Flashcards in Fitz- CML Module Deck (11):
What is the general MOA for STIs?
They bind to to the ATP binding site of TK
What are the general SE of STIs?
Generally have fewer SE than conventional therapies because they are target toward the specific defect of a particular cancer.
CAN cause CHF and MYOCARDIAL INFARCTION
Why is Imatinib so successful?
Targets a genetic defect that is perfectly selective to cancer cells
What are the TUs for imatinib?
Complete hematological/cytological response in 85-95% of pts w/ chronic CML
Delay death in 25% of pts in blast crisis
Gastroinstestinal stormal tumors expressing c-kit
Where does imatinib act?
Competitive antagonist at the ATP binding site of:
c-KIT--altered in GIST
What does DASTAINIB specifically target?
A TK whose expression is up-regulated in several types of cancer
What are common toxicities associated w/ imatinib?
What are the therapeutic uses for gefitinib and erolotinib? What is weird about it in terms of efficacy?
Metastatic non-small cell lung cancer after failure of standard chemotherapies
different populations experience varying efficacies--> having the right mutation means the diff between a cure and a response
What is the MOA for efitinib and erolotinib? what does it commonly target?
competitive antagonists of ATP binding site of EGFR TK
EGFR TK is overexpressed in epithelial derived cancers
Interstitial pneumonia is associated w/ what drugs?
Erlotinib and gefitinib