Small molecule therapy pt 2

competes with the ATP for the binding site at the kinase which stops the functionality of the kinase because it cant bind to ATP

mutations in the drug target, which impacts drug binding, bypass signalling, which maintains oncogenic signalling and mutations in downstream effetors which causes alterations in genes regulating the cell cycle

by combining drugs - this increases potency and reduces the ability to develop drug resistance

<p>BCL-2 inhibitors</p> Signup and view all the answers

<p>extrinsic pathway and intrinsic pathway</p> Signup and view all the answers

<p>binding to a receptor activates caspases responsible for apoptosis</p> Signup and view all the answers

<p>BH3 mimetics bind to anti-apoptotic Bcl-2 family members, preventing them from trapping pro-apoptotic proteins like Bax/Bak. this leads to the activation of Bak/Bax and changes in the mitochondria leading to cell death.</p> Signup and view all the answers

<p>Rituximab</p> Signup and view all the answers

<p>mutations can cause BCL-2 to become resistant to BH3 mimetics, resistance can either be innate or acquired</p> Signup and view all the answers

<p>familial breast and ovarian cancer</p> Signup and view all the answers