Bombesin/GRP receptor agonist derived from the pro-apoptotic protein BIM, which is a member of the BCL-2 family proteins and activates the BAX and BAK proteins to promote apoptosis.

The process of apoptosis can be activated by the intrinsic or extrinsic pathways, the former is activated by stress stimuli such as DNA damage and nutrient deficiency, while the latter is induced through activation of the death receptors FAS and TRAIL.

The BCL-2 family’s transmembrane anchor at the C-terminus allows them to locate at the mitochondrial outer membrane and play a vital role in apoptosis.

Within the mitochondria BIM is a member of the BH3 molecules alongside, BIM, PUMA and NOXA which can all be activated by the intrinsic pathway. These in turn can initiate the homo-oligomerisation of BAX and BAK which induce mitochondrial outer membrane permeabilisation (MOMP) and the release of cytochrome c into the cytosol. Here cytochrome c associates with APAF-1 and dATP, ultimately activating effector caspase3/7 and apoptosis.

BIM can be activated by CHOP-mediated transcription and phosphatase 2A-mediated dephosphorylation during endoplasmic reticulum stress. However when BIM is phosphorylated it undergoes degradation by the proteasome.