing, and being maintained beyond 100 days. Furthermore, pre-clinical data also indicates that AZD9291 could target tumours that have acquired resistance to the more recently identified HER2-amplification mechanism, thus potentially extending its benefit in TKI resistant patients.


  99.8% Purity Pharmaceutical Raw Osimertinib Powder Azd9291 Mesylate for Lung Cancer 1421373-66-1

1. AZD-9291 Details:
Name:AZD-9291
Synonyms:N(2{[2(diMethylaMino)ethyl](Methyl)aMino}4Methoxy5{[4(1Methyl1Hindol3yl)pyriMidin2yl]aMino}phenyl)prop2enaMide;
N-[2-[[2-(Dimethylamino)ethyl]methylamino]-4-methoxy-5-[[4-(1-methyl-1H-indol-3-yl)-2-pyrimidinyl]amino]phenyl]-2-propenamide;AZD9291;
CAS:1421373-65-0 
MF:C28H33N7O2 
MW:499.61 
Feature:Orally bioavailable mutant-selective EGFR inhibitor that has been tested in Phase III clinical trials for treatment of Non-Small Cell Lung Cancer.

2. AZD-9291 Usage:
Cell lines.
Human lung cancer cells with EGFR-mutations or wild type EGFR stable expression

Preparation method
The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.
 
3. AZD-9291 Application:
AZD9291 administered once daily orally at 5 mg/kg caused profound regression of tumours across EGFRm+ (PC9; 178% growth inhibition) and EGFRm+/T790M (H1975; 119% growth inhibition) tumour models in vivo,after 14 days dosing. Furthermore 5 mg/kg AZD9291 was sufficient to cause significant shrinkage of EGFRm+ and EGFRm+/T790M transgenic mouse lung tumours. Tumour growth inhibition was associated with profound inhibition of EGFR phosphorylation and key downstream signaling pathways such as AKT and ERK. Chronic long-term treatment of PC9 and H1975 xenograft tumours with AZD9291 led to a complete and sustained macroscopic response, with no visible tumours after 40 days dosing, and being maintained beyond 100 days. Furthermore, pre-clinical data also indicates that AZD9291 could target tumours that have acquired resistance to the more recently identified HER2-amplification mechanism, thus potentially extending its benefit in TKI resistant patients.


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